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Andre, Jane. "Earthworm adaptations to metals : inorganic speciation, biochemical fingerprinting and molecular genetics." Thesis, University of Reading, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497024.
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An organisms' ability to adapt to environmental stress and tolerate novel habitats remains one of the most intriguing phenomena in evolutionary biology. This study examined the lead-related microevolutionary responses of the cosmopolitan earthworm species Lumbricus rubellus inhabiting contrasting metalliferous soils: circumneutra Cwmystwyth Cottage (CC) and Draethen Hollow (DH), acidic Cwmystwyth Stream (CS), East (E) and MWest (W) and unpolluted reference sites, Pontcanna (P) and Dinas Powys (DP). Techniques used ranged from mitochondrial (COII) and nuclear (AFLP) genotyping markers, cellular fractionation, synchrotron-based whole-worm X-ray absorption spectroscopy (XAS: EXAFS and XANES), biochemical fingerprinting of individual cells by high energy Fourier-Transform Infra-Red (FTIR) microspectroscopy, and a variety of molecular-genetic tools including Expressed Sequence Tag (EST) sequencing of Pb-exposed worms (www.earthworms.org) and specific target gene sequencing.
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Golińska, Monika Anna. "The molecular and metabolic adaptations of HIF-1β deficient tumour cells." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609977.
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Brown, Elizabeth Anne. "Metabolic Adaptations in Modern Human Populations: Evidence, Theory, and Investigation." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17463979.
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Diverse climates, infectious agents, and subsistence patterns drove humans to adapt metabolically to different environments since the migration out of Africa 100,000 years ago. In this dissertation, I review current literature on the genetic underpinnings, and the molecular and physiological manifestations of these metabolic adaptations in diverse human populations. Then, I develop a theory regarding pregnancy as a critical period in life history that mediated recent selection on human metabolism. Finally, I investigate the function and evidence for selection of derived genetic variants at increased frequency in East Asian populations. I find multiple standing variants that increase expression of the gene IVD and increase the efficiency of leucine catabolism, which lie on positively selected haplotypes in East Asians. I use this research process as a model for how to develop and study novel hypotheses of human metabolic adaptation. Such adaptations often impact health in the modern environment, so more evolutionary research will provide useful guidance to the medical community in how to treat people from diverse ethnicities.Human Evolutionary Biology
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Calay, Ediz Suha. "Cellular and Systemic Metabolic Adaptations to Energy Status." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11547.
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Hussain, Muhammad Zubair. "Molecular Adaptations in the Endogenous Opioid System in Human and Rodent Brain." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-205133.
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The aims of the thesis were to examine i) whether the endogenous opioid system (EOS) is lateralized in human brain areas involved in processing of emotions and pain; ii) whether EOS responses to unilateral brain injury depend on side of lesion, and iii) whether in human alcoholics, this system is involved in molecular adaptations in brain areas relevant for cognitive control of addictive behavior and habit formation. The main findings were that (1) opioid peptides but not opioid receptors and classic neurotransmitters are markedly lateralized in the anterior cingulate cortex involved in processing of positive and negative emotions and affective component of pain. The region-specific lateralization of neuronal networks expressing opioid peptides may underlie in part lateralization of higher functions in the human brain including emotions and pain. (2) Analysis of the effects of traumatic brain injury (TBI) demonstrated predominant alteration of dynorphin levels in the hippocampus ipsilateral to the injury, while injury to the right hemisphere affected dynorphin levels in the striatum and frontal cortex to a greater extent than that to the left hemisphere. Thus, trauma reveals a lateralization in the mechanisms mediating the response of dynorphin expressing neuronal networks in the brain. These networks may differentially mediate effects of left or right brain injury on lateralized brain functions. (3) In human alcoholics, the enkephalin and dynorphin systems were found to be downregulated in the caudate nucleus and / or putamen that may underlie in part changes in goal directed behavior and formation of a compulsive habit in alcoholics. In contrast to downregulation in these areas, PDYN mRNA and dynorphins in dorsolateral prefrontal cortex, k-opioid receptor mRNA in orbitofrontal cortex, and dynorphins in hippocampus were upregulated in alcoholics. Activation of the k-opioid receptor by upregulated dynorphins may underlie in part neurocognitive dysfunctions relevant for addiction and disrupted inhibitory control. We conclude that the EOS exhibits region-specific lateralization in human brain and brain-area specific lateralized response after unilateral TBI in mice; and that the EOS is involved in adaptive processes associated with specific aspects of alcohol dependence.
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Bovdilova, Anastasiia [Verfasser]. "Molecular adaptations and post-translational regulation of C4-NADP-malic enzyme / Anastasiia Bovdilova." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1210700492/34.
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Hales, Kimberly. "Neuronal and Molecular Adaptations of GABA Neurons in the Ventral Tegmental Area to Chronic Alcohol." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd2182.pdf.
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Philip-Couderc, Pierre. "ADAPTATIONS DU SYSTEME NERVEUX VEGETATIF ET DU TRANSCRIPTOME CARDIAQUE AU COURS DE L'OBESITE." Phd thesis, Université Paul Sabatier - Toulouse III, 2004. http://tel.archives-ouvertes.fr/tel-00105596.
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La prévalence de l'obésité suit une progression sans précédent dans les pays industrialisés et augmente dramatiquement la morbimortalité cardiovasculaire. Le développement excessif du tissu adipeux a un impact direct sur le tissu myocardique au travers des peptides et cytokines qu'il sécrète et un impact indirect au travers de l'augmentation de la volémie. Ces changements induisent des modifications de l'expression génique dans les cardiomyocytes et les fibroblastes cardiaques. Par exemple, l'expression du récepteur M2 diminue dans l'OD de chiens rendus obèses hypertendus.Dans ce modèle canin, nous avons montré dans la voie M2/eNOS qu'il existait des régulations compensatoires au niveau de la eNOS. Nous avons également montré que l'adrénomedulline, peptide impliqué dans l'homéostasie tensionnelle et sécrété par le tissu adipeux, détermine la surexpression compensatoire du récepteur M2, dans le modèle de cardiomyocytes de la lignée P19.
Nous avons entrepris une étude globale au niveau du transcriptome dans le but d'identifier l'ensemble des modifications induites dans le cœur de l'obèse. Ces études, dans le modèle de chien obèse hypertendu, puis chez l'Homme ont montré que le cœur de l'obèse modifiait très précocement l'expression de ses gènes et qu'il avait un profil transcriptionnel unique. Ces régulations convergent notamment vers la voie TGF Β et la voie Wnt, toutes deux normalement impliquées dans la cardiogénèse. Enfin, ces travaux ont initié l'étude de gènes nouveaux inconnus (PPR1 & PPR2).
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Moustafa, Moustafa Bayoumi. "Molecular adaptations of cardiac and skeletal muscles to endurance training in a canine model of sudden death." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1133375886.
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van, der Vaart Andrew D. "Molecular Brain Adaptations to Ethanol: Role of Glycogen Synthase Kinase-3 Beta in the Transition to Excessive Consumption." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5510.
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Alcoholism is a complex neuropsychiatric disease that is characterized by compulsive alcohol use and intensifying cravings and withdrawals, often culminating in physiologic dependency. Fundamental alterations in brain chemistry underlie the transition from initial ethanol exposure to repetitive excessive use. Key mediators of this adaptation include changes in gene expression and signal transduction. Here we investigated gene expression pathways in prefrontal cortex and nucleus accumbens following acute or chronic ethanol treatment, to identify genes with potentially conserved involvement in the long-term response of the corticolimbic system to repeated ethanol exposure. We investigated Gsk3b, which encodes glycogen synthase kinase 3-beta, as a highly ethanol responsive gene associated with risk for long-term maladaptive responses to ethanol. On the level of the protein, we found that GSK3B and to a lesser extent the GSK3A isoform showed robust increases in inhibitory phosphorylation following acute ethanol. This inhibition may underlie aspects of the behavioral response to acute ethanol, as pre-treatment with a GSK3B inhibitor (tideglusib) augmented ethanol’s locomotor effects. Following long term ethanol exposure, we re-tested GSK3B phosphorylation and found that its ethanol response is blunted, consistent with molecular tolerance as a corollary to increased consumption. As the prefrontal cortex (PFC) plays a vital role in the reward pathway via its glutamatergic projections to the nucleus accumbens, we investigated the role of the Gsk3b gene specifically in PFC and in glutamatergic neurons. Overexpression of Gsk3b in the PFC robustly increased ethanol consumption, while deletion in Camk2a-positive neurons significantly attenuated ethanol consumption. Pharmacologic antagonism of GSK3B also decreased drinking in a model of binge-like consumption. Collectively this data implicates GSK3B as a mediator of excessive ethanol intake via its kinase activity, wherein inhibition of the kinase via phosphorylation exerts a protective effect in the context of acute ethanol, but desensitizes with repeated exposure.
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Malinovska, Liliana. "Specific adaptations in the proteostasis network of the social amoebae Dictyostelium discoideum lead to an unusual resilience to protein aggregation." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-144848.
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A key prerequisite for cellular and organismal health is a functional proteome. A variety of human protein misfolding diseases are associated with the occurrence of amyloid protein aggregates, such as amyotrophic lateral sclerosis (ALS) or Huntington’s disease. The proteins involved in disease manifestation all contain aggregation-prone sequences of low compositional complexity. Such sequences are also known as prion-like, because of their sequence similarity to yeast prions. Yeast prion proteins are a specific subset of amyloid forming proteins with distinct physio-chemical and functional features, which give them transmissible properties. The aggregation properties of yeast prions and disease-related prion-like proteins reside in structurally independent, prion-forming domains (PrDs). These domains are highly enriched for uncharged polar amino acids, such as glutamine (Q) and asparagine (N). These compositional features can be used to predict prion-like proteins bioinformatically. To investigate the prevalence of prion-like proteins across different organisms, we analyzed a range of eukaryotic proteomes. Our analysis revealed that the slime mold D. discoideum contains the highest number of prion-like N/Q-rich proteins of all organisms. Based on this finding, we hypothesized that D. discoideum could be a valuable model system to study protein homeostasis (proteostasis) and the molecular basis of protein misfolding diseases. To explore how D. discoideum manages its highly aggregation-prone proteome, we analyzed the behavior of several well-characterized misfolding-prone marker proteins (variants of the disease-causing exon 1 of the huntingtin protein as well as wildtype and variant versions of the Q/N-rich yeast prion Sup35NM). Intriguingly, these proteins did not form cytosolic aggregates in D. discoideum, as they do in other organisms. Aggregates, however, formed as a result of heat stress, which indicates that the tested proteins have the capacity to aggregate, but are kept under tight control under normal conditions. Furthermore, when the stress level was reduced, the stress-induced aggregates dissolved, suggesting that D. discoideum has evolved mechanisms to reverse aggregation after a period of acute stress. Together, these findings reveal an unusual resilience of D. discoideum to aggregation-prone proteins, which very likely results from specific adaptations in its proteostasis network. By studying these specific adaptations, we could get important insight into the strategies that nature employs to control and maintain a highly aggregation-prone proteome. So far, our experimental investigations have revealed evidence for three specific adaptations. First, we identified the disaggregase Hsp101 as a key player in the acute stress response of D. discoideum. A functional analysis of Hsp101 in yeast and D. discoideum revealed that it supports thermotolerance. Second, we found evidence for an important role of the nucleus and nucleolus in proteostasis. We discovered that a small fraction of highly aggregation-prone proteins accumulated in the nucleus or nucleolus of D. discoideum cells. The magnitude of this nuclear accumulation could be increased by proteasome impairment, which suggests that the ubiquitin-proteasome system (UPS) is involved. This finding is consistent with previous studies in other organisms and hints at the possibility that D. discoideum disposes of aggregation-prone proteins by degrading them in the nucleus/nucleolus. Third and finally, we found that cells containing nuclear accumulations are asymmetrically distributed in the multicellular developmental stage (slug), suggesting that D. discoideum employs cell-sorting mechanisms to dispose of cells with accumulated protein damage. Although our current understanding of proteostasis in D. discoideum is preliminary, we have gained important insight into the molecular mechanisms and cellular pathways that D. discoideum uses to counteract protein aggregation. Findings from this work will inform similar comparative studies in other organisms and will impact our molecular understanding of protein misfolding diseases and agingEine wesentliche Voraussetzung für die Gesundheit von Zellen und Organismen ist ein funktionales Proteom. Eine Reihe von humanen Protein- Missfaltungs-Erkrankungen, wie Chorea Huntington und Amyotrophe Lateralsklerose (ALS) werden mit dem Auftreten von amyloiden Protein- Aggregaten in Verbindung gebracht. Sämtliche Proteine, die in der Pathogenese dieser Krankheiten eine Rolle spielen, enthalten aggregations-anfällige Sequenzen mit geringer Sequenzkomplexität. Solche Sequenzen werden als Prion-ähnlich bezeichnet, da sie in ihrer Zusammensetzung den Prionen aus der Hefe S. cerevisiae gleichen. Die Prion-Proteine der Hefe gehören zu einer Unterart von amyloid-aggregierenden Proteinen, die durch bestimmte physikochemische und funktionelle Eigenschaften einen infektiösen Charakter erhalten. Die Aggregations-Eigenschaften von Hefeprionen und aggregationsanfällige Proteinen, die mit Erkrankungen in Verbindung gebracht werden, basieren auf strukturell unabhängigen, Prion-bildenden Domänen (prion domain, PrD). Diese Domänen sind angereichert mit polaren Aminosäuren wie Glutamin und Asparagin. Diese Zusammensetzung kann dazu verwendet werden prion-ähnliche Proteine bioinformatisch vorherzusagen. Um die Verbreitung von Prion-ähnlichen Proteinen in verschiedenen Organismen zu untersuchen, analysierten wir eine Reihe von eukaryotischen Proteomen. Unsere Analyse zeigte, dass der Schleimpilz D. discoideum die höchste Anzahl von Prion-ähnlichen N/Q-reichen Proteinen aufzeigt. Aufgrund dieser Erkenntnisse erstellten wir die Hypothese, dass D. discoideum ein nützlicher Modellorganismus sein könnte, um Protein Homöostase (Proteostase) sowie die molekulare Basis von Proteins-Missfaltungs-Erkrankungen zu ergründen. Um zu analysieren, wie D. discoideum mit seinem höchst aggregations-anfälligen Proteom umgehen kann, untersuchten wir das Verhalten mehrerer bereits charakterisierter aggregations-anfälliger Marker-Proteine in D. discoideum. Hierbei verwendeten wir Varianten des krankheits-erzeugenden Exon 1 des humanen Huntingtin Protein sowie den wild-typ und Varianten des N/Q-reichen Hefe Prions Sup35. Interessanterweise bildeten diese Proteine, anders als in anderen Organismen, keine zytosolischen Aggregate in D. discoideum aus. Aggregate wurden jedoch unter Hitzestress-Bedingungen gebildet. Dies deutet darauf hin, dass die getesteten Proteine durchaus das Vermögen zu aggregieren besitzen, jedoch unter normalen Wachstumsbedingungen streng kontrolliert werden. Wenn, darüberhinaus das Stress- Level gesenkt wurde, kam es zur Auflösung der stress-induzierten Aggregate. Dies deutet darauf hin, dass D. discoideum Mechanismen entwickelt hat, um Aggregate nach Perioden von akutem Stress wieder aufzulösen. Zusammengenommen enthüllen diese Erkenntnisse eine ungewöhnliche Widerstandsfähigkeit gegenüber aggregations-anfälligen Proteinen. Diese beruht höchstwahrscheinlich auf spezifischen Modifikationen im Proteostase Netzwerk. Durch die Analyse dieser spezifischen Anpassungen könnten wichtige Einblicke in die Strategien gewährt werden, welche die Natur benutzt, um ein höchst aggregations-anfälliges Proteom zu erhalten und zu kontrollieren. Bisher erbrachten unsere Experimente Anhaltspunkte für drei spezifische Anpassungen. Erstens zeigten wir, dass die Disaggregase Hsp101 eine Schlüsselrolle in der akuten Stressantwort in D. discoideum einnimmt. Eine funktionale Analyse von Hsp101 in D. discoideum und Hefe zeigte, dass die Disaggregase Thermotoleranz fördert. Zweitens haben wir Anhaltspunkte, dass der Nukleus und der Nukleolus eine wichtige Rolle in der Proteostase einnehmen. Eine geringe Fraktion der überaus aggregations-anfälligen Proteine akkumuliert im Nukleus oder Nukleolus von D. discoideum. Das Ausmaß der nuklearen Akkumulation konnte erhöht werden, wenn das Proteasom beeinträchtigt wird. Dies deutet darauf hin, dass das Ubiquitin-Proteasom-System involviert sein könnte. Diese Beobachtung ist im Einklang mit jüngsten Berichten aus anderen Organismen und daraus folgt, dass D. discoideum möglicherweise aggregations-anfällige Proteine durch Abbau im Nukleus entsorgt. Drittens konnten wir feststellen, dass Zellen, die nukleare Akkumulationen enthalten, asymmetrisch in der multizellulären Entwicklungs-Struktur des Pseudoplasmodiums verteilt sind. Dies deutet darauf hin, dass D. discoideum möglicherweise den Zellsortierungsmechanismus während der Entwicklung nutzen kann, um Zellen mit angereicherten Protein-Schäden zu beseitigen. Auch wenn das gegenwärtige Verständnis der Proteostase in D. discoideum nur vorläufig ist, haben wir wichtige Einblicke in die molekularen Mechanismen und zellulären Prozesse erhalten, die D. discoideum verwendet, um Protein-Aggregation zu verhindern. Die Ergebnisse dieser Arbeit werden ähnliche vergleichende Studien in anderen Organismen beeinflussen und Auswirkungen auf unser molekulares Verständnis über Protein-Missfaltungs-Erkrankungen und das Altern haben
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Rittershaus, Emily S. C. "Identification of Essential Metabolic and Genetic Adaptations to the Quiescent State in Mycobacterium Tuberculosis: A Dissertation." eScholarship@UMMS, 2012. http://escholarship.umassmed.edu/gsbs_diss/876.
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Mycobacterium tuberculosis stably adapts to respiratory limited environments by entering into a nongrowing but metabolically active state termed quiescence. This state is inherently tolerant to antibiotics due to a reduction in growth and activity of associated biosynthetic pathways. Understanding the physiology of the quiescent state, therefore, may be useful in developing new strategies to improve drug efficiency. Here, we used an established in vitro model of respiratory stress, hypoxia, to induce quiescence. We utilized metabolomic and genetic approaches to identify essential and active pathways associated with nongrowth. Our metabolomic profile of hypoxic M. tuberculosis revealed an increase in several free fatty acids, metabolite intermediates in the oxidative pathway of the tricarboxylic acid (TCA) cycle, as well as, the important chemical messenger, cAMP. In tandem, a high-throughput transposon mutant library screen (TnSeq) revealed that a cAMP-regulated protein acetyltransferase, MtPat, was conditionally essential for survival in the hypoxic state. Via 13C-carbon flux tracing we show an MtPat mutant is deficient in re-routing hypoxic metabolism away from the oxidative TCA cycle and that MtPat is involved in inhibiting fatty-acid catabolism in hypoxia. Additionally, we show that reductive TCA metabolism is required for survival of hypoxia by depletion of an essential TCA enzyme, malate dehydrogenase (Mdh) both in in vitro hypoxia and in vivo mouse infection. Inhibition of Mdh with a novel compound resulted in a significantly greater killing efficiency than the first-line anti-M. tuberculosis drug isoniazid (INH). In conclusion, we show that understanding the physiology of the quiescent state can lead to new drug targets for M. tuberculosis.
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Rittershaus, Emily S. C. "Identification of Essential Metabolic and Genetic Adaptations to the Quiescent State in Mycobacterium Tuberculosis: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/876.
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Mycobacterium tuberculosis stably adapts to respiratory limited environments by entering into a nongrowing but metabolically active state termed quiescence. This state is inherently tolerant to antibiotics due to a reduction in growth and activity of associated biosynthetic pathways. Understanding the physiology of the quiescent state, therefore, may be useful in developing new strategies to improve drug efficiency. Here, we used an established in vitro model of respiratory stress, hypoxia, to induce quiescence. We utilized metabolomic and genetic approaches to identify essential and active pathways associated with nongrowth. Our metabolomic profile of hypoxic M. tuberculosis revealed an increase in several free fatty acids, metabolite intermediates in the oxidative pathway of the tricarboxylic acid (TCA) cycle, as well as, the important chemical messenger, cAMP. In tandem, a high-throughput transposon mutant library screen (TnSeq) revealed that a cAMP-regulated protein acetyltransferase, MtPat, was conditionally essential for survival in the hypoxic state. Via 13C-carbon flux tracing we show an MtPat mutant is deficient in re-routing hypoxic metabolism away from the oxidative TCA cycle and that MtPat is involved in inhibiting fatty-acid catabolism in hypoxia. Additionally, we show that reductive TCA metabolism is required for survival of hypoxia by depletion of an essential TCA enzyme, malate dehydrogenase (Mdh) both in in vitro hypoxia and in vivo mouse infection. Inhibition of Mdh with a novel compound resulted in a significantly greater killing efficiency than the first-line anti-M. tuberculosis drug isoniazid (INH). In conclusion, we show that understanding the physiology of the quiescent state can lead to new drug targets for M. tuberculosis.
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Rojas-Rodriguez, Raziel. "Adaptations of Adipose Tissue Expandability in Gestation are Associated with Maternal Glucose Metabolism." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1048.
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Pregnancy induces maternal metabolic adaptations including mild glucose intolerance and weight gain in order to support fetal development and lactation. Adipose tissue (AT) function in gestation is featured by reduced insulin sensitivity and fat mass accrual which partly accounts for the weight gain in pregnant women and adaptation of glucose metabolism. A common metabolic pregnancy complication is gestational diabetes mellitus (GDM), a disease characterized by impaired glucose tolerance with onset in gestation. However, the relationship between AT expandability and glucose metabolism in gestation is not well understood. The goal of this thesis was to investigate the adaptations of human AT expansion induced by pregnancy, how these changes are reflected in pregnancies complicated with GDM and characterize a mouse model to study the mechanisms underlying this disease. This dissertation illustrates that pregnancy promotes AT expandability by a signaling mechanism between placental pregnancy-associated plasma protein-A (PAPP-A) and AT- insulin-like growth factor binding protein-5 (IGFBP5). In addition, gravidas with GDM showed impaired AT expansion. Studies investigating the relationship between PAPP-A and glycemic state demonstrated that low levels of PAPP-A in the 1sttrimester are highly associated with the development of GDM. Moreover, PAPP-A knockout mice exhibit reduced insulin sensitivity and impaired AT growth exclusively in gestation. These results expand the knowledge of AT biology in gestation and have the potential to improve maternal care by proposing PAPP-A as an early biomarker and possible therapeutic for GDM. It also introduces a new mouse model to study the etiology of gestational diabetes.
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Romero, Pedro [Verfasser], Markus [Akademischer Betreuer] [Gutachter] Pfenninger, and Imke [Gutachter] Schmitt. "Evolution of the terrestrial invasion in Panpulmonata (Mollusca, Gastropoda): molecular adaptations in the context of realm transitions / Pedro Romero ; Gutachter: Markus Pfenninger, Imke Schmitt ; Betreuer: Markus Pfenninger." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2017. http://d-nb.info/1138276863/34.
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Kremer, Débora. "O GÊNERO TILLANDSIA L. (BROMELIACEAE-TILLANDSIOIDEAE) NO ESTADO DO PARANÁ, BRASIL." UNIVERSIDADE ESTADUAL DE PONTA GROSSA, 2011. http://tede2.uepg.br/jspui/handle/prefix/952.
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Tillandsia L. is the largest genus of the subfamily Tillandsioideae (Bromeliaceae) with ca. 557 species. It is distributed from the southern U. S. A to central Argentina and Chile. Traditionally the genus has been divided into seven subgenera: Tillandsia subg. Allardtia (A. Dietrich) Baker, Tillandsia subg. Anoplophytum (Beer) Baker, Tillandsia subg. Phytarrhiza (Vis.) Baker, Tillandsia subg. Diaphoranthema (Beer) Baker, Tillandsia subg. Tillandsia L., Tillandsia subg. Pseudalcantarea Mez and Tillandsia subg. Pseudo-Catopsis Baker. The taxonomic study of the species Tillandsia in the Paraná state was presented. Were found 17 species in 4 subgenera:Tillandsia subg. Diaphoranthema -Tillandsia loliacea Mart. ex Schult. & Schult.f., Tillandsia recurvata (L.) L, Tillandsia tricholepis Baker and Tillandsia usneoides (L.) L.; Tillandsia subg. Anoplophytum -Tillandsia didisticha (E. Morren) Baker, Tillandsia gardneri Lindley, Tillandsia geminiflora Brong., Tillandsia lineares Vell., Tillandsia lorentziana Griseb.; Tillandsia pohliana Mez, Tillandsia recurvifolia Hooker, Tillandsia stricta Solander, Tillandsia tenuifolia L.; Tillandsia subg. Phytarrhiza - Tillandsia crocata (E. Morren) Baker, Tillandsia streptocarpa Baker; Tillandsia mallemontii Glazou ex Mez e Tillandsia subg. Tillandsia -Tillandsia polystachia (L.) L.. Identification Keys, as well as descriptions, illustrations, comments and distribuition patterns are presented. The results show that the Paraná has a high species richness when compared to neighboring states. Besides the taxonomic study, there were some evolutionary adaptations of species, fitting them in ecophysiological types proposed in the literature. Only T. polystachia presents wide rosette forming tank. The remaining species are characterized by the absence of the tank, the presence or absence of non-root in adulthood and four species were found to be minimized.
Tillandsia L. é o maior gênero da subfamília Tillandsioideae (Bromeliaceae) com 557 espécies, distribuídas desde o sul dos Estados Unidos até a Argentina e o Chile. Tradicionalmente, está dividido em sete subgêneros: Tillandsia subg. Allardtia (A. Dietrich) Baker, Tillandsia subg. Anoplophytum (Beer) Baker, Tillandsia subg. Phytarrhiza (Vis.) Baker, Tillandsia subg. Diaphoranthema (Beer) Baker, Tillandsia subg. Tillandsia L., Tillandsia subg. Pseudalcantarea Mez e Tillandsia subg. Pseudo- Catopsis Baker. Um estudo taxonômico de Tillandsia no Estado do Paraná foi realizado e foram encontrados 17 táxons, distribuídos em 4 subgêneros: Tillandsia subg. Diaphoranthema -Tillandsia loliacea Mart. ex Schult. & Schult.f., Tillandsia recurvata (L.) L, Tillandsia tricholepis Baker e Tillandsia usneoides (L.) L.; Tillandsia subg. Anoplophytum - Tillandsia didisticha (E. Morren) Baker, Tillandsia gardneri Lindley, Tillandsia geminiflora Brong., Tillandsia lineares Vell., Tillandsia lorentziana Griseb.; Tillandsia pohliana Mez, Tillandsia recurvifolia Hooker, Tillandsia stricta Solander, Tillandsia tenuifolia L.; Tillandsia subg. Phytarrhiza - Tillandsia crocata (E. Morren) Baker, Tillandsia streptocarpa Baker; Tillandsia mallemontii Glazou ex Mez e Tillandsia subg. Tillandsia – com apenas uma espécie Tillandsia polystachia (L.) L.. São apresentadas chaves de identificação, descrições, comentários,ilustrações e distribuição geográfica de cada táxon. Os resultados revelaram que a riqueza de espécies de Tillandsia no Paraná é maior quando comparada aos Estados vizinhos. Além do estudo taxonômico, foram observadas algumas adaptações evolutivas das espécies, enquadrando-as nos tipos ecofisiológicos propostos em literatura. Apenas T. polystachia apresenta roseta ampla formando tanque. As demais espécies são caracterizadas pela ausência de tanque, a presença ou não de raiz na fase adulta e quatro delas, foram consideradas espécies minimizadas.
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Coffey, Vernon Glenn, and vernon coffey@rmit edu au. "The Molecular Bases of Training Adaptation." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070131.123552.
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The molecular events that promote or inhibit specific training adaptations (i.e. skeletal muscle hypertrophy or mitochondrial biogenesis) are not completely understood. Accordingly, there is a need to better define both the acute and chronic responses to divergent exercise stimuli in order to elucidate the specific molecular mechanisms that ultimately determine skeletal muscle phenotype. Therefore, the primary aims of the studies undertaken for this thesis were to examine the acute molecular adaptation responses in skeletal muscle following resistance and endurance training. In order to determine the acute molecular events following repeated bouts of exercise, the study described in Chapter Two compared a high-frequency stacked training regimen designed to generate a summation of transient exercise-induced signalling responses with a conventional-frequency resistance training protocol. Groups (n= 6) of Sprague-Dawley rats performed either high-frequency training (four exercise bouts consisting of 3 - 10 repetitions separated by 3 h) or conventional-frequency training (three exercise bouts consisting of 4 - 10 repetitions with 48 h between sessions). Protocols were matched for total work, and repetitions were performed at 75% one-repetition maximum with 3 min recovery between sets. White quadriceps muscle was extracted 3 h after every training bout, and 24 and 48 h following the final exercise session of each protocol. AKT phosphorylation was significantly decreased 3 h following the 2nd bout of high-frequency training, an effect that persisted until 48 h after the final exercise bout (P less than 0.05), while the phosphorylation state of this kinase was unchanged with conventional training. These results suggest that high-frequency training suppressed IGF-1 mediated signalling. Furthermore, high-frequency training generated sustained and coordinated increases in TNFá and IKK phosphorylation (P less than 0.05), indicating an extended response of inflammatory signalling pathways. Conversely, and irrespective of an initial increase after the first bout of exercise, TNFá signalling ultimately returned to control Abstract values by DAY 5 of conventional-frequency training, indicative of a rapid adaptation to the exercise stimulus. Notably, despite differential AKT activation there were similar increases in p70 S6K phosphorylation with both training protocols. These results indicate high-frequency resistance training extends the transient activation of inflammatory cytokine-mediated signalling and results in a persistent suppression of AKT phosphorylation, but these events do not appear to inhibit kinase activity proximal to translation initiation. The aim of the study described in Chapter Three was to determine the effect of prior training history on selected signalling responses after an acute bout of resistance and endurance exercise. Following 24 h diet / exercise control 13 male subjects (7 strength-trained and 6 endurance-trained) performed a random order of either resistance (8 x 5 maximal leg extensions) or endurance exercise (1 h cycling at 70% peak O2 uptake). Muscle biopsies were taken from the vastus lateralis at rest, immediately and 3 h post-exercise. AMPK phosphorylation increased after cycling in strength-trained, but not endurance-trained subjects (P less than 0.05). Conversely, AMPK was elevated following resistance exercise in endurance-, but not strength-trained subjects (P less than 0.05). Thus, AMPK was elevated only when subjects undertook a bout of exercise in a mode of training to which they were unaccustomed. Surprisingly, there was no change in AKT phosphorylation following resistance exercise regardless of the training background of the subjects. In the absence of increased AKT phosphorylation, resistance exercise induced an increase in p70 S6K and ribosomal S6 protein phosphorylation in endurance-trained but not strength-trained subjects (Pless than 0.05). AKT phosphorylation was increased in endurance-trained, but not strength-trained subjects after cycling (P less than 0.05). These results show that a degree of signalling
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Caldwell, Elizabeth Frances. "Molecular evidence for dietary adaptation in humans." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445382/.
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Starch digestion begins in the mouth where it is hydrolysed into smaller polysaccharides by the enzyme salivary amylase. Three salivary amylase genes (AMY1A, B & C) and a pseudogene (AMYP1) have been described and are located in tandem on chromosome 1. Polymorphic variation has been demonstrated in Caucasians in the form of the number of repeats of the AMY1 genes, as follows: (lA-lB-Pl)n-lC. This variation has been reported to result in differing levels salivary amylase enzyme production and, as a result, differences in the efficiency of starch digestion in the mouth. It is proposed in this thesis that an increase in salivary gene copy number may be an adaptation to high starch diets as a result of the adoption of agriculture. Reliable high-throughput multiplex PCR based methods have been designed to quantify AMY1 gene copy number and to also to type 6 microsatellite markers closely linked to the AMY gene cluster. Data have been collected for 14 human populations, with different histories of cereal agriculture and ancestral levels of starch in the diet. Data have also been collected on AMY1 gene copy number in 5 chimpanzees (Pan troglodytes). The AMY1 allele frequency difference (measured using FST) between the two most extreme populations, the Mongolians and Saami, was not an outlier on a distribution of FST based on presumed neutral 11,024 SNPs from the human genome. The chimpanzee data suggest that the most frequent allele (AMY1*H1) in humans may not be the ancestral allele, as all chimpanzee chromosomes tested carried the AMY1*H0 allele (containing only one copy of the AMY1 gene). A more sensitive selection test, the analysis of the intra-allelic variability of the AMY1 repeat alleles using closely linked microsatellites, showed no compelling evidence for recent positive selection at the AMY1 locus in humans. As a result, genetic drift could not be ruled out as an explanation for the observed AMY1 allele frequency differences among populations. Alanine:glyoxylate aminotransferase (AGT) is an intermediary metabolic enzyme that is targeted to different organelles in different species. Previous studies have shown that there is a clear relationship between the organellar distribution of AGT and diet. Non-human primates show the herbivorous peroxisomal distribution of AGT. In humans a point mutation and insertion deletion polymorphism have been associated with peroxisome-to-mitochondria AGT mis-targeting. Data have been collected using a PCR/RFLP based method, in 11 human populations. In a comparison with FST values from 11.024 SNP loci, 94.5% of SNPs had a lower FST than a comparison of AGT allele frequencies for Saami and Chinese. This unusually high allele frequency difference between Chinese and Saami is consistent with the signature of recent positive selection driven by the unusually high meat content in the Saami diet.
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Cwiklinski, Emma. "Molecular Mechanisms Regulating SNAT2 Adaptation in Mlammalian Cells." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521651.
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Harrison, Michael Andrew. "Molecular mechanisms of adaptation in the photosynthetic apparatus." Thesis, University of Leeds, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.277375.
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Blazek, Alisa D. "Integrative Approach to Understanding the Multimodal Effects of Exercise Adaptation." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1439546709.
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Tan, Zhijia, and 谭志佳. "Molecular analyses of chondrocyte differentiation and adaptation to ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209435.
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Endochondral bone development depends on the progression of chondrocyte proliferation, hypertrophy and terminal differentiation, which requires precise transcriptional regulation and signaling coordination. Disturbance of this process would disrupt chondrocyte differentiation and lead to chondrodysplasias. In cells, a highly conserved mechanism, ER stress signaling, has been developed to sense the protein load and maintain the cellular homeostasis. In humans, mutations in COL10A1 induce ER stress and result in metaphyseal chondrodysplasia type Schmid (MCDS). Previous analysis of a MCDS mouse model (13deltg mouse) had revealed a novel mechanism of chondrocyte adaptation to ER stress. The hypertrophic chondrocytes survive ER stress by reverting to a pre-hypertrophic like state (Tsang et al., 2007). To dissect the underlying mechanisms that coordinate chondrocyte survival, reverted differentiation and adaptation to ER stress, different chondrocyte populations in the wild type and 13del growth plates were fractionated for global gene expression analyses.
The genome-wide expression profiles of proliferating chondrocytes, prehypertrophic chondrocytes, hypertrophic chondrocytes and terminally differentiated chondrocytes in the wild type growth plate provide molecular bases to understand the processes underlying both physiological and pathological bone growth. Systematic analyses of these transcriptomic data revealed the gene expression patterns and correlation in the dynamics of endochondral ossification. Genes associated with sterol metabolism and cholesterol biosynthesis are enriched in the prehypertrophic chondrocytes. Selected genes (Wwp2, Zbtb20, Ppa1 and Ptgis) that may potentially contribute to endochondral ossification were identified differentially expressed in the growth plate. Bioinformatics approaches were applied to predict regulatory networks in chondrocytes at different differentiation stages, implying the essential and dominant roles of Sox9 in coordination of stage specific gene expression. We further confirmed that Sox9 directly regulates the transcription of Cyr61, Lmo4, Ppa1, Ptch1 and Trps1, suggesting that Sox9 integrates different steps of chondrocyte differentiation via regulation of its target genes and partially crosstalk with IHH signaling pathway.
The information on gene expression and regulation from physiological growth plate provides important basis to understand the molecular defects of chondrodysplasia. The hypertrophic zone in 13del growth plate was fractionated into upper, middle and lower parts for microarray profiling, corresponding for the onset of ER stress, onset of reverted differentiation and adaptation phase. Comparative transcriptomics of wild type and 13del growth plates revealed genes related to glucose, amino acid and lipid metabolisms are up regulated in response to ER stress. Fgf21 was identified as a novel ER stress inducible factor regulated by ATF4. Removal of Fgf21 results in increasing cell apoptosis in 13del hypertrophic zone without affecting the reverted differentiation process. Up regulation of genes expression related to hypoxic stress (Slc2a1, Hyou1, Stc2 and Galectin3) in 13del hypertrophic chondrocytes suggested that survival and adaptation of chondrocytes to ER stress involve cross-regulation by other stress pathways. Our findings have provided a new insight into the mechanisms that facilitate chondrocyte survival under ER stress in vivo, and propose the integrative effects of hypoxic stress pathway during the stress adaptation process, which broaden the molecular horizons underlying chondrodysplasias caused by protein folding mutations.published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
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Punn, Anu. "The molecular basis of adaptation to ischaemia in cardiac myocytes." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418254.
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Niswander, Julie M. "Molecular Correlates of Adaptation and Apoptosis: p38 Signaling in Hippocampus." University of Toledo Health Science Campus / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=mco1085678685.
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Peccoux, Anthony. "Molecular and physiological characterization of grapevine rootstock adaptation to drought." Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21864/document.
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Dans le contexte du changement climatique, les prédictions réalisées mettent en évidence une altération de la disponibilité en eau dans de nombreuses régions viticoles ; ce qui, conjointement à l’augmentation de la population mondiale et la diminution des terres agricoles, va accroître la compétition pour l’utilisation des ressources hydriques. Par conséquent, améliorer l'adaptation à la sécheresse de la vigne est un des enjeux majeurs des prochaines années. Pour cela, une adaptation des pratiques culturales peut être proposée, en particulier le choix pertinent du matériel végétal et notamment du porte-greffe.Dans ce travail, le rôle du porte-greffe vis-à-vis de la réponse de la vigne greffée à la contrainte hydrique a été étudié, en utilisant des approches écophysiologiques, moléculaires et de modélisation. Des expériences ont été réalisées en conditions contrôlées afin d’étudier l’effet du déficit hydrique à court et long terme sur les réponses de différents porte-greffes greffés avec le même scion.Le modèle écophysiologique a démontré que les porte-greffes affectent l'ouverture stomatique du greffon par des processus coordonnés incluant les caractéristiques racinaires, les signaux hydrauliques et les signaux chimiques lors d’un déficit hydrique à court terme. La conductance stomatique, le taux de transpiration et la conductance hydraulique des feuilles ont été plus élevés en conditions irriguées et de stress hydriques modérés chez le génotype résistant à la sécheresse (110 Richter) par rapport au génotype sensible à la sécheresse (Vitis riparia cv. Gloire de Montpellier). Nous avons identifié plusieurs paramètres génétiques impliqués dans le contrôle de la régulation stomatique. Des différences d’architecture racinaire et de conductivité hydraulique des racines ont été identifiées entre les porte-greffes.Le déficit hydrique à long terme a entrainé des réponses adaptatives différentes entre les porte-greffes. Le génotype tolérant la sécheresse a induit une modification du diamètre des vaisseaux du xylème de la partie apicale de la racine en réponse au déficit hydrique modéré tandis que le génotype sensible n'a pas présenté de différence par rapport au contrôle. L’analyse transcriptomique des racines a identifié des gènes spécifiques aux différents génotypes, qui sont régulés en fonction du niveau de déficit hydrique. La comparaison entre les niveaux de stress et les génotypes a identifié 24 gènes intervenant dans l’interaction « traitement × génotype ». Ces gènes sont majoritairement impliqués dans le métabolisme des lipides et de la paroi cellulaire. Des courbes de réponse au déficit hydrique spécifiques aux différents génotypes ont été observées. La protection contre les dommages liés aux stress oxydatifs induits par le stress hydrique semble être un mécanisme important chez le porte-greffe résistant à la sécheresse. Le génotype sensible semble répondre au déficit hydrique par une modification des propriétés de la paroi cellulaire de la racineClimate change raises concerns about temporal and spatial water availability in many grape growing countries. The rapidly increasing world population and the scarcity of suitable land for agricultural food production, together with a changing climate, will increase competition with grape-producing areas for the use of land and resources. Consequently, other practices that can potentially improve water management of vineyards and water acquisition by grapevines need to be considered. Aside from canopy systems and their management, the choice of plant material is a key issue. Therefore, in the present work, the role of different rootstocks, regarding their tolerance to drought, was investigated for their potential effects on i) water uptake, ii) water transport and iii) shoot water use, using a combination of ecophysiological, modelling and transcriptomic approaches. Experiments were conducted under controlled conditions to decipher short and long term responses to drought of different rootstocks grafted with the same scion. An ecophysiological model was used to investigate the roles of rootstock genotypes in the control of stomatal aperture. Long-term steady state water-deficit conditions were used to examine the responses of i) whole plant growth, root anatomy and hydraulic properties and ii) transcriptome remodelling in the roots.Our model showed that rootstock affect stomatal aperture of the grafted scion via coordinated processes between root traits, hydraulic signals and chemical signals. Stomatal conductance, transpiration rate and leaf-specific hydraulic conductance were higher and better maintained under well-watered and moderate water-deficit conditions in the drought-tolerant genotype (110 Richter) compared to the drought-sensitive one (Vitis riparia cv. Gloire de Montpellier). We identified several genotype-specific parameters which play important roles, like root-related parameters, in the control of stomatal regulation. Additionally, root system architecture and root hydraulic properties are important constitutive traits identified between rootstocks.Long-term water-deficit induced genotype adaptive responses in the roots were evaluated. The drought-tolerant genotype exhibited a substantial shift in root tips xylem conduit diameter under moderate water-deficit while the drought-sensitive genotype did not respond. Transcriptomic analysis identified genotype-specific transcripts that are regulated by water-deficit levels. The comparison between stress levels and genotypes identified 24 significant genes in “treatment×genotype” interactions, most of them were involved in lipid metabolism and cell wall processes. These genes displayed genotype-specific water-deficit response curves. Protection against drought-induced oxidative damage was found to be an important mechanisms induced by the drought-tolerant rootstock, while the drought-sensitive one responds to water-deficit by modification of cell wall properties
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Crill, Wayne Douglass. "Experimental evolution and molecular basis of host-specific viral adaptation /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.
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Niswander, Julie Marie. "Molecular correlates of adaptation and apoptosis : p38 signaling in hippocampus." Connect to full-text via OhioLINK ETD Center, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1085678685.
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Thesis (Ph.D.)--Medical College of Ohio, 2004."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Linda A. Dokas. Document formatted into pages: iv, 150 p. Title from title page of PDF document. Bibliography: pages 44-52.
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Maher, Keri Renee. "A geographically constrained molecular phylogeny of Panamanian Aechmea species (Bromeliaceae, subfamily bromelioideae)." CSUSB ScholarWorks, 2007. https://scholarworks.lib.csusb.edu/etd-project/3280.
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This study lends strong support to the idea that members of Bromeliaceae have undergone a recent adaptive radiation, and therefore show that, at least in part, diversity in the tropics is due to a fast speciation rate and that the tropics can be a "cradle" for new diversification and exploitation of varying ecological niches through the diversification of ecophysiological traits within a lineage.
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Ruecker, Ovidiu Ludwig. "Molecular adaptation mechanisms of phototrophic sulfur bacteria to different light conditions." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-145970.
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D'Esposito, Daniela. "The molecular signature for local adaptation in the seagrass Posidonia oceanica." Thesis, Open University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590668.
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In the last century, seagrass ecosystems have suffered a worldwide decline ascribed to multiple environmental stressors, among which the reduction of light available for the photosynthesis and the increase in temperature represent the strongest constraints for their growth and survival. Despite conservation, this decline is at present still continuing. in order to understand the genetic adaptive response to light and temperature in the seagrass Posidonia ocxanica, two different strategies have been pursued: a genome scan approach along a latitudinal and a bathymetric gradient and a differential gene expression analysis along the bathymetric gradient, where light and temperature were the two main selective factors. For the genome scan approach 6 populations (Delimara - Malta, Lacco Ameno - Island of Ischia, Italy, Marettimo Island- Italy, Me10ria - Italy, Piombino - Italy and Stareso - Corsica, France) were sampled along the bathymetric gradient at two different depths (-5m and -25m). The same populations were used for the latitudinal gradient analysis by grouping them on the basis of their geographic location (Southern group: Delimara. Lacco Ameno and Marettimo; Northern group: Meloria, Piombino and Stareso). No genes under selection were identified in the genome scan along the bathymetric gradient. Three putative genes under selection were identified in the genome scan along the latitudinal gradient and were involved in the photosynthesis and in the translation process. For assessing differential gene expression, a transcriptome sequencing of plants sampled at two different depths and different times of the day in the Stareso meadow was performed by RNAseq technology. The analysis highlighted the capability of plants living in shallow waters to cope with environmental stresses imposed by high light and high temperature. Transcriptome data generated from this study increased the resources available in P. oceanica and will be very useful for further investigations of the adaptation of in this plant
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Baeshen, Naseebh. "Molecular basis of adaptation of enteroviruses to different cancer cell lines." Thesis, University of Essex, 2015. http://repository.essex.ac.uk/15694/.
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Viral oncolytic therapy, a novel treatment for cancer using specially designed viruses to kill malignant cells while leaving normal cells unharmed, is currently under intense investigation. Several receptors are up-regulated in cancer cells, including decay-accelerating factor (DAF; CD55) and integrins (αvβ3, αvβ6) and viruses which recognise these receptors could be useful for therapy. Several echoviruses, including Echovirus 11 (E11), bind to DAF; coxsackievirus A9 (CVA9) utilizes an RGD motif to bind to integrins, particularly αvβ6. Some isolates of CVA9 also bind to heparan sulfate proteoglycans (HSPG). This thesis describes work designed to improve our understanding of CVA9 and echovirus cell/receptor tropism. Several echoviruses and CVA9 variants were tested in a panel of 9 cell lines. Distinct patterns of infection were seen, but did not fully correlate with receptor expression, suggesting that other determinants also help to define tropism. To investigate this further, E11 was adapted by passaging on two cell lines, A549 and HeLa. Two mutations were seen in A549-adapted virus, and both mapped to the DAF-binding footprint, suggesting changes to E11/DAF interactions. A single mutation in VP4 was seen in HeLa-adapted virus, and may affect a later stage in cell entry. To investigate CVA9 binding to HSPG, 3 isolates were propagated on A549 cells and heparin-blocked mutants were isolated. Although the isolates are diverse, the same mutation (VP3 Q59R) was seen in two isolates and probably gives a positively-charged cluster with adjacent amino acids. Other mutations were seen close to the RGD motif, where there is already a highly basic sequence. The results suggest multiple potential mechanisms for HSPG-binding. Combinations of some of the adapting mutations discovered could significantly enhance the tropism of these viruses to specific cancer cells and optimise them as oncolytic agents.
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Smith, Gilbert. "Investigating the molecular basis of adaptation and speciation in divergent populations." Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/3678.
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The creation of biodiversity involves the evolution of new species. Recent trends in the study of speciation have increased the emphasis on the role of ecology in adaptation and the evolution of reproductive isolation. This includes examining the relative contributions of different types of selection, the role of gene flow and the genomic changes that occur during ecological speciation. The search for speciation genes continues, however our growing knowledge of how the genome translates into phenotypes means we should now consider a broader molecular basis of speciation, which includes genetic, transcriptomic and potentially epigenetic variation that contribute to phenotypic variation. This thesis addresses the molecular basis of speciation by using three different complementary methods to examine the early stages of ecological speciation and the evolution of premating reproductive isolation between two incipient species of the cactophilic fly, Drosophila mojavensis. First, the genetic basis was examined through the sequencing of two candidate genes underlying reproductive isolation (Chapter 2). Second, the historical biogeography of population divergence was uncovered using multiple sequenced loci (Chapter 3). Lastly, gene expression across the whole transcriptome associated with phenotypic plasticity and mating success was assessed (Chapter 4). Further, the role of epigenetic imprinting in the population divergence of a freshwater fish, Girardinichthys multiradiatus, was examined through sequencing of a well known gene involved in sexual conflict (Chapter 5). These studies find that uncovering the genetic variation underlying speciation is difficult, especially when there is extensive phenotypic plasticity. Further, gene expression plasticity may play an important role in the evolution of premating isolation, and this includes a role for epigenetic mechanisms of gene expression. Additionally, it is important to assess the demographic scenario of population divergence to put into context the ecological and functional data on divergent groups. Through these studies this thesis examines the genetic, expression and epigenetic variation associated with on-going population divergence, and emphasises the need to consider the potential role of the full range of gene expression changes during ecological speciation.
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Rees, David J. "Colonisation and adaptation in Nesotes beetles on the Canary Islands." Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327605.
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Belzer, Clara. "Surviving the Enterohepatic Tract: Molecular Mechanisms of Stress Adaptation in Helicobacter hepaticus." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2007. http://hdl.handle.net/1765/10647.
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Markov, Peter V. "Molecular epidemiology, evolution and adaptation of hepatitis C virus to population immunity." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.711633.
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Nilsson, Christina. "Genome-plasticity and adaptation in Helicobacter pylori /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-189-X/.
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Sullivan, Christopher James. "The role of fibroblast growth factor-2 (FGF2) in vascular remodeling and adaptation." Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/284317.
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The goal of this dissertation was to test the hypothesis that fibroblast growth factor-2 (FGF2) is required during diseased-related vascular growth and remodeling in the adult organism. Given previous research, it is generally assumed that FGF2 is an important regulator of vessel growth during various pathophysiological processes (e.g. tissue ischemia, vessel injury, and flow-dependent remodeling). However, such studies only indirectly implicate FGF2 in vascular adaptation and remodeling. In contrast, experiments using mice with a targeted disruption of the Fgf2 gene have allowed direct determination of the biological roles of endogenous FGF2. Thus, experimental models of flow-dependent remodeling and ischemic revascularization were used to compare the responses of Fgf2⁻/⁻ and Fgf2⁺/⁺ mice to directly identify the function of FGF2 during vascular adaptation in the adult animal. Surprisingly, the lack of FGF2 did not appear to affect vascular growth in these models. First, using a novel model of flow-dependent remodeling, Fgf2⁻/⁻ mice had equivalent carotid artery adaptation in response to both high-flow and low-flow was as wildtype counterparts. Second, angiogenesis and arteriogenesis were not different between the ischemic limbs Fgf2⁺/⁺ and Fgf2⁻/⁻ mice, demonstrating that FGF2 is not required for vascular adaptation in response to ischemia. However, these experiments led to the observation that reactive hyperemia was impaired in ischemic limb of Fgf2⁻/⁻ mice. These results indicate that vessel responsiveness is altered in the collateral circulation of the ischemic Fgf2⁻/⁻ limb. This possible identification of FGF2 as a "functional" factor in the collateral circulation suggests a novel, non-mitogenic role for endogenous growth factors. Finally, Fgf2⁻/⁻ mice had altered gene expression in the ischemic limb as evaluated using cDNA microarrays. The significance of differential gene expression in the absence of FGF2 is unknown. It is unclear whether such changes in gene expression are related to the FGF2 hyperemia phenotype or whether they are related to an unknown phenotype present in the ischemic limb of Fgf2⁻/⁻ mice. Overall, this dissertation provides new evidence that endogenous FGF2 has important actions in the remodeling vasculature during ischemic revascularization. Specifically, endogenous FGF2 appears to modulate vascular reactivity of the collateral circulation of the hindlimb.
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Alvarado, Sebastian. "Genomic adaptation to disease: A role for DNA demethylation of microRNA regulation in cancer and chronic neuropathic pain." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116896.
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Cancer and chronic pain are two common pathologies affecting millions of patients worldwide. Much like most other disease states, they can be determined genetically, environmentally, or both. Unlike the static genome, the epigenome is responsible for interpreting environmental interactions and is often altered in disease states. A subset of epigenetic modifications, known as DNA methylation, is capable of mediating gene silencing. In this thesis, two cases will be explored probing the nature of DNA methylation in cancer and in peripheral neuropathy. Aberrant DNA methylation is a common hallmark of cancer often resulting in the methylation of tumor suppressors and the demethylation of oncogenes. The identity of a DNA methylase, however, remains elusive. One candidate, methyl binding domain 2 (MBD2), has been previously characterized as a demethylase and also functions as a transcriptional repressor. One possible explanation for its role as a repressor may involve the direct activation of a repressor which can then mediate silencing. An attractive class of genes for this model are microRNAs, which are capable of binding several targets in the cell and mediate their silencing. We therefore test the hypothesis that MBD2 is capable of activating a microRNA which is capable of negatively-regulating target genes. In this thesis, we delineate mechanisms that demonstrate MBD2 is capable of binding a microRNA, mir-496, which is then capable of inducing itsiactivation. We further show that mir-496 can mediate a repressive action on three separate genes in the cell that have tumor suppressive roles in cancer. Chronic pain has been shown to alter gene expression and brain anatomy and is often accompanied with comorbidities that affect cognitive processing, sleep and anxiety. Interestingly, these changes have been shown to be reversible following effective treatment of pain, suggesting the mechanisms behind pain may also be reversible, thus prompting the study of pain epigenetics. We therefore proposed to test the hypothesis that the methylome and transcriptome are altered in the brain following peripheral nerve injury. We were able to identify a signature of DNA methylation and transcription specific to the prefrontal cortex and amygdala that accompanied peripheral nerve injury and behavioral signs of neuropathy. Furthermore we were able reverse behavioral signs of neuropathic pain and altered methylation states in the prefrontal cortex with environmental enrichment, demonstrating their reversible nature. Taken together, this thesis explores the role of DNA methylation in two complex diseases: through small scale processes in cancer and through broader changes at the level of the methylome and transcriptome in chronic pain. In identifying these molecular pathways and signatures, we hope to improve the mechanistic understanding of these pathologicaliistates, ultimately resulting in better treatment outcomes for millions of patients worldwide.Le cancer et la douleur chronique sont deux pathologies courantes qui affectent des millions de personnes à travers le monde. Comme beaucoup d'autres états pathologiques, ils peuvent être déterminés génétiquement et par l'environnement. Contrairement au génome qui est statique, l'épigénome est responsable de l'interprétation des interactions avec l'environnement et est souvent altéré dans des états pathologiques. Un sous-ensemble de modifications épigénétiques, appelé méthylation de l'ADN, est capable de médier l'inactivation génique. Dans cette thèse, deux cas seront explorés pour sonder la nature de la méthylation de l'ADN dans le cancer et dans la neuropathie périphérique. Une méthylation de l'ADN aberrante est une caractéristique commune du cancer qui entraîne souvent la méthylation de gènes suppresseurs de tumeurs et la déméthylation d'oncogènes. L'identité d'une déméthylase de l'ADN, cependant, reste insaisissable. Un candidat, "methyl binding domain 2" (MBD2), a été précédemment caractérisé comme étant une déméthylase et fonctionnant également comme un répresseur transcriptionnel. Une explication possible pour son rôle en tant que répresseur pourrait impliquer l'activation directe d'un répresseur qui pourrait ensuite servir de médiateur de la répression. Une classe de gènes intéressante dans ce modèle est celle des microARN, qui sont capables de se lier à plusieurs cibles dans la cellule et de conduire à leur répression. Nous avons donc testé l'hypothèse que MBD2 serait capable d'activer un micro-ARN capable de réguler négativement les gènes cibles. Dans cette thèse, nous avons étudié les mécanismes qui démontrent que MBD2 est capable de se lier à un microARN, mir-496, qui est alors capable d'induire son activation. Nous montrons en outre que mir-496 peut servir de médiateur d'une action répressive sur trois gènes distincts qui ont des rôles de suppresseurs de tumeur dans les cellules cancéreuses. La douleur chronique a été montrée comme modifiant l'expression des gènes et l'anatomie du cerveau. Elle est souvent accompagnée de comorbidités qui touchent le traitement cognitif, le sommeil et l'anxiété. Fait intéressant, ces changements se sont montrés réversibles après un traitement efficace de la douleur, suggérant que les mécanismes à l'origine de la douleur pourraient aussi être réversibles, incitant ainsi à l'étude de l'épigénétique de la douleur. Nous avons donc proposé de tester l'hypothèse que le méthylome et le transcriptome seraient altérés dans le cerveau après une lésion nerveuse périphérique. Nous avons pu identifier une signature de méthylation de l'ADN et de transcription spécifique au cortex préfrontal et à l'amygdale qui accompagne une lésion du nerf périphérique et les signes comportementaux de la neuropathie. En outre, nous avons pu inverser les signes comportementaux de la douleur neuropathique et les niveaux de méthylation dans le cortex préfrontal par un enrichissement de l'environnement, démontrant ainsi leur caractère réversible. L'ensemble de cette thèse explore le rôle de la méthylation de l'ADN dans deux maladies complexes : au travers de processus à petite échelle dans le cancer et par des changements plus larges au niveau du méthylome et du transcriptome dans la douleur chronique. En identifiant ces voies moléculaires et les signatures épigénétiques, nous espérons améliorer la compréhension mécanistique de ces états pathologiques, ouvrant la voie à de meilleurs traitements pour des millions de patients dans le monde.
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Grobbelaar, Melanie. "Adaptation of the Mycobacterium tuberculosis transcriptome in response to rifampicin." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20387.
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Thesis (MScMedSc)--Stellenbosch University, 2012.ENGLISH ABSTRACT: Anti-tuberculosis drugs target specific essential cellular processes and structural components. The first line drug, rifampicin (RIF) is a RNA polymerase inhibitor which targets the β-subunit and subsequently inhibits the initiation of transcription. Previous proteomic and transcriptomic analyses have shown that exposure to RIF for 24hrs significantly increased the abundance of proteins involved in energy metabolism in clinical isolates. No studies have been done to describe the transcriptional responses to RIF in an in vitro RIF resistant M. tuberculosis isolate. Application of in vitro mutants is novel since it will exclude most of the confounding factors which may be present in clinical isolates obtained from patients where the bacterium may have been incubated for several weeks or even years. This study aimed to determine the effect of prolonged exposure to RIF and the effect of the rpoB Ser531Leu mutation on the expression of energy metabolism genes, sigma factors and a regulator in RIF mono-resistant in vitro mutants with different levels of RIF resistance (minimum inhibitory concentration (MIC): 40μg/ml and 70μg/ml). RIF mono-resistant in vitro mutants were generated from a pan susceptible Beijing cluster 208 progenitor using the Luria Delbruck assay. In vitro RIF mono-resistant mutants harbouring the Ser531Leu rpoB mutation and which displayed different levels of RIF resistance were selected. To assess the effect of prolonged RIF exposure on the expression of candidate genes, the in vitro mutants were cultured in liquid media and exposed to RIF for 1, 7 and 14 days. High quality RNA was extracted from these cultures at each time point and Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR) was done on the selected candidate genes. The results indicate that limited expression of energy metabolism genes and sigma factors was observed after prolonged RIF exposure. In addition, the activity of the regulator (Rv1846c) was down-regulated in the presence of RIF explaining the up-regulated state of energy metabolism genes. To assess the effect of the rpoB Ser531Leu mutation on the candidate genes, RNA was extracted from the RIF unexposed culture at mid-log phase. RT-qPCR was done for each in vitro mutant in addition to the wild-type progenitor isolate. These results show that energy metabolism genes and sigma factors were significantly up-regulated in the RIF resistant mutantss harbouring an rpoB Ser531Leu mutation. This suggests that the mutation had a significant effect on the cellular energy cost due to the up-regulated state of the energy metabolism genes. In addition, an increase in the expression of sigma factors may be required to compensate for the rpoB mutation by enforcing the binding of the RNA polymerase and sigma factors to the promoter for transcription to be initiated. It is therefore important to assess these candidate genes for their potential as novel candidates for future drug design as this is an important aspect to influence tuberculosis control.
AFRIKAANSE OPSOMMING: Teen-tuberkulose middels teiken essensiële sellulêre prosesse en strukturele komponente. Die eerste linie teen-tuberkulose middel, rifampisien (RIF) is ʼn RNS polimerase inhibeerder wat die β-subeenheid teiken en daarna die inisiasie van transkripsie onderdruk. Vorige proteomiese en transkriptomiese analises het getoon dat blootstelling aan RIF vir 24 uur beduidende styging in sekere protiene wat verband hou met energie metabolisme in kliniese isolate veroorsaak. Die huidige studie poog om die effek van langdurige RIF blootstelling, asook die effek van die rpoB Ser531Leu mutasie op die uitdrukking van energie metabolisme gene, sigma faktore en reguleerders op RIF-enkel weerstandige in vitro mutante by verskillende vlakke van RIF weerstandigheid (Minimum Inhiberende Konsentrasie (MIK): 40μg/ml en 70μg/ml) te ondersoek. RIF-enkelweerstandige in vitro mutante isolate is gegenereer van ʼn sensitiewe Beijing 208 stamfamilielid deur die Luria Delbruck metode. In vitro RIF enkelweerstandige mutante met die rpoB Ser531Leu mutasie en verskillende vlakke van RIF weerstandigheid is geselekteer. Om die langdurige effek van RIF blootstelling op kandidaat geen uitdrukking te ondersoek, is in vitro mutante isolate gegroei in vloeibare medium en blootgestel aan RIF vir 1, 7 en 14 dae. Goeie kwaliteit RNS is geëkstraheer van hierdie kulture by elke tydpunt om Werklike-tyd Kwantitatiewe Polimerase Ketting Reaksie (RT-qPCR) op die kandidaat gene uit te voer. Die resultate toon dat ʼn beperkte aantal energie metabolisme en sigma faktor gene uitgedruk was na RIF blootstelling. Verder is die uitdrukking van die reguleerder (Rv1846c) af gereguleer in die teenwoordigheid van RIF en dit verduidelik die op gereguleerde energie metaboliese geen patroon. Om die effek van die rpoB Ser531Leu mutasie op die kandidaat gene te evalueer, is RNS geëkstraheer van ʼn weerstandige en RIF sensitiewe kultuur wat nie blootgestel was aan RIF nie. RT-qPCR is uit gevoer op elke in vitro mutante isolaat asook op ʼn sensitiewe isolaat sonder ʼn mutasie. Hierdie resultate toon dat energie metabolisme gene en sigma faktore beduidend opreguleer word in die isolate met ʼn rpoB Ser531Leu mutasie. Dit dui daarop dat die mutasie ʼn beduidende effek op die sellulêre energie koste het, omdat die energie metabolisme gene op gereguleer is. Verder kan ʼn toename in die uitdrukking van sigma faktore benodig word om die effek van die rpoB mutasie te oorkom deur binding van die RNS polimerase en die sigma faktore aan die promotor om transkripsie inisiasie te forseer. Dit is daarom belangrik om hierdie kandidaat gene verder te ondersoek vir toekomstige ontwikkeling van teenmiddels teen tuberkulose.
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Knies, Jennifer Lynn Burch Christina L. "Thermal adaptation of the phage G4 and molecular evolution of RNA secondary structure." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1241.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.Title from electronic title page (viewed Mar. 26, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Genetics and Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.
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Vidanes, Genevieve M. "Suppression of the DNA damage checkpoint by the Saccharomyces cerevisiae polo-like kinase, CDC5, to promote adaptation." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3352477.
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Werzner, Annegret [Verfasser], and Wolfgang [Akademischer Betreuer] Stephan. "Local adaptation in Drosophila melanogaster : Molecular and morphological aspects / Annegret Werzner. Betreuer: Wolfgang Stephan." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2011. http://d-nb.info/1018615679/34.
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Guo, Baoqing. "Molecular basis of Campylobacter antibiotic resistance and adaptation to the intestinal tract of chickens." [Ames, Iowa : Iowa State University], 2007.
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Muaddi, Hala. "Phosphorylation of eukaryotic initiation factor 2-alpha at serine 51 is an important determinant of cell survival and adaptation to glucose deficiency." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:8881/R/?func=dbin-jump-full&object_id=92253.
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Whiteley, Rachel. "Quantitative and molecular genetic variation in Ulmus laevis Pall. /." Uppsala : Dept. of Plant Biology and Forest Genetics, Swedish Univ. of Agricultural Sciences, 2004. http://epsilon.slu.se/s313.pdf.
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Ostrowski, Martin Biotechnology & Biomolecular Sciences Faculty of Science UNSW. "Physiological adaptation to nutrient limitation in a marine oligotrophic ultramicrobacterium Sphingopyxis alaskensis." Awarded by:University of New South Wales. School of Biotechnology and Biomolecular Sciences, 2006. http://handle.unsw.edu.au/1959.4/27422.
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Sphingopyxis (formerly Sphingomonas) alaskensis, a numerically abundant species isolated from Alaskan waters and the North Sea represents one of the only pure cultures of a typical oligotrophic ultramicrobacterium isolated from the marine environment. In this study, physiological and molecular characterization of an extinction dilution isolate from the North Pacific indicate that it is a strain of Sphingopyxis alaskenis, extending the known geographical distribution of this strain and affirming its importance as a model marine oligotroph. Given the importance of open ocean systems in climatic processes, it is clearly important to understand the physiology and underlying molecular biology of abundant species, such as S. alaskensis, and to define their role in biogeochemical processes. S. alaskensis is thought to proliferate by growing slowly on limited concentrations of substrates thereby avoiding outright starvation. In order to mimic environmental conditions chemostat culture was used to study the physiology of this model oligotroph in response to slow growth and nutrient limitation. It was found that the extent of nutrient limitation and starvation has fundamentally different consequences for the physiology of oligotrophic ultramicrobacteria compared with well-studied copiotrophic bacteria (Vibrio angustum S14 and Escherichia coli). For example, growth rate played a critical role in hydrogen peroxide resistance of S. alaskensis with slowly growing cells being 10, 000 times more resistant than fast growing cells. In contrast, the responses of V. angustum and E. coli to nutrient availability differed in that starved cells were more resistant than growing cells, regardless of growth rate. In order to examine molecular basis of the response to general nutrient limitation, starvation and oxidative stress in S. alaskensis we used proteomics to define differences in protein profiles of chemostat-grown cultures at various levels of nutrient limitation. High-resolution two-dimensional electrophoresis (2DE) methods were developed and 2DE protein maps were used to define proteins regulated by the level of nutrient limitation. A number of these proteins were identified with the aid of mass spectrometry and cross-species database matching. The identified proteins are involved in fundamental cellular processes including protein synthesis, protein folding, energy generation and electron transport, providing an important step in discovering the molecular basis of oligotrophy in this model organism.
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David, Maude. "Bacterial adaptation to the chlorinated compounds." Thesis, Ecully, Ecole centrale de Lyon, 2009. http://www.theses.fr/2009ECDL0026/document.
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Le travail présenté dans cette thèse porte sur l'adaptation bactérienne aux molécules chlorées, tant au niveau des ressources génétiques nécessaires à la mise en place des gênes de dégradation qu'au niveau de la structure de la communauté microbienne observée durant la dégradation de ces composés. La première partie de ce document est une bibliographie qui se focalise sur les mécanismes développés par les bactéries pour répondre aux stress environnementaux, et sur les possibles origines des gènes responsables des premières étapes de dégradation des composés chlorés : les dehalogenases (qui réalisent les étapes de déchloration). Le deuxième chapitre de cette thèse porte sur des essais expérimentaux de remodelage génétique, dans le but de valider les hypothèses présentées lors de la bibliographie quant aux mécanismes qui ont pu conduire à la génération de nouveaux gênes de dégradation. Ces remodelages in vitro et in vivo ont été effectués en utilisant les gènes linB et dhaA. Le chapitre suivant examine la structure de la communauté bactérienne lors de la dégradation réductive du tetrachloroéthylène (PCE). Pour cette étude, des outils de biologie moléculaire, plus spécifiquement des puces phylogénétiques, ont été utilisés pour étudier la structure de la communauté microbienne depuis l'introduction du polluant jusqu'à sa dégradation. Afin d'élucider les fonctions métaboliques qui peuvent être corrélées avec la dégradation du PCE, les résultats des puces phylogénétiques ont été comparés avec un suivi chimique des métabolites de dégradation de ce composé, lors d'une étude en microcosmes. L'objectif du dernier chapitre de la thèse a été de relier la structure de la communauté microbienne avec la cinétique de dégradation des composés chimiques étudiés. Pour cela, une étude globale comportant à la fois un suivi chimique des métabolites de dégradation, une quantification des gènes de dégradation impliqués dans la déchloration réductive du PCE ainsi que l'étude de la structure de la communauté microbienne ont été mis en place. Cette étude a permis de corréler les conditions environnementales nécessaires à la déchloration et la communauté microbienne associée avec l'expression des déhalogénases quantifiées. En résumé, cette thèse explore à la fois les mécanismes mis en place par les bactéries pour dégrader ces composés polluants et la structure de la communauté bactérienne durant la dégradation de ce polluant. Comprendre ces deux étapes dans l'adaptation bactérienne peut contribuer à améliorer l'utilisation des capacités bactériennes utilisées en bioremédiationThis thesis concerns the bacterial adaptation to the chlorinated compounds at both the gene level and the microbial community level. The bibliography will focus on the adaptation mechanisms developed by bacteria to respond to environmental stresses and on the possible origins of the genes responsible for the first steps of chlorinated compound degradation, those encoding for the dehalogenases, which perform the dechlorination or chlorine removal step. The second chapter of the thesis consists of an experimental exploration of the gene shuffling hypothesis presented in the bibliography, using linB and dhaA genes. The next chapter examines the bacterial community structure in relation to compound degradation using the reductive dechlorination of tetrachloroethylene. For this study, molecular biology tools, specifically phylochip microarrays were used to examine bacterial community structure from the moment of pollutant introduction to the environment and during bioremediation. In order to elucidate the metabolic functions, which correlate the PCE degradation, phylogenetic results were compared with functional genes in the microcosms studied. The last chapter of this global study on chlorinated compound degradation genes was to link the microbial community structure kinetics with the chemical degradation kinetics. In order to evaluate the molecular biological parameters of the microbial community, all the genes known to be involved in the entire pathway of PCE reductive dechlorination were quantified. This global study, incorporating chemical monitoring, dehalogenase quantification and microbial community structure, produced correlations between the environmental conditions necessary for dechlorination and the microbial community associated with dehalogenase expression. In summary, both the mechanisms implemented by the bacteria to degrade this compound pollutant and the bacterial community structure during the pollutant degradation were addressed. Improving the understanding of these two steps in bacterial adaptation can contribute to the understanding of bacterial and environmental cleanup capabilities
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Paris, Josephine Rosanna. "Brown trout and toxic metals : local adaptation to the legacy of Britain's mining history." Thesis, University of Exeter, 2017. http://hdl.handle.net/10871/29554.
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The effect of human activity on the natural world is increasingly shaping the evolution of species. The capacity of evolution to occur in individuals of a species, via natural selection acting on the genotypes of local populations through successive generations, is known as local adaptation. In southwest England, historical mining activity has resulted in a patchwork of highly metal-contaminated rivers across the region. Where the ecological diversity in many of these rivers has been decimated, metal-tolerant brown trout (Salmo trutta L.) populations seem to thrive. What are the mechanisms underlying this apparent metal-tolerance? And can it be attributed to processes of local adaptation? This thesis takes a multi-faceted approach in assessing this, by exploring the patterns and processes involved in metal-tolerance in brown trout populations in southwest England. A series of investigations were undertaken, including the use of neutral genetic markers (microsatellites), reduced representation genome sequencing (RAD-seq), common-garden exposure experiments, and genome-wide analysis of hepatic gene expression (RNA-seq). The microsatellite analysis illustrated that metal-tolerant trout have a different genetic architecture compared to fish in clean rivers and, using Bayesian analysis, these demographic differences were correlated with key periods of mining history. We then developed an approach to facilitate robust screening of genome-wide polymorphic loci through a method of parameter optimisation for RAD-seq. This approach formed the basis for identifying loci for investigating the genomic processes of local adaptation in metal-tolerant trout. We present genome-wide (RAD-seq) data highly indicative that neighbouring trout populations, differently impacted by unique ‘cocktails’ of metal pollutants have evolved both parallel and convergent mechanisms of metal tolerance. Through a common garden experiment, exposing metal-tolerant and metal-naïve fish to a mixture of metals, we were able to hone in on the physiological mechanisms underlying metal-tolerance. Finally, through RNA-seq, we observed that metal-tolerant fish showed little to no changes in hepatic gene expression when exposed to metals, pointing to innate mechanisms of metal handling. Together, the marriage of these various investigations showcases the remarkable ability of local adaptation in conferring metal-tolerance to brown trout populations in southwest England, and, importantly, the resilience of species’ in the face of human-altered environments.
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Bayonne, Mboumba Georges. "Assessment of quantitative and genetic molecular variation of Acacia karroo in two extreme populations." Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019/497.
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Voigt, Susanne [Verfasser], and Wolfgang [Akademischer Betreuer] Stephan. "Molecular evolution in Drosophila melanogaster : genetic aspects of thermal adaptation / Susanne Voigt. Betreuer: Wolfgang Stephan." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1080122206/34.
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