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Relevant bibliographies by topics / Insertion mutations

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Academic literature on the topic 'Insertion mutations'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "Insertion mutations"

1

Ruan, Zheng, та Natarajan Kannan. "Altered conformational landscape and dimerization dependency underpins the activation of EGFR by αC–β4 loop insertion mutations". Proceedings of the National Academy of Sciences 115, № 35 (2018): E8162—E8171. http://dx.doi.org/10.1073/pnas.1803152115.

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Mutational activation of epidermal growth factor receptor (EGFR) in human cancers involves both point mutations and complex mutations (insertions and deletions). In particular, short in-frame insertion mutations within a conserved αC–β4 loop in the EGFR kinase domain are frequently observed in tumor samples and patients harboring these mutations are insensitive to first-generation EGFR inhibitors. Despite the prevalence and clinical relevance of insertion mutations, the mechanisms by which these mutations regulate EGFR activity and contribute to drug sensitivity are poorly understood. Using cell-based mutation screening, we find that the precise location, length, and sequence of the inserted segment are critical for ligand-independent EGFR activation and downstream signaling. We identify three insertion mutations (N771_P772insN, D770_N771insG, and D770>GY) that activate EGFR in a unique way by relying more on the “acceptor” interface for kinase activation. Our drug inhibition studies indicate that these activating insertion mutations respond more favorably to osimertinib, a recently Food and Drug Administration-approved EGFR inhibitor for T790M-positive patients with lung cancer. Molecular dynamics simulations and umbrella sampling of WT and mutant EGFR suggest a model in which activating insertion mutations increase catalytic activity by relieving key autoinhibitory interactions associated with αC-helix movement and by lowering the transition free energy (ΔGactive-inactive) between active and inactive states. Our studies also identify a transition state sampled by activating insertion mutations that can be exploited in the design of mutant-selective EGFR inhibitors.

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ZHU, YONG, JOAN E. STRASSMANN, and DAVID C. QUELLER. "Insertions, substitutions, and the origin of microsatellites." Genetical Research 76, no. 3 (2000): 227–36. http://dx.doi.org/10.1017/s001667230000478x.

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This paper uses data from the Human Gene Mutation Database to contrast two hypotheses for the origin of short DNA repeats: substitutions and insertions that duplicate adjacent sequences. Because substitutions are much more common than insertions, they are the dominant source of new 2-repeat loci. Insertions are rarer, but over 70% of the 2–4 base insertion mutations are duplications of adjacent sequences, and over half of these generate new repeat regions. Insertions contribute fewer new repeat loci than substitutions, but their relative importance increases rapidly with repeat number so that all new 4–5-repeat mutations come from insertions, as do all 3-repeat mutations of tetranucleotide repeats. This suggests that the process of repeat duplication that dominates microsatellite evolution at high repeat numbers is also important very early in microsatellite evolution. This result sheds light on the puzzle of the origin of short tandem repeats. It also suggests that most short insertion mutations derive from a slippage-like process during replication.

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3

Chang, D. Y., B. Wisely, S. M. Huang, and R. A. Voelker. "Molecular cloning of suppressor of sable, a Drosophila melanogaster transposon-mediated suppressor." Molecular and Cellular Biology 6, no. 5 (1986): 1520–28. http://dx.doi.org/10.1128/mcb.6.5.1520.

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A hybrid dysgenesis-induced allele [su(s)w20] associated with a P-element insertion was used to clone sequences from the su(s) region of Drosophila melanogaster by means of the transposon-tagging technique. Cloned sequences were used to probe restriction enzyme-digested DNAs from 22 other su(s) mutations. None of three X-ray-induced or six ethyl methanesulfonate-induced su(s) mutations possessed detectable variation. Seven spontaneous, four hybrid dysgenesis-induced, and two DNA transformation-induced mutations were associated with insertions within 2.0 kilobases (kb) of the su(s)w20 P-element insertion site. When the region of DNA that included the mutational insertions was used to probe poly(A)+ RNAs, a 5-kb message was detected in wild-type RNA that was present in greatly reduced amounts in two su(s) mutations. By using strand-specific probes, the direction of transcription of the 5-kb message was determined. The mutational insertions lie in DNA sequences near the 5' end of the 5-kb message. Three of the seven spontaneous su(s) mutations are associated with gypsy insertions, but they are not suppressible by su(Hw).

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4

Chang, D. Y., B. Wisely, S. M. Huang, and R. A. Voelker. "Molecular cloning of suppressor of sable, a Drosophila melanogaster transposon-mediated suppressor." Molecular and Cellular Biology 6, no. 5 (1986): 1520–28. http://dx.doi.org/10.1128/mcb.6.5.1520-1528.1986.

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A hybrid dysgenesis-induced allele [su(s)w20] associated with a P-element insertion was used to clone sequences from the su(s) region of Drosophila melanogaster by means of the transposon-tagging technique. Cloned sequences were used to probe restriction enzyme-digested DNAs from 22 other su(s) mutations. None of three X-ray-induced or six ethyl methanesulfonate-induced su(s) mutations possessed detectable variation. Seven spontaneous, four hybrid dysgenesis-induced, and two DNA transformation-induced mutations were associated with insertions within 2.0 kilobases (kb) of the su(s)w20 P-element insertion site. When the region of DNA that included the mutational insertions was used to probe poly(A)+ RNAs, a 5-kb message was detected in wild-type RNA that was present in greatly reduced amounts in two su(s) mutations. By using strand-specific probes, the direction of transcription of the 5-kb message was determined. The mutational insertions lie in DNA sequences near the 5' end of the 5-kb message. Three of the seven spontaneous su(s) mutations are associated with gypsy insertions, but they are not suppressible by su(Hw).

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5

Quiñones-Mateu, Miguel E., Mahlet Tadele, Mariona Parera, et al. "Insertions in the Reverse Transcriptase Increase both Drug Resistance and Viral Fitness in a Human Immunodeficiency Virus Type 1 Isolate Harboring the Multi-Nucleoside Reverse Transcriptase Inhibitor Resistance 69 Insertion Complex Mutation." Journal of Virology 76, no. 20 (2002): 10546–52. http://dx.doi.org/10.1128/jvi.76.20.10546-10552.2002.

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ABSTRACT Recent studies have shown that the accumulation of multiple mutations associated with nucleoside reverse transcriptase inhibitor (NRTI) resistance may be grouped as multi-NRTI resistance (MNR) complexes. In this study, we have examined the viral fitness of recombinant viruses carrying the reverse transcriptase (RT) of a human immunodeficiency virus type 1 (HIV-1) primary isolate harboring mutations comprising the MNR 69 insertion complex. Different RT mutants were prepared in the sequence context of either the wild-type RT sequence of the HIV-1BH10 isolate or the sequence found in a clinical HIV-1 isolate with the MNR 69 insertion mutation. As expected, in the presence of zidovudine, recombinant viruses harboring the MNR RT from the patient were more fit than wild-type viruses. However, in the absence of drug, the virus with the RT from the original clinical isolate (SS) was more fit than (i) the wild-type virus with an engineered serine insertion between residues 69 and 70 (T69SSS) and (ii) the recombinant virus with the MNR RT where the insertion was removed (2S0S). These results suggest that RT insertions, in the right sequence context (i.e., additional mutations contained in the MNR 69 insertion complex), enhance NRTI resistance and may improve viral fitness. Thus, comparing complex mutation patterns with viral fitness may help to elucidate the role of uncharacterized drug resistance mutations in antiretroviral treatment failure.

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Mastrangelo, M. F., K. G. Weinstock, B. K. Shafer, A. M. Hedge, D. J. Garfinkel, and J. N. Strathern. "Disruption of a silencer domain by a retrotransposon." Genetics 131, no. 3 (1992): 519–29. http://dx.doi.org/10.1093/genetics/131.3.519.

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Abstract A galactose-inducible Ty element carrying the HIS3 gene has been used as an insertional mutagen to generate alpha-factor resistant mutants. This collection of Ty-induced mutations includes insertions into the gene for the alpha-factor receptor (STE2), several nonspecific STE genes, and mutations that lead to the expression of the normally silent HML alpha locus. The hml alpha "on" mutations fall into two classes, those that disrupt trans-acting regulators involved in silencing HML alpha and a novel class of mutations that activate HML alpha by insertion at that locus. The hml alpha::Ty "on" mutations illustrate the unusual ability of these retrotransposons to activate genes by overcoming gene silencing mechanisms. The hml alpha::Ty "on" mutations include examples of multimeric Ty arrays. Single Ty and solo delta insertion derivatives of these Ty multimers restore the ability of the silencing mechanism to repress HML alpha.

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Godwin, A. R., and R. M. Liskay. "The effects of insertions on mammalian intrachromosomal recombination." Genetics 136, no. 2 (1994): 607–17. http://dx.doi.org/10.1093/genetics/136.2.607.

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Abstract We examined the effects of insertion mutations on intrachromosomal recombination. A series of mouse L cell lines carrying mutant herpes simplex virus thymidine kinase (tk) heteroalleles was generated; these lines differed in the nature of their insertion mutations. In direct repeat lines with different large insertions in each gene, there was a 20-fold drop in gene conversion rate and only a five-fold drop in crossover rate relative to the analogous rates in lines with small insertions in each gene. Surprisingly, in direct repeat lines carrying the same large insertion in each gene, there was a larger drop in both types of recombination. When intrachromosomal recombination between inverted repeat tk genes with different large insertions was examined, we found that the rate of gene conversion dropped five-fold relative to small insertions, while the rate of crossing over was unaffected. The differential effects on conversion and crossing over imply that gene conversion is more sensitive to insertion mutation size. Finally, the fraction of gene conversions associated with a crossover increased from 2% for inverted repeats with small insertions to 18% for inverted repeats with large insertions. One interpretation of this finding is that during intrachromosomal recombination in mouse cells long conversion tracts are more often associated with crossing over.

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Fassler, J. S., and F. Winston. "Isolation and analysis of a novel class of suppressor of Ty insertion mutations in Saccharomyces cerevisiae." Genetics 118, no. 2 (1988): 203–12. http://dx.doi.org/10.1093/genetics/118.2.203.

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Abstract Using a new scheme for the isolation of suppressor of Ty insertion mutations (spt mutations) in yeast, we have identified six new SPT genes. Mutations in two of these genes, SPT13 and SPT14, exhibit a novel suppression pattern: suppression of complete Ty insertion mutations, but not of solo delta insertion mutations. Transcriptional analysis shows that spt13- and spt14-mediated suppression of Ty insertion mutations is the result of an elevation in the levels of adjacent gene transcription. In spite of the failure of these mutations to suppress solo delta insertion mutations, they do cause changes in transcription of at least one solo delta insertion mutation. In addition, spt13 and spt14 mutations are epistatic to mutations in certain other SPT genes that do suppress solo delta insertion mutations. These results suggest that the SPT13 and SPT14 gene products may act via sequences in both the delta and epsilon regions of Ty elements. Finally, mutations in SPT13 cause sporulation and mating defects and SPT14 is essential for growth, suggesting that these two genes have important roles in general cellular functions.

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Laudadio, Jennifer, Michael W. N. Deininger, Michael J. Mauro, Brian J. Druker, and Richard D. Press. "An Intron-Derived Insertion/Truncation Mutation in the BCR-ABL Kinase Domain in Three CML Patients Undergoing Kinase Inhibitor Therapy." Blood 110, no. 11 (2007): 1953. http://dx.doi.org/10.1182/blood.v110.11.1953.1953.

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Abstract Although targeted inhibition of BCR-ABL with imatinib is an effective therapy for patients with chronic myeloid leukemia, a minority acquire mutations in the kinase domain (KD) that cause imatinib resistance. The spectrum of KD mutations thus far discovered, although quite heterogeneous, includes almost exclusively single nucleotide substitutions in key amino acids regulating drug binding or BCR-ABL function. Here, we describe a KD insertion/truncation mutation in 3 CML patients undergoing kinase inhibitor therapy. Two of these patients were being treated with imatinib (for 12 and 17 months), and one with dasatinib (for 13 months after a prior relapse while on imatinib). Suspected drug resistance was assessed by direct DNA sequencing of a BCR-ABL PCR product extending to the end of the kinase domain. Each of these 3 patients had 35 nucleotides from ABL intron 8 inserted at the normal exon 8–9 splice junction, after nucleotide 1423 (amino acid 475) of Genbank cDNA clone NM_005157. In all 3 cases, the mutation was co-expressed with wild type BCR-ABL sequence. The inserted sequence is derived from intron 8, beginning 1151 bp downstream from the normal splice donor site at the end of exon 8. This 35 bp intronic sequence is flanked by excellent consensus splice donor and acceptor sequences, suggesting alternative splicing as the likely mutational mechanism. The insertion creates a premature translational stop codon after 10 intron-encoded amino acids (figure), thus truncating 653 C-terminal amino acids including part of the KD and the entire last exon region - including a proline-rich domain, 3 nuclear localization signals, a DNA-binding domain, an actin-binding domain, and a nuclear export signal. These 3 insertion mutation cases were detected in our diagnostic clinical molecular pathology laboratory after sequencing 174 cases referred to us for suspected kinase inhibitor resistance, 78 of which contained a detectable mutation. The estimated prevalence of the exon 8/9 insertion/truncation mutation is then approximately 1.7% among patients with suspected drug resistance, and this mutation constitutes approximately 3.8% of all mutations. Conclusion: Kinase domain insertions are an alternative (and not entirely uncommon) mutational mechanism in CML patients undergoing kinase inhibitor therapy. The functional significance in terms of kinase activity and drug resistance remains to be addressed. Figure: Amino acid sequence of the C-terminus of the BCR-ABL kinase domain for the wild type and insertion/truncation mutant (with numbering as per GenBank cDNA clone NM_005157). Figure: Amino acid sequence of the C-terminus of the BCR-ABL kinase domain for the wild type and insertion/truncation mutant (with numbering as per GenBank cDNA clone NM_005157).

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Skamaki, Kalliopi, Stephane Emond, Matthieu Chodorge, et al. "In vitro evolution of antibody affinity via insertional scanning mutagenesis of an entire antibody variable region." Proceedings of the National Academy of Sciences 117, no. 44 (2020): 27307–18. http://dx.doi.org/10.1073/pnas.2002954117.

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We report a systematic combinatorial exploration of affinity enhancement of antibodies by insertions and deletions (InDels). Transposon-based introduction of InDels via the method TRIAD (transposition-based random insertion and deletion mutagenesis) was used to generate large libraries with random in-frame InDels across the entire single-chain variable fragment gene that were further recombined and screened by ribosome display. Knowledge of potential insertion points from TRIAD libraries formed the basis of exploration of length and sequence diversity of novel insertions by insertional-scanning mutagenesis (InScaM). An overall 256-fold affinity improvement of an anti–IL-13 antibody BAK1 as a result of InDel mutagenesis and combination with known point mutations validates this approach, and suggests that the results of this InDel mutagenesis and conventional exploration of point mutations can synergize to generate antibodies with higher affinity.

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Dissertations / Theses on the topic "Insertion mutations"

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Edwards, Richard John. "The role of transient insertion mutations in the evolution and maintenance of bacterial transposable elements." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394867.

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Krouchi, Ahmed. "Mutations économiques et insertion des communautés immigrées en banlieue nord de Paris : Aubervilliers et Saint-Denis." Paris 4, 2003. http://www.theses.fr/2003PA040166.

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Cette recherche porte sur l'étude de l'évolution de deux phénomènes ambivalents et de leurs incidences sur l'insertion des populations immigrées. D'un coté, la récession économique engendrée par le premier choc pétrolier ; de l'autre, la recomposition de familles immigrées sur le sol d'accueil, suite à l'arrêt de l'immigration de travail. La conjugaison de ces deux phénomènes nous a amené à cerner les deux types de mutations intervenues au sein de ces populations. Il y a d'abord les mutations internes avec le changement des caractéristiques démographiques et des emplois occupés par leurs membres ; puis, des mutations externes liées à l'évolution du paysage économique local, après l'effondrement du secteur industriel. Le profond bouleversement des réalités locales, a donné lieu à une approche sur le terrain des problèmes d'insertion des immigrés, abordés surtout sous l'angle de l'exclusion urbaine<br>This research deals with the evolution of two ambivalent phenomena and their effects on the insertion of immigrant populations : on one side, the economic slow down born from the first oil shock : on the other, the reconstruction of immigrants families in France as a consequence of the end of labour migrations. The addition of these two phenomena led us to distinguish two types of mutations among these populations : first the internal mutations which were conducive to changes in the demographic and employment characteristics of their members; secondly the external mutations linked with the evolution of the local economic situation, after the collapse of the industrial sector. Because of the deep disruption of local realities, we focused our field work on the problems of immigrants, mainly those related to urban exclusion

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Han, Yi-Hong. "SEQUENCE SPECIFICITY OF TENIPOSIDE-INDUCED DELETION AND INSERTION MUTATIONS AT THE APRT LOCUS OF CHINESE HAMSTER CELLS." VCU Scholars Compass, 1992. http://scholarscompass.vcu.edu/etd/4921.

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Previous studies suggested that teniposide is a strong clastogen, and that the DNA breakage effect of this drug is mediated by the nuclear enzyme topoisomerase II. Ripley et al found evidence for a correspondence between sites of acridine-induced frameshift mutations in bacteriophage T4 and sites of in Vitro DNA cleavage by T4 topoisomerase II. To identify the sequence specificity of teniposide-induced deletion and insertion mutations in mammalian cells, the CHO-D422 cell line, which is hemizygous at the aprt locus, was employed in this study. Sixty-eight teniposide-induced and 42 spontaneous aprt mutants were analyzed at the DNA sequence level. Compared with the spectrum of spontaneous mutations in which two thirds of the mutations are base substitutions, two thirds of teniposide-induced mutations are deletions and insertions of different sizes. Significant site correspondence between teniposide-induced deletion/insertion mutations and in vitro DNA double strand cleavages by purified mammalian topoisomerase II was also found in this study, which suggests that the majority of teniposide-induced deletions and insertions observed in this study were generated at the sites of topoisomerase II mediated DNA double strand breaks in the cells. However, considering the positions of the double cleavage sites in the mutation sequences, no consistent pattern was found which could suggest a unified mechanism of DNA double strand break repair. Three models are proposed to try to explain the possible events occurring in the cells following teniposide exposure which resulted in observed deletion and insertion mutations.

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Indukuri, Vijaya Varma. "Transposon based mutagenesis and mapping of transposon insertion sites within the Ehrlichia chaffeensis genome using semi random two-step PCR." Thesis, Kansas State University, 2013. http://hdl.handle.net/2097/16329.

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Master of Science<br>Department of Diagnostic Medicine/Pathobiology<br>Roman Reddy Ganta<br>Ehrlichia chaffeensis a tick transmitted Anaplasmataceae family pathogen responsible for human monocytic ehrlichiosis. Differential gene expression appears to be an important pathogen adaptation mechanism for its survival in dual hosts. One of the ways to test this hypothesis is by performing mutational analysis that aids in altering the expression of genes. Mutagenesis is also a useful tool to study the effects of a gene function in an organism. Focus of my research has been to prepare several modified Himar transposon mutagenesis constructs for their value in introducing mutations in E. chaffeensis genome. While the work is in progress, research team from our group used existing Himar transposon mutagenesis plasmids and was able to create mutations in E. chaffeensis. Multiple mutations were identified by Southern blot analysis. I redirected my research efforts towards mapping the genomic insertion sites by performing the semi-random two step PCR (ST-PCR) method, followed by DNA sequence analysis. In this method, the first PCR is performed with genomic DNA as the template with a primer specific to the insertion segment and the second primer containing an anchored degenerate sequence segment. The product from the first PCR is used in the second PCR with nested transposon insertion primer and a primer designed to bind to the known sequence portion of degenerate primer segment. This method aided in identifying the genomic locations of four E. chaffeensis mutants and also was valuable in confirming four other sites mapped previously by the rescue cloning method. This is the first mutational analysis study in the genome of an Ehrlichia species. Mapping the genomic transposon insertion sites is the first critical step needed for the continued research to define the importance of the mutations in understanding the pathogenesis caused by the organism.

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Lecuir-Nemo, Geneviève. "Femmes et vocation missionnaire, permanence des congrégations féminines au Sénégal de 1819 à 1960$$eadaptation ou mutations ? Impact et insertion." Paris 1, 1995. http://www.theses.fr/1995PA010596.

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L'arrivée à Saint-Louis du Sénégal des premières religieuses de Saint-Joseph de Cluny le 19 mars 1819, se fait dans le cadre de la restauration et de la reprise par la France des vestiges de son premier empire colonial; la fondatrice, Mère Javouhey, donne ainsi à la jeune congrégation sa dimension missionnaire. Les premières à aborder le sol africain sont chargées de la gestion des hôpitaux, du soin des malades et de l'ouverture d'écoles pour les filles. Les sœurs de Notre-Dame de l'immaculée-conception de castres les rejoignent en 1848, envoyées par leur fondatrice, Mère Marie de Villeneuve, pour seconder les missionnaires sur la presqu'ile du Cap-Vert ou nait bientôt le port de Dakar. Puis, pour atténuer les résistances à la christianisation (Islam), une congrégation autochtone est fondée : les filles du saint-cœur de Marie. La présence et les activités de ces religieuses sont le résultat de l'option missionnaire prise par leurs fondatrices, dans un double contexte, colonial et religieux. Jusqu'en 1904, les religieuses ont un rôle essentiel assurant presque exclusivement l'éducation des filles et l'action sociale et secondant les missionnaires. Les lois laïques de 1904, rompent momentanément leurs liens étroits avec l'administration coloniale. Les guerres mondiales, les profonds changements politiques et sociaux qui en découlent leur permettent de poursuivre leur action, avec une remarquable faculté d'adaptation et de renouvellement aux nouvelles conditions de leur présence, suivant les transformations de la conception de la mission<br>The arrival in Saint-Louis du Senegal of the first nuns from the order of saint-Joseph-de-Cluny, on march 19th 1819, takes place within and as a part of the French restoration, enablinbg France to recover the remnants of its former colonial empire. Its founder, Mother Javouhey, thus gives her young community its missionary dimension. The first nuns to land in Africa are in charge of hospital management, medical care and the opening of schools for girls. The nuns from Notre-Dame de l'Immaculée-Conception-de-Castres join them in 1848, sent by their founder, Mother Marie de Villeneuve, to help the missionaries of the Cap-Vert peninsula where Dakar is soon to develop. Then, to reduce the opposition to Christianization (Islam), a native religious community is founded : les filles du Saint-Coeur-De-Marie. The presence and activities of these nuns are a consequence of their founders' missionary option in a twofold context, both colonial and religious. Up to 1904, the nuns have an essential role : they are almost exclusively in charge of girls' education and welfare activities, and support the missionaries. The 1904 lay laws temporarily sever their close links with the colonial administration. The world wars and the following deep political and social changes enales to continue their work with a surprisingly active sense of adaptation and renovation, allowing them to meet the new conditions of their presence - following a change in the very idea of the missionary activity. Nuns arriving from other communities bring a fresh and important addition of their workforce, and contribute to the expansion of Catholicism

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Lahiouel, Ridha. "Mutations démographiques et emploi : le cas des étudiants du Sud-Est tunisien." Thesis, Paris 10, 2014. http://www.theses.fr/2014PA100110/document.

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En Tunisie, la massification et la démocratisation de l’enseignement supérieur ont explosé le nombre de diplômés qui éprouvent des difficultés d’insertion professionnelle depuis le début des années 1980, cette conjoncture a été l’un des principaux déclencheurs de la révolution du 14 janvier 2011.Comme dans plusieurs des pays, l’origine du chômage des diplômés tunisiens réside essentiellement dans le déphasage entre les formations (investissement en capital humain) et les besoins des entreprises (l’investissement en matière d’emploi).Ce phénomène ne manque pas d’avoir des conséquences sociodémographiques importantes. En effet, les individus en difficulté d’insertion sont souvent victimes d’un sentiment de marginalisation, voire d’exclusion, notamment des transactions matrimoniales (retard de leur date de mise en couple qui aura des conséquences sur la fécondité). Les diplômés développent alors des stratégies pour échapper au chômage tels que l’émigration, la poursuite des études surtout pour les filles ou la création d’entreprises si la situation financière le permet.L’objectif de cette thèse consiste à étudier et à comprendre les interactions entre l’emploi et les phénomènes démographiques<br>In Tunisia, the massification and democratization of higher education have exploded the number of graduates who have employability problems since the early 1980s, this situation was one of the main triggers of the Revolution of January 14, 2011. As in many countries, causing the unemployment Tunisian graduates lies essentially in the phase shift between training (human capital investment), and business needs (investment in employment). This phenomenon does not fail to have significant sociodemographic consequences. Indeed, individuals with insertion difficulties often experience a sense of marginalization or exclusion, including matrimonial transactions (delay their date of couple formation will affect fertility). Graduates eek to developing strategies to escape unemployment to escape unemployment such as emigration, further education especially for girls or business creation if the financial situation allows.The objective of this thesis is to study and understand the interactions between employment and demographic phenomena

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Arpino, James. "From single amino acid deletions to whole domain insertions : engineering GFP through polypeptide backbone mutations." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/14266/.

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With an ever-expanding protein engineering toolbox different mutational techniques can be used to engineer new or altered function into protein scaffolds without the restriction of sampling just simple substitution mutagenesis. These include approaches that target backbone as well as side chain changes, such as single amino acid deletions or whole domain insertion. The problem with utilizing these mutational approaches is the difficulty in predicting both local and global structural changes on changing the backbone conformation. The aim of this thesis is to demonstrate the tolerance and beneficial influence of backbone targeted mutations using a mutant library-based screening approach, and to provide an understanding of their mechanism of action. A directed evolution transposon-based approach was used to generate libraries of single amino acid deletion and whole domain insertions into enhanced green fluorescent protein (EGFP). The later involved the insertion of cyt b562 as the donating insert domain. Library analysis revealed a wide range of sites were sampled across the backbone of EGFP. Library screening revealed widespread tolerance of EGFP to single amino acid deletions. Using the crystal structure of EGFP determined here, it was found that that loop regions where particularly tolerant. Two variants with residues G4 or A227 deleted conferred increased protein fluorescence to cell cultures with respect to EGFP. Spectral characterization and unfolding experiments identified that rather than altering the fluorescent properties of EGFP the mutations elicited their effects through altered protein folding and stability. Screening of the domain insert library revealed that sites spread along the backbone of EGFP were tolerant to cyt b562 insertion. Particularly tolerant were loops and the C-terminal end of β-strand 7, with the linker sequences playing a key role. One integral domain fusion scaffold, termed CG6, was identified in which the functions of the two individual domains were highly coupled. CG6 exhibited almost 100% fluorescence quenching upon the binding of haem to the cyt b562 domain. CG6 was also shown to potentially act as a sensor for redox state and reactive oxygen species such as H2O2 via a haem-dissociation dependent mechanism. The structure of CG6, determined by X-ray crystallography, provided the molecular basis for the functional coupling of the two domains. Critical was the side-by-side domain arrangement caused by differential linker lengths at the pivot position re-enforced by a domain-domain interface that placed the chromophores within 17-18Å of each other. Further rational design of a cyt b562-EGFP integral fusion scaffold (CG15) was performed to create novel ratiometric fluorescent redox sensors, termed CG15CC variants. The CG15CC variants have been shown to have the most reducing redox midpoint potentials of any protein based redox sensor studied to date. One of the CG15CC variants also has the fastest redox kinetics observed to date. The survey of the tolerance and influence of single amino acid deletions in EGFP conducted here has highlighted the potential beneficial nature of deletion mutagenesis and has helped provide a molecular understanding of their effect. Through domain insertion mutagenesis and retrospective structure analysis the mechanism behind the functional coupling of two domains has been described and will also help guide future work in the development of novel biomolecular switches.

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Signorelli, Katherine Louise. "Characterization of an insertional mutation in a line of transgenic mice /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=744576231&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Callahan, Jennifer Ware. "Analysis of mutations that suppress transport defects in Escherichia coli /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10276.

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Bellanger, Fabienne. "La mutagenèse par insertion d'ADN chez Chlamydomonas reinhardtii : une nouvelle voie pour l'élucidation de la biosynthèse." Compiègne, 1994. http://www.theses.fr/1994COMP686S.

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Une souche sans paroi de l'algue verte unicellulaire chlamydomonas reinhardtii auxotrophe pour l'arginine a été transformée par le plasmide parg 7. 8 par agitation en présence de billes de verre. Les cellules ayant intégré une copie fonctionnelle du plasmide ont été sélectionnées par leur capacité à croître sur un milieu dépourvu d'arginine, le plasmide portant le gène de l'argino-succinate lyase sauvage complémentant l'auxotrophie. Des souches déficientes pour la biosynthèse de l'amidon ont été sélectionnées parmi les transformants. Parmi les 16 souches présentant un phénotype mutant pour la synthèse d'amidon, 10 accumulent de très faibles quantités du polysaccharide (inferieure à 5% de la quantité mesurée chez la souche sauvage). Deux souches sont mutées pour la synthèse de l'amylose et 4 autres accumulent une amylopectine modifiée. Une analyse génétique de la souche BAF R1 a permis de mettre en évidence l'intégration d'un plasmide parg 7. 8 fonctionnel au locus ST-2, conduisant à la délétion du gène de structure de la GBSS (Granule Bound Starch Synthase). Ceci nous a permis de prouver que la synthèse de longs glucanes n'est pas un prérequis pour la synthèse de l'amylopectine. L'un des mutants pauvres en amidon ne présente pas d'activité ADP-GLC pyrophosphorylase détectable. Cette délétion complémente la mutation ST-1-1 précédemment caractérisée comme défectueuse pour la même activité enzymatique. Ceci suggère que la transformation a conduit à la mutation du deuxième gène de structure de l'ADP-GLC pyrophosphorylase. La présence d'un polysaccharide soluble fortement branché, de type phytoglycogène, a été détectée chez un autre des mutants pauvres en amidon. 50 souches ont également été sélectionnées suite à un maintien de l'amidon dans des conditions qui induisent sa dégradation chez le sauvage.

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Books on the topic "Insertion mutations"

1

Small, Sheridan James. Molecular analysis of the recessive lethal insertional mutation in the ZDC2 transgenic line of mice (Mus musculus). typescript, 1999.

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E, Lambert Michael, McDonald John F. 1947-, Weinstein I. Bernard, Cold Spring Harbor Laboratory, and Abbott Laboratories, eds. Eukaryotic transposable elements as mutagenic agents. Cold Spring Harbor Laboratory, 1988.

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Lambert, Michael E., and John F. McDonald. Eukaryotic Transposable Elements As Mutagenic Agents (Banbury Report) (Banbury Report). Cold Spring Harbor Laboratory Pr, 1988.

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Wen, Xiao-Yan. Characterization of a mouse insertional mutation lpd associated with a deffect in triglyceride metabolism. 1995.

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Arthur, Brown. Molecular analysis of an insertional mutation at the mouse dt locus: the identification of a candidate dt gene. 1993.

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Book chapters on the topic "Insertion mutations"

1

Coury, D. A., and K. A. Feldmann. "T-DNA Insertion Mutagenesis and the Untagged Mutants." In Somaclonal Variation and Induced Mutations in Crop Improvement. Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-015-9125-6_26.

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Elena, Santiago F., Lynette Ekunwe, Neerja Hajela, Shenandoah A. Oden, and Richard E. Lenski. "Distribution of fitness effects caused by random insertion mutations in Escherichia coli." In Mutation and Evolution. Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5210-5_28.

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Fujii, Ryota, Motomitsu Kitaoka, and Kiyoshi Hayashi. "Random Insertional–Deletional Strand Exchange Mutagenesis (RAISE): A Simple Method for Generating Random Insertion and Deletion Mutations." In Methods in Molecular Biology. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1053-3_10.

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Bae, Taeok, Elizabeth M. Glass, Olaf Schneewind, and Dominique Missiakas. "Generating a Collection of Insertion Mutations in the Staphylococcus aureus Genome Using bursa aurealis." In Microbial Gene Essentiality: Protocols and Bioinformatics. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-321-9_7.

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Oldenburg, J., J. Schröder, C. Schmitt, H. H. Brackmann, and R. Schwaab. "Small Deletion/Insertion Mutations Within Poly-A Runs of the Factor VIII Gene Mitigate the Severe Haemophilia A Phenotype." In 28. Hämophilie-Symposion Hamburg 1997. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59915-6_27.

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York, Daniel S., Vincent M. Blum, Jonathan A. Low, et al. "Phylogenetic signals from point mutations and polymorphic Alu insertions." In Transposable Elements and Genome Evolution. Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4156-7_18.

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Pearson, Melanie M., Stephanie D. Himpsl, and Harry L. T. Mobley. "Insertional Mutagenesis Protocol for Constructing Single or Sequential Mutations." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9601-8_7.

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Kalkreuth, Roman. "An Empirical Study on Insertion and Deletion Mutation in Cartesian Genetic Programming." In Studies in Computational Intelligence. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70594-7_4.

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Churkin, Alexander, and Danny Barash. "A Biologically Meaningful Extension of the Efficient Method for Deleterious Mutations Prediction in RNAs: Insertions and Deletions in Addition to Substitution Mutations." In Bioinformatics Research and Applications. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94968-0_15.

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Wang, Wenyan, and Bruce A. Malcolm. "Two-Stage Polymerase Chain Reaction Protocol Allowing Introduction of Multiple Mutations, Deletions, and Insertions, Using QuikChangeTM Site-Directed Mutagenesis." In In Vitro Mutagenesis Protocols. Humana Press, 2002. http://dx.doi.org/10.1385/1-59259-194-9:037.

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Conference papers on the topic "Insertion mutations"

1

Lee, Yusoo, Tae Min Kim, Dong-Wan Kim, et al. "Abstract 3157: Osimertinib (AZD9291) is effective against NSCLC cells harboringEGFRexon 20 insertion mutations." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3157.

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Balado, Félix. "On the embedding capacity of DNA strands under substitution, insertion, and deletion mutations." In IS&T/SPIE Electronic Imaging, edited by Nasir D. Memon, Jana Dittmann, Adnan M. Alattar, and Edward J. Delp III. SPIE, 2010. http://dx.doi.org/10.1117/12.838537.

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Kim, Sunghwan, Younho Lee, Hwan Kim, et al. "Abstract B002: Discovery of selective and potent EGFR kinase inhibitors for exon20 insertion mutations." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-b002.

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Marhäll, Alissa, Thomas Fischer, Florian Heidel, Julhash U. Kazi, and Lars Rönnstrand. "Abstract 2380: Insertion mutations in the tyrosine kinase domain of FLT3 display a higher oncogenic potential than the D835Y mutation in acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2380.

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Yasuda, Hiroyuki, Natasha J. Sng, Wee-Lee Yeo, Lorena L. Figueiredo-Pontes, Susumu Kobayashi, and Daniel B. Costa. "Abstract 23: Sensitivity ofEGFRexon 20 insertion mutations to EGFR inhibitors is determined by their location within the tyrosine kinase domain of EGFR." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-23.

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Ichihara, Eiki, Hiroyuki Yasuda, Yuta Takashima, et al. "Abstract CT106: Phase I/II study of osimertinib in EGFR exon 20 insertion mutations in non-small cell lung cancer patients: AEX20." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-ct106.

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Xu, Yan, Lin Zhang, Lifang Zhu, Yingchun Wang, Mei Wang, and Zhenfan Yang. "Abstract 3081: DZD9008, an oral, wild type selective EGFR inhibitor for the treatment of non-small-cell lung cancer with Exon20 insertion and other activating mutations." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3081.

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Xu, Yan, Lin Zhang, Lifang Zhu, Yingchun Wang, Mei Wang, and Zhenfan Yang. "Abstract 3081: DZD9008, an oral, wild type selective EGFR inhibitor for the treatment of non-small-cell lung cancer with Exon20 insertion and other activating mutations." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3081.

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Nazeri, Zeinab, and Leyli Mohammad Khanli. "An insertion mutation operator for solving project scheduling problem." In 2014 Iranian Conference on Intelligent Systems (ICIS). IEEE, 2014. http://dx.doi.org/10.1109/iraniancis.2014.6802537.

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Busby, S., K. Berkner, L. Halfpap, J. Gambee, and A. Kumar. "ALTERATION OF PROPTIDE SEQUENCE IMPAIRS BIOLOGICAL ACTIVITY OF HUMAN FACTOR VII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643784.

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We have investigated the effect of altering the leader sequence of human factor VII on its biological activity. Factor VII is a vitamin K-dependent blood coagulation protein whose activity depends on the presence of gamma-carboxyglutamic acid (gla) residues in its amino terminal region. Since factor VII and other vitamin K-dependent proteins exhibit structural homology in the propeptide, it has been suggested that the propeptide is involved in gamma-carboxylation. Recently, two factor IX patients were identified with point mutations which prevented the processing of the propeptide and generated a factor IX with greatly reduced biological activity (Diuguid et al., PNAS 83; 5803; Bentley et al., Cell 45: 343). To examine this question using recombinant DNA technology, we altered the sequence of the factor VII propeptide by in vitro mutagenesis of the factor VII cDNA and then expressed the altered genes in baby hamster kidney (BHK) cells. For the 60 and 38 aa leader forms of factor VII, the arg (R) at -1 was changed to ser (S), yielding the sequence HRRRS before the +1 ala. In addition, for the 60 aa leader form, a ser was inserted after the arg at -1, resulting in the sequence HRRRRS before the +1 ala. As determined by ELISA, the mutant proteins were synthesized and secreted by BHK cells at levels comparable to the wild-type forms of factor VII. Analysis by radioimmune precipitation and SDS-PAGE indicated that substitution of arg by ser at -1 prohibits processing of the factor VII propeptide, whereas, insertion of a ser after the four arg's does not. However, all three proteins have reduced biological activity by approximately 5-fold when compared to the wild-type forms with the one-stage clotting assay. All three proteins are also quantitatively precipitated by Ba citrate, indicating they are at least partially gamma-carboxylated. These results suggest that the correct sequence of the propeptide, not just cleavage of the propeptide, is necessary for generating a biologically active molecule. The effect of these sequence alterations on gamma-carboxylation will be evaluated further by analysis of the amino acid sequence and composition of the mutant proteins.

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