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| Author | : José Luis Sardina |
| Publisher | : Frontiers Media SA |
| Total Pages | : 171 |
| Release | : 2021-10-20 |
| Genre | : Science |
| ISBN | : 2889715108 |
| Author | : Chin-Hsing Annie Lin |
| Publisher | : Frontiers Media SA |
| Total Pages | : 104 |
| Release | : 2016-06-24 |
| Genre | : Genetics |
| ISBN | : 2889198529 |
The fundamental question of how an undifferentiated progenitor cell adopts a more specialized cell fate that then contributes to the development of specialized tissues, organs, organ systems and ultimately a unique individual of a given species has intrigued cell and developmental biologists for many years. Advances in molecular and cell biology have enabled investigators to identify genetic and epigenetic factors that contribute to these processes with increasing detail and also to define the various molecular characteristics of each cell fate with greater precision. Understanding these processes have also provided greater insights into disorders in which the normal mechanisms of cell fate determination are altered, such as in cancer and inherited malformations. With these advances have come techniques that facilitate the manipulation of cell fate, which have the potential to revolutionize the field of medicine by facilitating the repair and/or regeneration of diseased organs. Given the rapid advances that are occurring in the field, the articles in this eBook are both relevant and timely. These articles originally appeared online as part of the Research Topic “Cell Fate” overseen by my colleagues Dr. Lin, Dr. Buttitta, Dr. Maves, Dr. Dilworth, Dr. Paladini and myself and have been viewed extensively. Because of their popularity, they are now made available as an eBook, in a more easily downloadable form. Michael T. Chin
| Author | : Anita Göndör |
| Publisher | : Academic Press |
| Total Pages | : 496 |
| Release | : 2016-10-25 |
| Genre | : Science |
| ISBN | : 0128034025 |
Chromatin Regulation and Dynamics integrates knowledge on the dynamic regulation of primary chromatin fiber with the 3D nuclear architecture, then connects related processes to circadian regulation of cellular metabolic states, representing a paradigm of adaptation to environmental changes. The final chapters discuss the many ways chromatin dynamics can synergize to fundamentally contribute to the development of complex diseases. Chromatin dynamics, which is strategically positioned at the gene-environment interface, is at the core of disease development. As such, Chromatin Regulation and Dynamics, part of the Translational Epigenetics series, facilitates the flow of information between research areas such as chromatin regulation, developmental biology, and epidemiology by focusing on recent findings of the fast-moving field of chromatin regulation. Presents and discusses novel principles of chromatin regulation and dynamics with a cross-disciplinary perspective Promotes crosstalk between basic sciences and their applications in medicine Provides a framework for future studies on complex diseases by integrating various aspects of chromatin biology with cellular metabolic states, with an emphasis on the dynamic nature of chromatin and stochastic principles Integrates knowledge on the dynamic regulation of primary chromatin fiber with 3D nuclear architecture, then connects related processes to circadian regulation of cellular metabolic states, representing a paradigm of adaptation to environmental changes
| Author | : Tala H. Fakhouri |
| Publisher | : |
| Total Pages | : 328 |
| Release | : 2008 |
| Genre | : Caenorhabditis elegans |
| ISBN | : |
| Author | : Quang-Huy Le |
| Publisher | : |
| Total Pages | : |
| Release | : 2016 |
| Genre | : |
| ISBN | : |
| Author | : Jason Knott |
| Publisher | : Springer |
| Total Pages | : 85 |
| Release | : 2017-11-23 |
| Genre | : Medical |
| ISBN | : 331963187X |
Five leaders in the field of mammalian preimplantation embryo development provide their own perspectives on key molecular and cellular processes that mediate lineage formation during the first week of life. The first cell-fate decision involves the formation of the pluripotent inner cell mass (ICM) and extraembryonic trophectoderm (TE). The second cell-fate choice encompasses the transformation of ICM into extraembryonic primitive endoderm (PE) and pluripotent epiblast. The processes, which occur during the period of preimplantation development, serve as the foundation for subsequent developmental events such as implantation, placentation, and gastrulation. The mechanisms that regulate them are complex and involve many different factors operating spatially and temporally over several days to modulate embryonic chromatin structure, impose cellular polarity, and direct distinct gene expression programs in the first cell lineages.
| Author | : Katharine Schulz |
| Publisher | : |
| Total Pages | : 0 |
| Release | : 2018 |
| Genre | : |
| ISBN | : |
Cell fate transitions are initiated by key transcription factors with a potent ability to reprogram the transcriptome. These master regulator transcription factors have been identified in numerous cellular contexts, yet, the mechanisms by which they produce global transcriptional change remain unclear. To further our understanding of how these factors function, I have studied a factor that initiates a massive transcriptional shift during embryogenesis. In animals, the genome remains transcriptionally dormant following fertilization and development is launched by maternally supplied RNAs and proteins. Yet, within a matter of hours, the genome must undergo widespread transcriptional activation for development to proceed. In [Drosophila melanogaster] the transcription factor Zelda (ZLD) directs zygotic genome activation (ZGA). ZLD is required for the expression of hundreds of genes during ZGA, but the mechanisms by which ZLD initiates this widespread activation were initially unknown. In this thesis, I present evidence that ZLD shapes the chromatin landscape to poise the zygotic genome for activation. I begin by introducing ZGA in Chapter 1, drawing on work from a range of model organisms. In Chapter 2, I include published work that demonstrates a role for ZLD in chromatin regulation. Here, we found that ZLD is required to maintain chromatin accessibility at a subset of its binding sites, and that this accessibility facilitates transcription factor binding and gene expression. Notably, we identified thousands of ZLD-binding sites that do not require ZLD for accessibility, and we determined that the chromatin regulator GAGA Factor (GAF) is enriched at these loci. Based on this finding, we proposed that GAF may serve as a co-regulator of ZGA. In Chapter 3, I describe my plan to assess this potential role for GAF using MS2-based reporters. Finally, to better understand how ZLD might regulate chromatin, I recently tested the ability of ZLD to bind to nucleosomes [in vitro]. In Chapter 4, I include evidence that ZLD has a unique ability to target nucleosomal DNA.
| Author | : Bingfei Yu |
| Publisher | : |
| Total Pages | : 170 |
| Release | : 2018 |
| Genre | : |
| ISBN | : |
CD8 + T cells are a central component of the adaptive immune system. Upon infection, a naive CD8 + T cell will differentiate into a heterogeneous population of effector T cells composed of terminal-effector and memory-precursor CD8 + T cells. Terminal-effector T cells rapidly decay after pathogens are eradicated while memory-precursor T cells survive during the contraction phase to become memory T cells, providing long-term protection from reinfection. Similar to the heterogeneity of effector T cells, memory T cells can also be divided into central-memory, effector-memory and tissue-resident memory subsets based on trafficking, location, proliferation potential and cytotoxic function. These memory subsets collaborate together to enhance the pathogen clearance and vaccine efficacy. The differentiation of a naive CD8 + T cell into a specific effector or memory subset is influenced by cell-extrinsic environmental signals and cell-intrinsic factors including transcription factors (TFs), epigenetic modification and chromatin organization. Considerable advances have been made to identify key TFs that regulate these T cell fate decisions. However, the TF-mediated transcriptional network responsible for specific subset differentiation and how epigenetic modifications and chromatin configuration modulate CD8 + T cell fate determination is still largely unknown. To address these questions, we deciphered epigenetic landscapes in effector and memory CD8 + T cells in response to bacterial infection by characterizing the genome-wide histone modification, chromatin accessibility and transcriptional program. Integrative analysis of epigenomics data showed that subset-specific enhancers established by key TFs foreshadow the specific lineage differentiation. To better identify cruicial TFs from multilayered epigenetic landscapes, we developed a webpage ranking-based algorithm (PageRank) to rank the importance of TFs from transcriptional network and identified a novel function of two TFs: YY1 and Nr3c1 to regulate terminal-effector and memory-precursor subset differentiation, respectively. By leveraging the PageRank analysis and chromatin accessibility data, we developed a computational screen to predict key TFs for tissue-resident memory T cell differentiation. Combining this approach with shRNA functional screen, we identified the role of Runx3 in programming tissue-residency signatures in non-lymphoid tissues and tumors. Finally, we discovered a novel role for the genome organizer CTCF in CD8 + T cell fate decisions illustrating the impact of chromatin organization on effector and memory T cell differentiation. Taken together, we uncovered a multi-layered regulation of chromatin state, accessibility and organization, that influences T cell fate decisions by fine-tuning transcriptional circuits. We further constructed a computational framework that integrates these high-dimensional data, facilitating identification of key transcriptional regulators and providing valuable biological insights.
| Author | : Catherine Soo Rhee |
| Publisher | : |
| Total Pages | : 252 |
| Release | : 2016 |
| Genre | : |
| ISBN | : |
The placenta is a transient but vital organ mediating a myriad of interactions between maternal and embryonic tissues. The cells in the trophectoderm (TE) lineage are responsible for proper implantation, placentation, and immunological functions of the placenta. However, our understanding of molecular mechanisms underlying placentation and TE development is still rudimentary. Deciphering the mechanisms by which key TE-specific transcription factors (TFs) control the first cell fate decision, as well as the maintenance and differentiation of TE, is a prerequisite for understanding early embryonic development and ultimately improving healthy pregnancy. First, using a combination of functional genomics, bioinformatics, and mouse genetics, I revealed that Arid3a is a critical regulator for controlling the first cell fate decision and placental development. Ectopically expressed Arid3a induces TE-like gene expression programs in embryonic stem (ES) cells. Moreover, Arid3a is not only essential for maintaining self-renewing TS cells, but also for promoting further differentiation of trophoblastic lineages. Consistently, Arid3a-/- mice suffer from severely impaired post-implantation development, resulting in early embryonic lethality. I further showed that Arid3a directly activates TE-specific genes while repressing pluripotency genes by recruiting HDAC1. Second, I studied the mechanisms underlying TF-mediated conversion of ES to trophoblast stem (TS)-like cells. Upon overexpression of TS cell-specific TFs, Cdx2, Arid3a, and Gata3 (CAG factors) in ES cells, I performed time–course profiling of chromatin accessibility, transcriptomes, and occupancy of these reprogramming factors during reprogramming. Using an integrative analysis, I discovered that CAG factors orchestrate the conversion via a sequential two-step regulation in a timely, ordered manner, with repression of pluripotency genes by decommissioning active enhancers, followed by activation of TS cell-specific genes as pioneer factors that can access closed chromatin. Taken together, my studies unveiled that Arid3a functions as a pivotal regulator of TE and placental development by regulating the commitment to the first cell fate, as well as by executing TE lineage differentiation. I advanced our understanding of the mechanisms underlying TF-mediated reprogramming of ES to TS-like cells, in particular Arid3a-mediated transcriptional and epigenetic regulation. Thus, my studies will be beneficial for enhancing clinical applications such as disease modeling, drug screening, and regenerative therapies.
| Author | : Valeriya Malysheva |
| Publisher | : |
| Total Pages | : 0 |
| Release | : 2016 |
| Genre | : |
| ISBN | : |
The cell fate acquisition is a highly complex phenomenon that involves a plethora of intrinsic and extrinsic instructive signals. However, despite the important progress in identification of key regulatory factors of this process, the mechanistic links between transcription factors, epigenome and chromatin structure which coordinate the regulation of cell differentiation and deregulation of gene networks during cell transformation are largely unknown. To address these questions for two model systems of cell fate transitions, namely the neuronal and endodermal cell differentiation induced by the morphogen retinoic acid and the stepwise tumorigenesis of primary human cells, we conducted integrative transcriptome, epigenome and chromatin architecture studies. Through extensive integration with thousands of available genomic data sets, we deciphered the gene regulatory networks of these processes and revealed new insights in the molecular circuitry of cell fate acquisition. The understanding of regulatory mechanisms that underlie the cell fate decision processes not only brings the fundamental understanding of cause-and-consequence relationships inside the cell, but also open the doors to the directed trans-differentiation.
