| Citation | Tabuchi TM, Rechtsteiner A, Strome S, Hagstrom KA. Opposing activities of DRM and MES-4 tune gene expression and X-chromosome repression in Caenorhabditis elegans germ cells. G3 (Bethesda), 2014. |
| PubMed ID | 24281426 |
| Short Description | Opposing activities of DRM and MES-4 tune gene expression and X-chromosome repression in Caenorhabditis elegans germ cells. GEO Record: GSE52064 Platform: GPL200 Download gene-centric, log2 transformed data: WBPaper00044545.ce.mr.csv |
| # of Conditions | 12 |
Full Description
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During animal development, gene transcription is tuned to tissue-appropriate levels. Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 (Maternal Effect Sterile-4) marks genes expressed in the germline with methylated lysine on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosome. The DRM transcription factor complex, named for its Dp/E2F, Retinoblastoma-like, and MuvB subunits, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 and the DRM subunit lin-54 oppositely skew the transcript levels of their common targets and cause sterility. A double mutant restores target gene transcript levels closer to wild type, and the concomitant loss of lin-54 suppresses the severe germline proliferation defect observed in mes-4 single mutants. Together, "yin-yang" regulation by MES-4 and DRM ensures transcript levels appropriate for germ-cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage. Experimental Details: WBPaper00044545:N2_1 WBPaper00044545:N2_2 WBPaper00044545:N2_3 WBPaper00044545:lin-54(n3423)_1 WBPaper00044545:lin-54(n3423)_2 WBPaper00044545:lin-54(n3423)_3 WBPaper00044545:mes-4(ok2326)_1 WBPaper00044545:mes-4(ok2326)_2 WBPaper00044545:mes-4(ok2326)_3 WBPaper00044545:lin-54(n3423);mes-4(ok2326)_1 WBPaper00044545:lin-54(n3423);mes-4(ok2326)_2 WBPaper00044545:lin-54(n3423);mes-4(ok2326)_3. |
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