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[
International Worm Meeting,
2019]
Organization of the genome into domains of euchromatin and heterochromatin is a conserved and essential feature of all eukaryotes. Heterochromatin plays important roles in repression of transcription, chromosome segregation, and maintenance of genome integrity. Heterochromatin can be divided into constitutive heterochromatin and facultative heterochromatin, which can be distinguished by their associated histone modifications. Methylation of lysine 27 on histone H3 (H3K27me) is associated with facultative heterochromatin, while methylation of lysine 9 on histone H3 (H3K9me) is associated with constitutive heterochromatin. In mouse, fungus, and Drosophila, these two marks largely anticorrelate. However, in C. elegans, H3K27me and H3K9me show a surprising positive correlation, suggesting a species-specific difference in the organization of heterochromatin. In C. elegans, H3K27me represses transcription of the X chromosome in the germline, and its loss leads to a maternal-effect sterile (Mes) phenotype. Intriguingly, Gaydos et al. (Science, 2014) showed that mes mutant males that inherited their single X chromosome from the father are usually fertile and that the fertility of those males is dependent on H3K9me. Together, these observations suggest a potential redundant function of H3K27me and H3K9me in repressing the single X chromosome in the male germline to promote fertility in subsequent generations. We are investigating the potential redundant functions of H3K27me and H3K9me in the C. elegans male germline. First, by generating chimeric animals whose germlines inherit only paternal chromosomes, we have shown that mes mutant XX hermaphrodites are rendered fertile when both of their X chromosomes, which lack H3K27me, are inherited from the father. Furthermore, as in males, fertility is dependent on H3K9me. Second, we are comparing misexpression of genes and repetitive elements in hermaphrodite and male germlines lacking either H3K27me or H3K9me or lacking both marks, to investigate cross-talk between those two marks and differential responses of hermaphrodite (XX) and male (XO) germlines. Lastly, we are examining other species of Caenorhabditis. Early results suggest that C. briggsae accomplishes X-chromosome repression differently than C. elegans.
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[
International Worm Meeting,
2021]
Organization of the genome into domains of euchromatin and heterochromatin is a conserved feature of all eukaryotes and precise regulation of these domains is important for organism health and development. Proper formation of heterochromatin is crucial for transcriptional repression, chromosome segregation, and maintenance of genome integrity. Heterochromatin can be categorized as either facultative or constitutive. These two types of heterochromatin are often distinguished by their associated histone modifications: methylation of lysine 27 or lysine 9 on histone H3. H3K27me is associated with facultative heterochromatin, and its domains are found throughout genomes, often with developmentally regulated genes. H3K9me is associated with constitutive heterochromatin, and is generally concentrated in gene-poor, repeat-rich regions such as pericentric regions. Thus, anticorrelation of H3K27me and H3K9me domains is observed in many model organisms. However, in C. elegans, H3K27me and H3K9me domains show a surprising amount of positive correlation, suggesting a species-specific mechanism for organizing facultative and constitutive heterochromatin. In the C. elegans germline, H3K27me is enriched on the X chromosome, and its loss leads to sterility in the F2 generation. Interestingly, H3K27me(-) F2 males that inherit a paternal X chromosome (Xp) and no maternal X chromosome (Xm) are usually fertile. The fertility of these males is dependent on H3K9me, which is enriched on the single X chromosome in the male germline. These observations suggest a potential redundant function of H3K27me and H3K9me in repressing the X chromosome in the male germline to promote fertility in subsequent generations. We are investigating the organization and functions of H3K27me and H3K9me in the C. elegans male germline. By generating chimeric animals whose germlines inherit only paternal chromosomes (XpXp), we've shown that a double dose of paternal chromosomes lacking H3K27me can also support fertile hermaphrodite germline development in an H3K9me-dependent manner. We are comparing misexpression of genes and repetitive elements in hermaphrodite and male germlines lacking H3K27me, H3K9me, or both. Lastly, we are using CUT&RUN to examine the distribution of H3K27me in germ cells and to test whether H3K9me regulates this distribution, as it does in Mouse and Neurospora.
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[
Worm Breeder's Gazette,
1994]
Cloning
mua-3: some observations on the new Molecular Era John Plenefisch and Edward Hedgecock, Dept. of Biology, Johns Hopkins University, Baltimore MD 21218
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[
Worm Breeder's Gazette,
1994]
Tc4 and Tc5: what makes them move and why it matters Christi Parham, Kristie Butze, Joanna Beinhorn and John Collins. Dept. of Biochemistry and Molecular Biology, University of New Hampshire. Durham, NH 03824
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[
Worm Breeder's Gazette,
1994]
Function of a Domain of the Myosin Heavy Chain Implicated in Familial Hypertrophic Cardiomyopathy Craig A. Almeida, Kerry E. Swift and John J. Collins Department of Biochemistry and Molecular, University of New Hampshire, Durham, NH 03820
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[
J Neurobiol,
1993]
Mutations causing a touch-insensitive phenotype in the nematode Caenorhabditis elegans have been the basis of studies on the specification of neuronal cell fate, inherited neurodegeneration, and the molecular nature of mechanosensory transduction. (C) 1993 John Wiley & sons, Inc.
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[
Worm Breeder's Gazette,
1994]
Mutations that enhance
glp-1 identify genes required for various aspects of germline development. Eleanor Maine, Li Qiao, Jim Lissemore-, Pei Shu, Anne Smardon, and Melanie Gelber. Biology Dept., Syracuse University, Syracuse, NY 13244 and Biology Dept., John Carroll University, Cleveland, OH 44118.
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[
Nature,
1998]
In 1983, John Sulston and Alan Coulson began to construct a complete physical map of the genome of the nematode worm Caenorhabditis elegans, and started what became known as the C. elegans Genome Project. At the time, several people wondered why John, who had just described all of the cell divisions in C. elegans (the cell lineage), was interested in this project rather than in a more 'biological' problem. He replied by joking that he had a "weakness for grandiose, meaningless projects". In 1989, as the physical map approached completion, the Genome Project, now including Bob Waterston and his group, embarked on the even more ambitious goal of obtaining the complete genomic sequence
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[
Parasitol Today,
1993]
Arrested development dramatically alters the life history of some species of soil-transmitted nematodes and elicits profound variations in the epidemiology of the infections they cause. Here, Peter Hotez, John Hawdon and Gerhard Schad show how an understanding of the cellular and molecular bases of arrested development may lead to new approaches for the control of ancylostomiasis and related infections.
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[
J Neurogenet
]
John Sulston changed the way we do science, not once, but three times - initially with the complete cell lineage of the nematode <i>Caenorhabditis elegans</i>, next with completion of the genome sequences of the worm and human genomes and finally with his strong and active advocacy for open data sharing. His contributions were widely recognized and in 2002 he received the Nobel Prize in Physiology and Medicine.