Gene expression changes upon depletion of H3K36 methylation by mutating met-1 and RNAi depleting mes-4 in worm L1 larvae
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ABSTRACT:
PROVIDER: PRJNA476763 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7364790.fastq.gz | Fastqsanger.gz | |||
| SRR7364787.fastq.gz | Fastqsanger.gz | |||
| SRR7364788.fastq.gz | Fastqsanger.gz | |||
| SRR7364789.fastq.gz | Fastqsanger.gz |
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Project description:We compared wild type N2 fed L4440 control RNAi to met-1 mutants fed mes-4 RNAi food. Genes tend to be upregulated rather than downregulated in these mutants. Comparison to available ChIPseq datasets indicates that the upregulated genes are heterochromatic and are not enriched for H3K36 methylation, indicating that H3K36me loss derepresses heterochromatin indirectly.
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2010-12-17 | PRD000256 | Pride
Project description:Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, 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 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. 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.
2013-11-05 | GSE52064 | GEO
Project description:Here we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, 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 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. 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. We compared germline gene expression profile of wild-type N2 C. elegans, lin-54(n3423) M+Z- mutant, mes-4(ok2326) M+Z- mutant, and lin-54(n3423);mes-4(ok2326) M+Z-mutant grown at 20C. 50~70 Germlines were dissected from young adults (24hours after L4 stage), and region from the tip until late pachytene stage of meiosis were collected. Three biological replicates for each strain were performed.
2013-11-05 | E-GEOD-52064 | biostudies-arrayexpress
Project description:Trascriptional profiling of C. elegans adult germ lines comparing mes-2(bn11)unc-4(e120) mutants and unc-4(e120) (wild type), mes-4(bn85) mutants and N2 (wild type), mes-2(bn11)unc-4(e120); mes-4(bn85) and unc-4(e120) (wild type) at 20 degrees.
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Project description:Maternally synthesized products play critical roles in development of offspring. A premier example is the C. elegans H3K36 methyltransferase MES-4, which is essential for germline survival and development in offspring. How maternal MES-4 protects the germline is not well understood, but its role in H3K36 methylation hinted that it may regulate gene expression in Primordial Germ Cells (PGCs). We tested this hypothesis by profiling transcripts from nascent germlines (PGCs and their descendants) dissected from wild-type and mes-4 mutant (lacking maternal and zygotic MES-4) larvae. mes-4 nascent germlines displayed down-regulation of some germline genes, up-regulation of some somatic genes, and dramatic up-regulation of hundreds of genes on the X chromosome. We demonstrated that up-regulation of 1 or more genes on the X is the cause of germline death by generating and analyzing mes-4 mutants that inherited different endowments of X chromosome(s). Intriguingly, removal of the THAP transcription factor LIN-15B from mes-4 mutants reduced X mis-expression and prevented germline death. lin-15B is X-linked and mis-expressed in mes-4 PGCs, identifying it as a critical target for MES-4 repression. The above findings extend to the H3K27 methyltransferase MES-2/3/6, the C. elegans version of Polycomb Repressive Complex 2. We propose that maternal MES-4 and PRC2 cooperate to protect germline survival by preventing synthesis of germline-toxic products encoded by genes on the X chromosome, including the key transcription factor LIN-15B.
2022-03-16 | GSE198552 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE38158: mes-2, mes-4 or mes-2; mes-4 mutants vs. wild type GSE38159: Strome MES-4, H3K36me3 and H3K27me3 in mes-4 RNAi EEMB GSE38180: Strome Mes-4, H3K36me3 and H3K27me3 in N2 EEMB Refer to individual Series
2012-05-29 | E-GEOD-38160 | biostudies-arrayexpress
Project description:Trascriptional profiling of C. elegans adult germ lines comparing mes-2(bn11)unc-4(e120) mutants and unc-4(e120) (wild type), mes-4(bn85) mutants and N2 (wild type), mes-2(bn11)unc-4(e120); mes-4(bn85) and unc-4(e120) (wild type) at 20 degrees. One-condition experiment, mutant vs. WT. Biological replicates 4 mutant, 4 wildtype harvested indepedently. One mutant replicate and one WT replicate per array.
2012-05-29 | E-GEOD-38158 | biostudies-arrayexpress
Project description:Cell plasticity is needed during development and homeostasis to generate diverse cell types from stem and progenitor cells. Following differentiation, plasticity must be restricted in specialized cells to maintain tissue integrity and function. For this reason, specialized cell identity is highly stable under homeostatic conditions; however, cells in some tissues regain plasticity during injury-induced regeneration. While precise gene expression is needed to control these processes, the regulatory mechanisms that restrict or promote cell plasticity are poorly understood. Here, we use the mouse small intestine as a model system to study cell plasticity. We find that H3K36 methylation reinforces expression of cell type-associated genes to maintain specialized cell identity in intestinal epithelial cells. Depleting H3K36 methylation leads to defects in lineage commitment and activates a plastic, regenerative gene expression signature. Correspondingly, we observe rapid and reversible remodeling of H3K36 methylation following injury-induced regeneration. Together, these data suggest a fundamental role for H3K36 methylation in regulating cell plasticity and regeneration.
2024-10-25 | GSE275296 | GEO
Project description:Cell plasticity is needed during development and homeostasis to generate diverse cell types from stem and progenitor cells. Following differentiation, plasticity must be restricted in specialized cells to maintain tissue integrity and function. For this reason, specialized cell identity is highly stable under homeostatic conditions; however, cells in some tissues regain plasticity during injury-induced regeneration. While precise gene expression is needed to control these processes, the regulatory mechanisms that restrict or promote cell plasticity are poorly understood. Here, we use the mouse small intestine as a model system to study cell plasticity. We find that H3K36 methylation reinforces expression of cell type-associated genes to maintain specialized cell identity in intestinal epithelial cells. Depleting H3K36 methylation leads to defects in lineage commitment and activates a plastic, regenerative gene expression signature. Correspondingly, we observe rapid and reversible remodeling of H3K36 methylation following injury-induced regeneration. Together, these data suggest a fundamental role for H3K36 methylation in regulating cell plasticity and regeneration.
2024-10-25 | GSE275295 | GEO