[
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.