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| Author | : Cheryl Lynn Johnson |
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| Total Pages | : |
| Release | : 2012 |
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| ISBN | : 9780494971086 |
| Author | : Tim Schedl |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 434 |
| Release | : 2012-08-09 |
| Genre | : Medical |
| ISBN | : 1461440157 |
Germ cells in sexually reproducing metazoa, through the germline lineage, are the route by which genetic material and cytoplasmic constituents are passed from one generation to the next in the continuum of life. Chapters in this book review germ cell development in the model organism Caenorhabditis elegans, discussing the biology, the genetics and the molecular mechanisms for various processes, as well as drawing comparisons with other organisms. Processes discussed include specification of germ cell fate, meiosis, gametogenesis, environmental/ physiological controls, epigenetics and translational control, fertilization and the oocyte-to-embryo transition. This book thus provides a comprehensive picture of the germline lineage and the continuum of life for the worm.
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Background: In the hermaphrodite of the nematode Caenorhabditis elegans, the first germ cells differentiate as sperm. Later the germ line switches to the production of oocytes. This process requires the activity of a genetic regulatory network that includes among others the fem, fog and mog genes. The function of some of these genes is germline specific while others also act in somatic tissues. DEAD box proteins have been shown to be involved in the control of gene expression at different steps such as transcription and pre-mRNA processing. Results: We show that the Caenorhabditis elegans gene mel-46 (maternal effect lethal) encodes a DEAD box protein that is related to the mammalian DDX20/Gemin3/DP103 genes. mel-46 is expressed throughout development and mutations in mel-46 display defects at multiple developmental stages. Here we focus on the role of mel-46 in the hermaphrodite germ line. mel-46(yt5) mutant hermaphrodites are partially penetrant sterile and fully penetrant maternal effect lethal. The germ line of mutants shows variable defects in oogenesis. Further, mel-46(yt5) suppresses the complete feminization caused by mutations in fog-2 and fem-3, two genes that are at the top and the center, respectively, of the genetic germline sex determining cascade, but not fog-1 that is at the bottom of this cascade. Conclusion: The C. elegans gene mel-46 encodes a DEAD box protein that is required maternally for early embryogenesis and zygotically for postembryonic development. In the germ line, it is required for proper oogenesis. Although it interacts genetically with genes of the germline sex determination machinery its primary function appears to be in oocyte differentiation rather than sex determination.
| Author | : Julie Ahringer |
| Publisher | : |
| Total Pages | : 242 |
| Release | : 1991 |
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| Author | : Christopher James Wedeles |
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| Total Pages | : 0 |
| Release | : 2018 |
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Small RNA pathways related to RNA Interference (RNAi) are prevalent in species ranging from protozoa to mammals, including humans. These pathways contribute to organismal development and cellular function and elicit their gene-regulatory impacts through diverse modes of action. The soil nematode, Caenorhabditis elegans, has emerged as a powerful system to study the endogenous activities of these pathways. In the germline, the worm has evolved an intricate network of small RNA pathways, that jointly contribute to the transmission of epigenetic information through cell divisions and across generations. This activity is necessary for the maintenance of existing germline gene expression programs, and involves the dynamic regulation of mRNA transcripts, small RNA populations, and changes to the chromatin landscape. In this thesis, I demonstrate a role for the Argonaute CSR-1 (Chromosome Segregation and RNAi defecient-1) in this process. Using genetic approaches, I demonstrate that CSR-1 licenses genes for germline expression and overcomes the silencing activity of competing small RNA pathways. I explore the mechanisms by which CSR-1 elicits its licensing activity, and identify a role for the pathway in guiding the acquisition of H3K36me3 on a genome-wide scale. Using a combination of genetic and genome-wide approaches I describe the contribution of two H3K36 methyltransferases to the CSR-1 pathway. Finally, I identify a putative self-reinforcing loop involving H3K36me3 and small RNAs that together act to reinforce an epigenetic memory of past patterns of germline gene expression. Together, these studies contribute to the understanding of how various aspects of epigenetic regulation converge to faithfully maintain existing gene expression programs in eukaryotes.
| Author | : Joan Marsh |
| Publisher | : John Wiley & Sons |
| Total Pages | : 344 |
| Release | : 1994-08-16 |
| Genre | : Medical |
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Connects classical cellular descriptive studies with more recent work on the molecular and genetic aspects regarding germline development. Prominent scientists discuss research on a range of organisms including insects, worms, birds, fish, amphibia, mammals and green algae. Specification of germ cells, their migration to the gonads and subsequent interactions with the soma and evolutionary factors of their segregation are among the topics covered.
| Author | : Florence Louise Marlow |
| Publisher | : Morgan & Claypool Publishers |
| Total Pages | : 221 |
| Release | : 2010 |
| Genre | : Family & Relationships |
| ISBN | : 161504051X |
Eggs of all animals contain mRNAs and proteins that are supplied to or deposited in the egg as it develops during oogenesis. These maternal gene products regulate all aspects of oocyte development, and an embryo fully relies on these maternal gene products for all aspects of its early development, including fertilization, transitions between meiotic and mitotic cell cycles, and activation of its own genome. Given the diverse processes required to produce a developmentally competent egg and embryo, it is not surprising that maternal gene products are not only essential for normal embryonic development but also for fertility. This review provides an overview of fundamental aspects of oocyte and early embryonic development and the interference and genetic approaches that have provided access to maternally regulated aspects of vertebrate development. Some of the pathways and molecules highlighted in this review, in particular, Bmps, Wnts, small GTPases, cytoskeletal components, and cell cycle regulators, are well known and are essential regulators of multiple aspects of animal development, including oogenesis, early embryogenesis, organogenesis, and reproductive fitness of the adult animal. Specific examples of developmental processes under maternal control and the essential proteins will be explored in each chapter, and where known conserved aspects or divergent roles for these maternal regulators of early vertebrate development will be discussed throughout this review. Table of Contents: Introduction / Oogenesis: From Germline Stem Cells to Germline Cysts / Oocyte Polarity and the Embryonic Axes: The Balbiani Body, an Ancient Oocyte Asymmetry / Preparing Developmentally Competent Eggs / Egg Activation / Blocking Polyspermy / Cleavage/ Mitosis: Going Multicellular / Maternal-Zygotic Transition / Reprogramming: Epigenetic Modifications and Zygotic Genome Activation / Dorsal-Ventral Axis Formation before Zygotic Genome Activation in Zebrafish and Frogs / Maternal TGF-β and the Dorsal-Ventral Embryonic Axis / Maternal Control After Zygotic Genome Activation / Compensation by Stable Maternal Proteins / Maternal Contributions to Germline Establishment or Maintenance / Perspective / Acknowledgments / References
| Author | : Suk-Won Jin |
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| Total Pages | : 444 |
| Release | : 2000 |
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| Author | : Henry F. Epstein |
| Publisher | : Academic Press |
| Total Pages | : 687 |
| Release | : 1995 |
| Genre | : Caenorhabditis elegans |
| ISBN | : 0125641494 |
The first of its kind, this laboratory handbook emphasizes diverse methods and technologies needed to investigate C. elegans, both as an integrated organism and as a model system for research inquiries in cell, developmental, and molecular biology, as well as in genetics and pharmacology. Four primary sections--Genetic and Culture Methods, Neurobiology, Cell and Molecular Biology, and Genomics and Informatics--reflect the cross-disciplinary nature of C. elegans research. Because C. elegans is a simple and malleable organism with a small genome and few cell types, it provides an elegant demonstr.
| Author | : Laura Gaydos |
| Publisher | : |
| Total Pages | : 129 |
| Release | : 2014 |
| Genre | : |
| ISBN | : 9781321087444 |
To retain cell identity during development, cells must remember patterns of gene expression through cell division. The MES proteins in Caenorhabditis elegans are key regulators of gene expression in the germline and are necessary in parents for fertility in the next generation. MES-2, MES-3, and MES-6 form the C. elegans Polycomb Repressive Complex 2 (PRC2) and generate a repressive histone modification, methylation on Lysine 27 of Histone H3 (H3K27me), on genes repressed in the germline. MES-4 generates a different histone modification, H3K36me, on genes expressed in the germline. To further define the targets of MES protein regulation, determine if they work together to regulate gene expression, and investigate when they are important during germline development, I used genomics, genetics, and microscopy approaches. Transcript profiling of dissected mutant germlines revealed that MES-2/3/6 and MES-4 cooperate to promote expression of germline genes and repress somatic genes and genes on the X chromosome. Loss of MES-4 from germline genes causes H3K27me3 to spread to germline genes, resulting in reduced H3K27me3 elsewhere on the autosomes and especially on the X. This finding supports the model that methylation of H3K36 antagonizes methylation of H3K27 on the same histone tails. My finding that loss of MES-2, 3, or 6 results in expression from the X chromosomes and sterility, unless the X chromosome is repressed by other means, showed that the essential role of MES-2/3/6 in worms is repression of the X chromosomes in germ cells. I determined that repressive H3K27me3 is transmitted to embryos by both sperm and oocytes. By generating embryos containing some chromosomes with and some lacking H3K27me3, I showed that in embryos lacking MES-2/3/6 function, H3K27me3 is transmitted to daughter chromatids through several rounds of cell division. In embryos with MES-2/3/6 function, the mosaic pattern of H3K27me3 is perpetuated through embryogenesis. Subsequently, during germline proliferation in larval stages, H3K27me3 accumulates on all chromosomes. During germline proliferation in larvae is also when I found MES-3 to be most important for germline development in the next generation. These latter two findings suggest that germline memory is reset during germline proliferation. Taken together, my findings support a "germline memory model" in which MES-4 and H3K36me act as a memory of germline gene expression and help concentrate MES-2/3/6 repression on the X chromosome. MES-2/3/6 and H3K27me3 act as a memory of germline gene repression, most importantly on the X chromosomes. The germline memory generated by the MES proteins is epigenetically transmitted across generations and is critical for the proper development of nascent germ cells.
