Journal articles: 'Cellular contexts'

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Nair, Surag, Daniel S. Kim, Jacob Perricone, and Anshul Kundaje. "Integrating regulatory DNA sequence and gene expression to predict genome-wide chromatin accessibility across cellular contexts." Bioinformatics 35, no. 14 (July 2019): i108—i116. http://dx.doi.org/10.1093/bioinformatics/btz352.

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Abstract Motivation Genome-wide profiles of chromatin accessibility and gene expression in diverse cellular contexts are critical to decipher the dynamics of transcriptional regulation. Recently, convolutional neural networks have been used to learn predictive cis-regulatory DNA sequence models of context-specific chromatin accessibility landscapes. However, these context-specific regulatory sequence models cannot generalize predictions across cell types. Results We introduce multi-modal, residual neural network architectures that integrate cis-regulatory sequence and context-specific expression of trans-regulators to predict genome-wide chromatin accessibility profiles across cellular contexts. We show that the average accessibility of a genomic region across training contexts can be a surprisingly powerful predictor. We leverage this feature and employ novel strategies for training models to enhance genome-wide prediction of shared and context-specific chromatin accessible sites across cell types. We interpret the models to reveal insights into cis- and trans-regulation of chromatin dynamics across 123 diverse cellular contexts. Availability and implementation The code is available at https://github.com/kundajelab/ChromDragoNN. Supplementary information Supplementary data are available at Bioinformatics online.

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Schwartz, Michael H., and Tao Pan. "Function and origin of mistranslation in distinct cellular contexts." Critical Reviews in Biochemistry and Molecular Biology 52, no. 2 (January 11, 2017): 205–19. http://dx.doi.org/10.1080/10409238.2016.1274284.

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Suresh, Nallan C., and Gerard J. C. Gaalman. "Performance evaluation of cellular layouts: Extension to DRC system contexts." International Journal of Production Research 38, no. 17 (November 2000): 4393–402. http://dx.doi.org/10.1080/00207540050205172.

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Dong, Xianjun, Melissa C. Greven, Anshul Kundaje, Sarah Djebali, James B. Brown, Chao Cheng, Thomas R. Gingeras, et al. "Modeling gene expression using chromatin features in various cellular contexts." Genome Biology 13, no. 9 (2012): R53. http://dx.doi.org/10.1186/gb-2012-13-9-r53.

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Angermann, Bastian R., Frederick Klauschen, Alex D. Garcia, Thorsten Prustel, Fengkai Zhang, Ronald N. Germain, and Martin Meier-Schellersheim. "Computational modeling of cellular signaling processes embedded into dynamic spatial contexts." Nature Methods 9, no. 3 (January 29, 2012): 283–89. http://dx.doi.org/10.1038/nmeth.1861.

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de Jong, Paulus T. V. M. "Myopia: its historical contexts." British Journal of Ophthalmology 102, no. 8 (February 3, 2018): 1021–27. http://dx.doi.org/10.1136/bjophthalmol-2017-311625.

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Worldwide, and especially in Asia, myopia is a major vision-threatening disorder. From AD 1600 on, to prevent myopia, authors warned against near work without sufficient pauses. There was an abundance of theories about the causes of myopia, the most common one being the necessity of extra convergence on nearby work with thickened extraocular muscles and elevated intraocular pressure. Ocular tenotomies against myopia were in vogue for a while. Axial lengthening of the eye in myopia was mentioned around 1700, but it took 150 years to become accepted as the most prevalent sign of high myopia. In 1864, a lucid concept of myopia and other ametropias arose through a clear separation between accommodation and refraction. Posterior staphyloma was known around 1800 and its association with myopia became evident some 30 years later. There still seems to be no generally accepted classification of myopia and particularly not of degenerative or pathologic myopia. This review focuses on myopia from 350 BC until the 21st century and on the earliest writings on the histology of eyes with posterior staphyloma. A proposal for myopia classification is given.

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Nam, Jin-Wu, Olivia S. Rissland, David Koppstein, Cei Abreu-Goodger, Calvin H. Jan, Vikram Agarwal, Muhammed A. Yildirim, Antony Rodriguez, and David P. Bartel. "Global Analyses of the Effect of Different Cellular Contexts on MicroRNA Targeting." Molecular Cell 53, no. 6 (March 2014): 1031–43. http://dx.doi.org/10.1016/j.molcel.2014.02.013.

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Schwaid, Adam G., and Ivan Cornella-Taracido. "Causes and Significance of Increased Compound Potency in Cellular or Physiological Contexts." Journal of Medicinal Chemistry 61, no. 5 (August 18, 2017): 1767–73. http://dx.doi.org/10.1021/acs.jmedchem.7b00762.

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Ling, Guy, Danielle Miller, Rasmus Nielsen, and Adi Stern. "A Bayesian Framework for Inferring the Influence of Sequence Context on Point Mutations." Molecular Biology and Evolution 37, no. 3 (November 5, 2019): 893–903. http://dx.doi.org/10.1093/molbev/msz248.

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Abstract The probability of point mutations is expected to be highly influenced by the flanking nucleotides that surround them, known as the sequence context. This phenomenon may be mainly attributed to the enzyme that modifies or mutates the genetic material, because most enzymes tend to have specific sequence contexts that dictate their activity. Here, we develop a statistical model that allows for the detection and evaluation of the effects of different sequence contexts on mutation rates from deep population sequencing data. This task is computationally challenging, as the complexity of the model increases exponentially as the context size increases. We established our novel Bayesian method based on sparse model selection methods, with the leading assumption that the number of actual sequence contexts that directly influence mutation rates is minuscule compared with the number of possible sequence contexts. We show that our method is highly accurate on simulated data using pentanucleotide contexts, even when accounting for noisy data. We next analyze empirical population sequencing data from polioviruses and HIV-1 and detect a significant enrichment in sequence contexts associated with deamination by the cellular deaminases ADAR 1/2 and APOBEC3G, respectively. In the current era, where next-generation sequencing data are highly abundant, our approach can be used on any population sequencing data to reveal context-dependent base alterations and may assist in the discovery of novel mutable sites or editing sites.

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Tien, An-Chi, Akhila Rajan, and Hugo J. Bellen. "A Notch updated." Journal of Cell Biology 184, no. 5 (March 2, 2009): 621–29. http://dx.doi.org/10.1083/jcb.200811141.

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Cell–cell signaling mediated by the Notch receptor is iteratively involved in numerous developmental contexts, and its dysregulation has been associated with inherited genetic disorders and cancers. The core components of the signaling pathway have been identified for some time, but the study of the modulation of the pathway in different cellular contexts has revealed many layers of regulation. These include complex sugar modifications in the extracellular domain as well as transit of Notch through defined cellular compartments, including specific endosomes.

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Geisler, Sarah, and Jeff Coller. "RNA in unexpected places: long non-coding RNA functions in diverse cellular contexts." Nature Reviews Molecular Cell Biology 14, no. 11 (October 9, 2013): 699–712. http://dx.doi.org/10.1038/nrm3679.

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Zhang, Mengying, Kang Xu, Limei Fu, Qi Wang, Zhenghong Chang, Haozhe Zou, Yan Zhang, and Yongsheng Li. "Revealing Epigenetic Factors of circRNA Expression by Machine Learning in Various Cellular Contexts." iScience 23, no. 12 (December 2020): 101842. http://dx.doi.org/10.1016/j.isci.2020.101842.

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Corda, Daniela, Pasquale Zizza, Alessia Varone, Karol S. Bruzik, and Stefania Mariggiò. "The glycerophosphoinositols and their cellular functions." Biochemical Society Transactions 40, no. 1 (January 19, 2012): 101–7. http://dx.doi.org/10.1042/bst20110679.

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Interest in the glycerophosphoinositols has been increasing recently, on the basis of their biological activities. The cellular metabolism of these water-soluble bioactive phosphoinositide metabolites has been clarified, with the identification of the specific enzyme involved in their synthesis, PLA2IVα (phospholipase A2 IVα), and the definition of their phosphodiesterase-based catabolism, and thus inactivation. The functional roles and mechanisms of action of these compounds have been investigated in different cellular contexts. This has led to their definition in the control of various cell functions, such as cell proliferation in the thyroid and actin cytoskeleton organization in fibroblasts and lymphocytes. Roles for the glycerophosphoinositols in immune and inflammatory responses are also being defined. In addition to these physiological functions, the glycerophosphoinositols have potential anti-metastatic activities that should lead to their pharmacological exploitation.

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Lee, Y. J., and J. M. Hallenbeck. "Insights into cytoprotection from ground squirrel hibernation, a natural model of tolerance to profound brain oligaemia." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1295–98. http://dx.doi.org/10.1042/bst0341295.

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Progression of acute ischaemic brain damage is complex and multifactorial. Also, evidence suggests that participating molecules and signal transduction pathways can function differently in different cellular contexts. Hibernation torpor, a model of natural tolerance to profoundly reduced blood flow and oxygen delivery to brain, along with models of induced ischaemic tolerance can guide efforts to identify cytoprotective mechanisms that are multifactorial and that target multiple mechanisms in multiple cellular contexts. Post-translational modification of proteins by conjugation with the SUMO (small ubiquitin-related modifier) is massively increased in hibernation and may be such a mechanism.

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Yozwiak, Carrie E., Tal Hirschhorn, and Brent R. Stockwell. "Toward a Microparticle-Based System for Pooled Assays of Small Molecules in Cellular Contexts." ACS Chemical Biology 13, no. 3 (January 24, 2018): 761–71. http://dx.doi.org/10.1021/acschembio.8b00043.

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CHOUDHARY, ASHISH, JIANPING HUA, MICHAEL L. BITTNER, and EDWARD R. DOUGHERTY. "THE EFFECT OF POPULATION CONTEXTS ON CLASSIFIER PERFORMANCE." Journal of Biological Systems 16, no. 04 (December 2008): 495–517. http://dx.doi.org/10.1142/s0218339008002587.

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Classifying a patient based on disease type, treatment prognosis, survivability, or other such criteria has become a major focus of genomics and proteomics. From the perspective of the general population of a particular kind of cell, one would like a classifier that applies to the whole population; however, it is often the case that the population is sufficiently structurally diverse that a satisfactory classifier cannot be designed from available sample data. In such a circumstance, it can be useful to identify cellular contexts within which a disease can be reliably diagnosed, which in effect means that one would like to find classifiers that apply to different sub-populations within the overall population. Using a model-based approach, this paper quantifies the effect of contexts on classification performance as a function of the classifier used and the sample size. The advantage of a model-based approach is that we can vary the contextual confusion as a function of the model parameters, thereby allowing us to compare the classification performance in terms of the degree of discriminatory confusion caused by the contexts. We consider five popular classifiers: linear discriminant analysis, three nearest neighbor, linear support vector machine, polynomial support vector machine, and Boosting. We contrast the case where classification is done with a single classifier without discriminating between the contexts to the case where there are context markers that facilitate context separation before classifier design. We observe that little can be done if there is high contextual confusion, but when the contextual confusion is low, context separation can be beneficial, the benefit depending on the classifier.

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Sharma, Divya Khandige, Kamiko Bressler, Harshil Patel, Nirujah Balasingam, and Nehal Thakor. "Role of Eukaryotic Initiation Factors during Cellular Stress and Cancer Progression." Journal of Nucleic Acids 2016 (2016): 1–19. http://dx.doi.org/10.1155/2016/8235121.

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Protein synthesis can be segmented into distinct phases comprising mRNA translation initiation, elongation, and termination. Translation initiation is a highly regulated and rate-limiting step of protein synthesis that requires more than 12 eukaryotic initiation factors (eIFs). Extensive evidence shows that the transcriptome and corresponding proteome do not invariably correlate with each other in a variety of contexts. In particular, translation of mRNAs specific to angiogenesis, tumor development, and apoptosis is altered during physiological and pathophysiological stress conditions. In cancer cells, the expression and functions of eIFs are hampered, resulting in the inhibition of global translation and enhancement of translation of subsets of mRNAs by alternative mechanisms. A precise understanding of mechanisms involving eukaryotic initiation factors leading to differential protein expression can help us to design better strategies to diagnose and treat cancer. The high spatial and temporal resolution of translation control can have an immediate effect on the microenvironment of the cell in comparison with changes in transcription. The dysregulation of mRNA translation mechanisms is increasingly being exploited as a target to treat cancer. In this review, we will focus on this context by describing both canonical and noncanonical roles of eIFs, which alter mRNA translation.

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Tominaga, Kana, and Hiroshi I. Suzuki. "TGF-β Signaling in Cellular Senescence and Aging-Related Pathology." International Journal of Molecular Sciences 20, no. 20 (October 10, 2019): 5002. http://dx.doi.org/10.3390/ijms20205002.

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Aging is broadly defined as the functional decline that occurs in all body systems. The accumulation of senescent cells is considered a hallmark of aging and thought to contribute to the aging pathologies. Transforming growth factor-β (TGF-β) is a pleiotropic cytokine that regulates a myriad of cellular processes and has important roles in embryonic development, physiological tissue homeostasis, and various pathological conditions. TGF-β exerts potent growth inhibitory activities in various cell types, and multiple growth regulatory mechanisms have reportedly been linked to the phenotypes of cellular senescence and stem cell aging in previous studies. In addition, accumulated evidence has indicated a multifaceted association between TGF-β signaling and aging-associated disorders, including Alzheimer’s disease, muscle atrophy, and obesity. The findings regarding these diseases suggest that the impairment of TGF-β signaling in certain cell types and the upregulation of TGF-β ligands contribute to cell degeneration, tissue fibrosis, inflammation, decreased regeneration capacity, and metabolic malfunction. While the biological roles of TGF-β depend highly on cell types and cellular contexts, aging-associated changes are an important additional context which warrants further investigation to better understand the involvement in various diseases and develop therapeutic options. The present review summarizes the relationships between TGF-β signaling and cellular senescence, stem cell aging, and aging-related diseases.

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Gisselbrecht, Stephen S., Alexandre Palagi, Jesse V. Kurland, Julia M. Rogers, Hakan Ozadam, Ye Zhan, Job Dekker, and Martha L. Bulyk. "Transcriptional Silencers in Drosophila Serve a Dual Role as Transcriptional Enhancers in Alternate Cellular Contexts." Molecular Cell 77, no. 2 (January 2020): 324–37. http://dx.doi.org/10.1016/j.molcel.2019.10.004.

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Banerjee, Navonil, and Elissa A. Hallem. "The role of carbon dioxide in nematode behaviour and physiology." Parasitology 147, no. 8 (October 11, 2019): 841–54. http://dx.doi.org/10.1017/s0031182019001422.

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AbstractCarbon dioxide (CO2) is an important sensory cue for many animals, including both parasitic and free-living nematodes. Many nematodes show context-dependent, experience-dependent and/or life-stage-dependent behavioural responses to CO2, suggesting that CO2 plays crucial roles throughout the nematode life cycle in multiple ethological contexts. Nematodes also show a wide range of physiological responses to CO2. Here, we review the diverse responses of parasitic and free-living nematodes to CO2. We also discuss the molecular, cellular and neural circuit mechanisms that mediate CO2 detection in nematodes, and that drive context-dependent and experience-dependent responses of nematodes to CO2.

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Calcinotto, Arianna, Jaskaren Kohli, Elena Zagato, Laura Pellegrini, Marco Demaria, and Andrea Alimonti. "Cellular Senescence: Aging, Cancer, and Injury." Physiological Reviews 99, no. 2 (April 1, 2019): 1047–78. http://dx.doi.org/10.1152/physrev.00020.2018.

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Cellular senescence is a permanent state of cell cycle arrest that occurs in proliferating cells subjected to different stresses. Senescence is, therefore, a cellular defense mechanism that prevents the cells to acquire an unnecessary damage. The senescent state is accompanied by a failure to re-enter the cell cycle in response to mitogenic stimuli, an enhanced secretory phenotype and resistance to cell death. Senescence takes place in several tissues during different physiological and pathological processes such as tissue remodeling, injury, cancer, and aging. Although senescence is one of the causative processes of aging and it is responsible of aging-related disorders, senescent cells can also play a positive role. In embryogenesis and tissue remodeling, senescent cells are required for the proper development of the embryo and tissue repair. In cancer, senescence works as a potent barrier to prevent tumorigenesis. Therefore, the identification and characterization of key features of senescence, the induction of senescence in cancer cells, or the elimination of senescent cells by pharmacological interventions in aging tissues is gaining consideration in several fields of research. Here, we describe the known key features of senescence, the cell-autonomous, and noncell-autonomous regulators of senescence, and we attempt to discuss the functional role of this fundamental process in different contexts in light of the development of novel therapeutic targets.

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Xu, Hua, Ariamala Gopalsamy, Erik C. Hett, Shores Salter, Ann Aulabaugh, Robert E. Kyne, Betsy Pierce, and Lyn H. Jones. "Cellular thermal shift and clickable chemical probe assays for the determination of drug-target engagement in live cells." Organic & Biomolecular Chemistry 14, no. 26 (2016): 6179–83. http://dx.doi.org/10.1039/c6ob01078d.

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Alim, Zahara, Cheryl Hartshorn, Oliver Mai, Iain Stitt, Colin Clay, Stuart Tobet, and Ulrich Boehm. "Gonadotrope Plasticity at Cellular and Population Levels." Endocrinology 153, no. 10 (October 1, 2012): 4729–39. http://dx.doi.org/10.1210/en.2012-1360.

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Abstract Hormone-secreting cells within the anterior pituitary gland may form organized and interdigitated networks that adapt to changing endocrine conditions in different physiological contexts. For gonadotropes, this might reflect a strategy to cope with acute changes throughout different female reproductive stages. The current study examined gonadotropes in female mice at characteristically different hormonal stages: prepubertal, postpubertal, and lactating. Gonadotrope plasticity was examined at the level of the whole population and single cells at different stages by imaging both fixed and live pituitary slices. The use of a model animal providing for the identification of selectively fluorescent gonadotropes allowed the particular advantage of defining cellular plasticity specifically for gonadotropes. In vivo analyses of gonadotropes relative to vasculature showed significantly different gonadotrope distributions across physiological states. Video microscopy studies using live slices ex vivo demonstrated pituitary cell plasticity in the form of movements and protrusions in response to GnRH. As positive feedback from rising estradiol levels is important for priming the anterior pituitary gland for the LH surge, experiments provide evidence of estradiol effects on GnRH signaling in gonadotropes. The experiments presented herein provide new insight into potential plasticity of gonadotropes within the anterior pituitary glands of female mice.

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Vallot, Céline, Jean-François Ouimette, and Claire Rougeulle. "Establishment of X chromosome inactivation and epigenomic features of the inactive X depend on cellular contexts." BioEssays 38, no. 9 (July 8, 2016): 869–80. http://dx.doi.org/10.1002/bies.201600121.

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Ferrario, Carrie R., and Lawrence P. Reagan. "Insulin-mediated synaptic plasticity in the CNS: Anatomical, functional and temporal contexts." Neuropharmacology 136 (July 2018): 182–91. http://dx.doi.org/10.1016/j.neuropharm.2017.12.001.

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Meimaridou, Eirini, Sakina B. Gooljar, and J. Paul Chapple. "From hatching to dispatching: the multiple cellular roles of the Hsp70 molecular chaperone machinery." Journal of Molecular Endocrinology 42, no. 1 (October 13, 2008): 1–9. http://dx.doi.org/10.1677/jme-08-0116.

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Molecular chaperones are best recognized for their roles in de novo protein folding and the cellular response to stress. However, many molecular chaperones, and in particular the Hsp70 chaperone machinery, have multiple diverse cellular functions. At the molecular level, chaperones are mediators of protein conformational change. To facilitate conformational change of client/substrate proteins, in manifold contexts, chaperone power must be closely regulated and harnessed to specific cellular locales – this is controlled by cochaperones. This review considers specialized functions of the Hsp70 chaperone machinery mediated by its cochaperones. We focus on vesicular trafficking, protein degradation and a potential role in G protein-coupled receptor processing.

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Marguet, Philippe, Frederick Balagadde, Cheemeng Tan, and Lingchong You. "Biology by design: reduction and synthesis of cellular components and behaviour." Journal of The Royal Society Interface 4, no. 15 (January 23, 2007): 607–23. http://dx.doi.org/10.1098/rsif.2006.0206.

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Biological research is experiencing an increasing focus on the application of knowledge rather than on its generation. Thanks to the increased understanding of cellular systems and technological advances, biologists are more frequently asking not only ‘how can I understand the structure and behaviour of this biological system?’, but also ‘how can I apply that knowledge to generate novel functions in different biological systems or in other contexts?’ Active pursuit of the latter has nurtured the emergence of synthetic biology. Here, we discuss the motivation behind, and foundational technologies enabling, the development of this nascent field. We examine some early successes and applications while highlighting the challenges involved. Finally, we consider future directions and mention non-scientific considerations that can influence the field's growth.

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Martinec Nováková, Lenka, and Radka Vojtušová Mrzílková. "Children’s exposure to odors in everyday contexts predicts their odor awareness." Chemosensory Perception 9, no. 2 (April 6, 2016): 56–68. http://dx.doi.org/10.1007/s12078-016-9205-3.

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Kotrys, Anna V., and Roman J. Szczesny. "Mitochondrial Gene Expression and Beyond—Novel Aspects of Cellular Physiology." Cells 9, no. 1 (December 19, 2019): 17. http://dx.doi.org/10.3390/cells9010017.

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Mitochondria are peculiar organelles whose proper function depends on the crosstalk between two genomes, mitochondrial and nuclear. The human mitochondrial genome (mtDNA) encodes only 13 proteins; nevertheless, its proper expression is essential for cellular homeostasis, as mtDNA-encoded proteins are constituents of mitochondrial respiratory complexes. In addition, mtDNA expression results in the production of RNA molecules, which influence cell physiology once released from the mitochondria into the cytoplasm. As a result, dysfunctions of mtDNA expression may lead to pathologies in humans. Here, we review the mechanisms of mitochondrial gene expression with a focus on recent findings in the field. We summarize the complex turnover of mitochondrial transcripts and present an increasing body of evidence indicating new functions of mitochondrial transcripts. We discuss mitochondrial gene regulation in different cellular contexts, focusing on stress conditions. Finally, we highlight the importance of emerging aspects of mitochondrial gene regulation in human health and disease.

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Dan, Songsong, Bo Kang, Xiaotao Duan, and Ying-Jie Wang. "A cell-free system toward deciphering the post-translational modification barcodes of Oct4 in different cellular contexts." Biochemical and Biophysical Research Communications 456, no. 3 (January 2015): 714–20. http://dx.doi.org/10.1016/j.bbrc.2014.12.043.

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Hewton, Keeley G., Amritpal S. Johal, and Seth J. Parker. "Transporters at the Interface between Cytosolic and Mitochondrial Amino Acid Metabolism." Metabolites 11, no. 2 (February 16, 2021): 112. http://dx.doi.org/10.3390/metabo11020112.

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Mitochondria are central organelles that coordinate a vast array of metabolic and biologic functions important for cellular health. Amino acids are intricately linked to the bioenergetic, biosynthetic, and homeostatic function of the mitochondrion and require specific transporters to facilitate their import, export, and exchange across the inner mitochondrial membrane. Here we review key cellular metabolic outputs of eukaryotic mitochondrial amino acid metabolism and discuss both known and unknown transporters involved. Furthermore, we discuss how utilization of compartmentalized amino acid metabolism functions in disease and physiological contexts. We examine how improved methods to study mitochondrial metabolism, define organelle metabolite composition, and visualize cellular gradients allow for a more comprehensive understanding of how transporters facilitate compartmentalized metabolism.

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Latroche, Claire, Cyril Gitiaux, Fabrice Chrétien, Isabelle Desguerre, Rémi Mounier, and Bénédicte Chazaud. "Skeletal Muscle Microvasculature: A Highly Dynamic Lifeline." Physiology 30, no. 6 (November 2015): 417–27. http://dx.doi.org/10.1152/physiol.00026.2015.

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Skeletal muscle is highly irrigated by blood vessels. Beyond oxygen and nutrient supply, new vessel functions have been identified. This review presents vessel microanatomy and functions at tissue, cellular, and molecular levels. Mechanisms of vessel plasticity are described during skeletal muscle development and acute regeneration, and in physiological and pathological contexts.

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Demmig-Adams, Barbara, Jared J. Stewart, and William W. Adams. "Less photoprotection can be good in some genetic and environmental contexts." Biochemical Journal 476, no. 14 (July 18, 2019): 2017–29. http://dx.doi.org/10.1042/bcj20190328.

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Abstract Antioxidant systems modulate oxidant-based signaling networks and excessive removal of oxidants can prevent beneficial acclimation responses. Evidence from mutant, transgenic, and locally adapted natural plant systems is used to interpret differences in the capacity for antioxidation and formulate hypotheses for future inquiry. We focus on the first line of chloroplast antioxidant defense, pre-emptive thermal dissipation of excess absorbed light (monitored as nonphotochemical fluorescence quenching, NPQ) as well as on tocopherol-based antioxidation. Findings from NPQ-deficient and tocopherol-deficient mutants that exhibited enhanced biomass production and/or enhanced foliar water-transport capacity are reviewed and discussed in the context of the impact of lower levels of antioxidation on plant performance in hot/dry conditions, under cool temperature, and in the presence of biotic stress. The complexity of cellular redox-signaling networks is related to the complexity of environmental and endogenous inputs as well as to the need for intensified training and collaboration in the study of plant–environment interactions across biological sub-disciplines.

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Zaman, Sojib Bin, Naznin Hossain, Shad Ahammed, and Zubair Ahmed. "Contexts and Opportunities of e-Health Technology in Medical Care." Journal of Medical Research and Innovation 1, no. 2 (May 1, 2017): AV1—AV4. http://dx.doi.org/10.15419/jmri.62.

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Keeping up with a sound health is a fundamental right for the human beings. It also acts as an indicator of the socio-economic development of a country. However, nowadays keeping sound health is challenging because of rapidly increasing non-communicable diseases. Concurrently, we are on the edge of very fast technological advancement which includes usage of cellular technology, high-speed internet and wireless communications. These technologies and their unique applications are creating lots of new dimensions in health care system which is known as e-Health. The medical call centers, emergency toll-free telephone services are being used in all over the world. The newly developed electronic health system can play a vital role in the remote regions of emerging and developing countries although sometimes it seems difficult due to the lack of communication infrastructure. E-Health can be a promising aspect for providing public health benefits if it integrates with the conventional medical system. More strategic approaches are necessary for the planning, development, and evaluation of e-Health. This article is written to depict the existing and future opportunities of e-Health in health support system.

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Chan, Candace S. Y., Nicolas Lonfat, Rong Zhao, Alexander E. Davis, Liang Li, Man-Ru Wu, Cheng-Hui Lin, Zhe Ji, Constance L. Cepko, and Sui Wang. "Cell type- and stage-specific expression of Otx2 is regulated by multiple transcription factors and cis-regulatory modules in the retina." Development 147, no. 14 (July 6, 2020): dev187922. http://dx.doi.org/10.1242/dev.187922.

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ABSTRACTTranscription factors (TFs) are often used repeatedly during development and homeostasis to control distinct processes in the same and/or different cellular contexts. Considering the limited number of TFs in the genome and the tremendous number of events that need to be regulated, re-use of TFs is necessary. We analyzed how the expression of the homeobox TF, orthodenticle homeobox 2 (Otx2), is regulated in a cell type- and stage-specific manner during development in the mouse retina. We identified seven Otx2 cis-regulatory modules (CRMs), among which the O5, O7 and O9 CRMs mark three distinct cellular contexts of Otx2 expression. We discovered that Otx2, Crx and Sox2, which are well-known TFs regulating retinal development, bind to and activate the O5, O7 or O9 CRMs, respectively. The chromatin status of these three CRMs was found to be distinct in vivo in different retinal cell types and at different stages. We conclude that retinal cells use a cohort of TFs with different expression patterns and multiple CRMs with different chromatin configurations to regulate the expression of Otx2 precisely.

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Bell, Karen F. S. "Insight into a neuron's preferential susceptibility to oxidative stress." Biochemical Society Transactions 41, no. 6 (November 20, 2013): 1541–45. http://dx.doi.org/10.1042/bst20130245.

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Neurons are more vulnerable to oxidative stress than astrocytes, the reasons for which have yet to be fully elucidated. Understanding the cellular and molecular mechanisms which contribute to this enhanced vulnerability is key to efforts aimed at ameliorating neuronal health and resilience to oxidative stress, particularly in the context of neurodegenerative disease, which is characterized by progressive dysfunction and loss of neurons specifically, and in which oxidative stress is considered a central aetiological contributor. Biological factors which may influence neuronal susceptibility to oxidative stress, in normal and neurodegenerative contexts, are reviewed in the present article, with a focus on properties intrinsic to the neuronal cell type and on properties related to neuronal reliance on surrounding astrocytes.

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De Graeve, Fabienne, and Florence Besse. "Neuronal RNP granules: from physiological to pathological assemblies." Biological Chemistry 399, no. 7 (June 27, 2018): 623–35. http://dx.doi.org/10.1515/hsz-2018-0141.

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Abstract Neuronal cells rely on macro- and micro-cellular compartmentalization to rapidly process information, and respond locally to external stimuli. Such a cellular organization is achieved via the assembly of neuronal ribonucleoprotein (RNP) granules, dynamic membrane-less organelles enriched in RNAs and associated regulatory proteins. In this review, we discuss how these high-order structures transport mRNAs to dendrites and axons, and how they contribute to the spatio-temporal regulation of localized mRNA translation. We also highlight how recent biophysical studies have shed light on the mechanisms underlying neuronal RNP granule dynamic assembly, remodeling and maturation, in both physiological and pathological contexts.

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Smith, Keriayn N., Sarah C. Miller, Gabriele Varani, J. Mauro Calabrese, and Terry Magnuson. "Multimodal Long Noncoding RNA Interaction Networks: Control Panels for Cell Fate Specification." Genetics 213, no. 4 (December 2019): 1093–110. http://dx.doi.org/10.1534/genetics.119.302661.

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Lineage specification in early development is the basis for the exquisitely precise body plan of multicellular organisms. It is therefore critical to understand cell fate decisions in early development. Moreover, for regenerative medicine, the accurate specification of cell types to replace damaged/diseased tissue is strongly dependent on identifying determinants of cell identity. Long noncoding RNAs (lncRNAs) have been shown to regulate cellular plasticity, including pluripotency establishment and maintenance, differentiation and development, yet broad phenotypic analysis and the mechanistic basis of their function remains lacking. As components of molecular condensates, lncRNAs interact with almost all classes of cellular biomolecules, including proteins, DNA, mRNAs, and microRNAs. With functions ranging from controlling alternative splicing of mRNAs, to providing scaffolding upon which chromatin modifiers are assembled, it is clear that at least a subset of lncRNAs are far from the transcriptional noise they were once deemed. This review highlights the diversity of lncRNA interactions in the context of cell fate specification, and provides examples of each type of interaction in relevant developmental contexts. Also highlighted are experimental and computational approaches to study lncRNAs.

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Steffens Reinhardt, Luiza, Xiajie Zhang, Anna Wawruszak, Kira Groen, Geoffry N. De Iuliis, and Kelly A. Avery-Kiejda. "Good Cop, Bad Cop: Defining the Roles of Δ40p53 in Cancer and Aging." Cancers 12, no. 6 (June 23, 2020): 1659. http://dx.doi.org/10.3390/cancers12061659.

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The tumour suppressor p53 is essential for maintaining DNA integrity, and plays a major role in cellular senescence and aging. Understanding the mechanisms that contribute to p53 dysfunction can uncover novel possibilities for improving cancer therapies and diagnosis, as well as cognitive decline associated with aging. In recent years, the complexity of p53 signalling has become increasingly apparent owing to the discovery of the p53 isoforms. These isoforms play important roles in regulating cell growth and turnover in response to different stressors, depending on the cellular context. In this review, we focus on Δ40p53, an N-terminally truncated p53 isoform. Δ40p53 can alter p53 target gene expression in both a positive and negative manner, modulating the biological outcome of p53 activation; it also functions independently of p53. Therefore, proper control of the Δ40p53: p53 ratio is essential for normal cell growth, aging, and responses to cancer therapy. Defining the contexts and the mechanisms by which Δ40p53 behaves as a “good cop or bad cop” is critical if we are to target this isoform therapeutically.

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Mesquita, Diana, João D. Barros-Silva, Joana Santos, Rolf I. Skotheim, Ragnhild A. Lothe, Paula Paulo, and Manuel R. Teixeira. "Specific and redundant activities of ETV1 and ETV4 in prostate cancer aggressiveness revealed by co-overexpression cellular contexts." Oncotarget 6, no. 7 (February 14, 2015): 5217–36. http://dx.doi.org/10.18632/oncotarget.2847.

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Ehrlich, Marcelo. "Endocytosis and trafficking of BMP receptors: Regulatory mechanisms for fine-tuning the signaling response in different cellular contexts." Cytokine & Growth Factor Reviews 27 (February 2016): 35–42. http://dx.doi.org/10.1016/j.cytogfr.2015.12.008.

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Portegys, Thomas E. "Generating an Artificial Nest Building Pufferfish in a Cellular Automaton Through Behavior Decomposition." International Journal of Artificial Intelligence and Machine Learning 9, no. 1 (January 2019): 1–12. http://dx.doi.org/10.4018/ijaiml.2019010101.

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A species of pufferfish builds fascinating circular nests on the sea floor to attract mates. This project simulates the nest building behavior in a cellular automaton using the morphognosis model. The model features hierarchical spatial and temporal contexts that output motor responses from sensory inputs. By considering the biological neural network of the pufferfish as a black box, and decomposing only its external behavior, an artificial counterpart can be generated. In this way a complex biological system producing a behavior can be filtered into a system containing only functions that are essential to reproduce the behavior. The derived system not only has intrinsic value as an artificial entity but also might help to ascertain how the biological system produces the behavior.

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Peel, Andrew D. "The evolution of developmental gene networks: lessons from comparative studies on holometabolous insects." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1496 (January 11, 2008): 1539–47. http://dx.doi.org/10.1098/rstb.2007.2244.

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Recent comparative studies have revealed significant differences in the developmental gene networks operating in three holometabolous insects: the beetle Tribolium castaneum , the parasitic wasp Nasonia vitripennis and the fruitfly Drosophila melanogaster . I discuss these differences in relation to divergent and convergent changes in cellular embryology. I speculate on how segmentation gene networks have evolved to operate in divergent embryological contexts, and highlight the role that co-option might have played in this process. I argue that insects represent an important example of how diversification in life-history strategies between lineages can lead to divergence in the genetic and cellular mechanisms controlling the development of homologous adult structures.

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Pan, Zhijian, and James A. Reggia. "Computational Discovery of Instructionless Self-Replicating Structures in Cellular Automata." Artificial Life 16, no. 1 (January 2010): 39–63. http://dx.doi.org/10.1162/artl.2009.16.1.16104.

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Cellular automata models have historically been a major approach to studying the information-processing properties of self-replication. Here we explore the feasibility of adopting genetic programming so that, when it is given a fairly arbitrary initial cellular automata configuration, it will automatically generate a set of rules that make the given configuration replicate. We found that this approach works surprisingly effectively for structures as large as 50 components or more. The replication mechanisms discovered by genetic programming work quite differently than those of many past manually designed replicators: There is no identifiable instruction sequence or construction arm, the replicating structures generally translate and rotate as they reproduce, and they divide via a fissionlike process that involves highly parallel operations. This makes replication very fast, and one cannot identify which descendant is the parent and which is the child. The ability to automatically generate self-replicating structures in this fashion allowed us to examine the resulting replicators as their properties were systematically varied. Further, it proved possible to produce replicators that simultaneously deposited secondary structures while replicating, as in some past manually designed models. We conclude that genetic programming is a powerful tool for studying self-replication that might also be profitably used in contexts other than cellular spaces.

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Palermo, Giovanni, Sonia Mazzucchi, Alessandra Della Vecchia, Gabriele Siciliano, Ubaldo Bonuccelli, Carole Azuar, Roberto Ceravolo, Simone Lista, Harald Hampel, and Filippo Baldacci. "Different Clinical Contexts of Use of Blood Neurofilament Light Chain Protein in the Spectrum of Neurodegenerative Diseases." Molecular Neurobiology 57, no. 11 (August 9, 2020): 4667–91. http://dx.doi.org/10.1007/s12035-020-02035-9.

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Krämer, Anne I., and Christoph Handschin. "How Epigenetic Modifications Drive the Expression and Mediate the Action of PGC-1α in the Regulation of Metabolism." International Journal of Molecular Sciences 20, no. 21 (October 31, 2019): 5449. http://dx.doi.org/10.3390/ijms20215449.

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Epigenetic changes are a hallmark of short- and long-term transcriptional regulation, and hence instrumental in the control of cellular identity and plasticity. Epigenetic mechanisms leading to changes in chromatin structure, accessibility for recruitment of transcriptional complexes, and interaction of enhancers and promoters all contribute to acute and chronic adaptations of cells, tissues and organs to internal and external perturbations. Similarly, the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is activated by stimuli that alter the cellular energetic demand, and subsequently controls complex transcriptional networks responsible for cellular plasticity. It thus is of no surprise that PGC-1α is under the control of epigenetic mechanisms, and constitutes a mediator of epigenetic changes in various tissues and contexts. In this review, we summarize the current knowledge of the link between epigenetics and PGC-1α in health and disease.

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Moncho-Amor, Veronica, Probir Chakravarty, Christophe Galichet, Ander Matheu, Robin Lovell-Badge, and Karine Rizzoti. "SOX2 is required independently in both stem and differentiated cells for pituitary tumorigenesis in p27-null mice." Proceedings of the National Academy of Sciences 118, no. 7 (February 11, 2021): e2017115118. http://dx.doi.org/10.1073/pnas.2017115118.

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P27, a cell cycle inhibitor, is also able to drive repression of Sox2. This interaction plays a crucial role during development of p27−/− pituitary tumors because loss of one copy of Sox2 impairs tumorigenesis [H. Li et al., Cell Stem Cell 11, 845–852 (2012)]. However, SOX2 is expressed in both endocrine and stem cells (SCs), and its contribution to tumorigenesis in either cell type is unknown. We have thus explored the cellular origin and mechanisms underlying endocrine tumorigenesis in p27−/− pituitaries. We found that pituitary hyperplasia is associated with reduced cellular differentiation, in parallel with increased levels of SOX2 in stem and endocrine cells. Using conditional loss-of-function and lineage tracing approaches, we show that SOX2 is required cell autonomously in p27−/− endocrine cells for these to give rise to tumors, and in SCs for promotion of tumorigenesis. This is supported by studies deleting the Sox2 regulatory region 2 (Srr2), the target of P27 repressive action. Single cell transcriptomic analysis further reveals that activation of a SOX2-dependent MAPK pathway in SCs is important for tumorigenesis. Altogether, our data highlight different aspects of the role of SOX2 following loss of p27, according to cellular context, and uncover an unexpected SOX2-dependent tumor-promoting role for SCs. Our results imply that targeting SCs, in addition to tumor cells, may represent an efficient antitumoral strategy in certain contexts.

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Weissengruber, Sebastian, Sang Wan Lee, John P. O’Doherty, and Christian C. Ruff. "Neurostimulation Reveals Context-Dependent Arbitration Between Model-Based and Model-Free Reinforcement Learning." Cerebral Cortex 29, no. 11 (March 19, 2019): 4850–62. http://dx.doi.org/10.1093/cercor/bhz019.

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Abstract While it is established that humans use model-based (MB) and model-free (MF) reinforcement learning in a complementary fashion, much less is known about how the brain determines which of these systems should control behavior at any given moment. Here we provide causal evidence for a neural mechanism that acts as a context-dependent arbitrator between both systems. We applied excitatory and inhibitory transcranial direct current stimulation over a region of the left ventrolateral prefrontal cortex previously found to encode the reliability of both learning systems. The opposing neural interventions resulted in a bidirectional shift of control between MB and MF learning. Stimulation also affected the sensitivity of the arbitration mechanism itself, as it changed how often subjects switched between the dominant system over time. Both of these effects depended on varying task contexts that either favored MB or MF control, indicating that this arbitration mechanism is not context-invariant but flexibly incorporates information about current environmental demands.

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Pryor, John M., Crystal A. Waters, Ana Aza, Kenjiro Asagoshi, Christina Strom, Piotr A. Mieczkowski, Luis Blanco, and Dale A. Ramsden. "Essential role for polymerase specialization in cellular nonhomologous end joining." Proceedings of the National Academy of Sciences 112, no. 33 (August 3, 2015): E4537—E4545. http://dx.doi.org/10.1073/pnas.1505805112.

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Nonhomologous end joining (NHEJ) repairs chromosome breaks and must remain effective in the face of extensive diversity in broken end structures. We show here that this flexibility is often reliant on the ability to direct DNA synthesis across strand breaks, and that polymerase (Pol) μ and Pol λ are the only mammalian DNA polymerases that have this activity. By systematically varying substrate in cells, we show each polymerase is uniquely proficient in different contexts. The templating nucleotide is also selected differently, with Pol μ using the unpaired base adjacent to the downstream 5′ phosphate even when there are available template sites further upstream of this position; this makes Pol μ more flexible but also less accurate than Pol λ. Loss of either polymerase alone consequently has clear and distinguishable effects on the fidelity of repair, but end remodeling by cellular nucleases and the remaining polymerase helps mitigate the effects on overall repair efficiency. Accordingly, when cells are deficient in both polymerases there is synergistic impact on NHEJ efficiency, both in terms of repair of defined substrates and cellular resistance to ionizing radiation. Pol μ and Pol λ thus provide distinct solutions to a problem for DNA synthesis that is unique to this pathway and play a key role in conferring on NHEJ the flexibility required for accurate and efficient repair.

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Nam, Seungyoon, Xinghua Long, ChangHyuk Kwon, Sun Kim, and Kenneth P. Nephew. "An integrative analysis of cellular contexts, miRNAs and mRNAs reveals network clusters associated with antiestrogen-resistant breast cancer cells." BMC Genomics 13, no. 1 (2012): 732. http://dx.doi.org/10.1186/1471-2164-13-732.

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Journal articles on the topic 'Cellular contexts'

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