The Dream and MEC Complexes reinforce SPR-5 MET-2 maternal reprogramming to maintain the Germline-Soma distinction [mep-1 RNAseq]
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PROVIDER: PRJNA1294132 | ENA |
REPOSITORIES: ENA
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Project description:Proper regulation of tissue-specific gene expression is essential for cell fate determination and development. In Caenorhabditis elegans, the distinction between germline and somatic cell fates is partially established through maternally inherited histone modifications. During gametogenesis, germline genes acquire transcription-coupled chromatin marks such as histone methylation, which are inherited by the zygote and must be reprogrammed at fertilization to prevent inappropriate germline gene expression in somatic tissues. This maternal reprogramming is mediated by histone-modifying enzymes, including the demethylase SPR-5/LSD1 and the H3K9 methyltransferase MET-2/SETDB1. Together, these enzymes limit DNA accessibility to transcriptional machinery, thereby resetting the chromatin landscape in te newly formed zygote. Failure to reprogram inherited histone methylation, as in spr-5; met-2 mutants, results in the ectopic expression of MES-4-targeted germline genes in somatic tissues, leading to developmental delay and sterility. Here, we investigated whether transcriptional repressor complexes—the DREAM and MEC NuRD complexes—cooperate with SPR-5 and MET-2 to specify germline versus soma. Loss of DREAM or MEC NuRD components alone causes somatic expression of germline genes. Strikingly, combined loss with spr-5; met-2 enhances developmental arrest at the L1 stage and exacerbates germline gene misexpression. By re analyzing previous published ChIP-seq data, we confirmed direct binding of MEP-1 and LIN-35 to these misregulated genes. Our findings demonstrate that maternal reprogramming and conserved chromatin repressor complexes act synergistically to repress germline transcription in somatic tissues, ensuring proper somatic development and preventing soma-to-germline transformation.
2025-07-21 | GSE303085 | GEO
Project description:Proper regulation of tissue-specific gene expression is essential for cell fate determination and development. In Caenorhabditis elegans, the distinction between germline and somatic cell fates is partially established through maternally inherited histone modifications. During gametogenesis, germline genes acquire transcription-coupled chromatin marks such as histone methylation, which are inherited by the zygote and must be reprogrammed at fertilization to prevent inappropriate germline gene expression in somatic tissues. This maternal reprogramming is mediated by histone-modifying enzymes, including the demethylase SPR-5/LSD1 and the H3K9 methyltransferase MET-2/SETDB1. Together, these enzymes limit DNA accessibility to transcriptional machinery, thereby resetting the chromatin landscape in te newly formed zygote. Failure to reprogram inherited histone methylation, as in spr-5; met-2 mutants, results in the ectopic expression of MES-4-targeted germline genes in somatic tissues, leading to developmental delay and sterility. Here, we investigated whether transcriptional repressor complexes—the DREAM and MEC NuRD complexes—cooperate with SPR-5 and MET-2 to specify germline versus soma. Loss of DREAM or MEC NuRD components alone causes somatic expression of germline genes. Strikingly, combined loss with spr-5; met-2 enhances developmental arrest at the L1 stage and exacerbates germline gene misexpression. By re analyzing previous published ChIP-seq data, we confirmed direct binding of MEP-1 and LIN-35 to these misregulated genes. Our findings demonstrate that maternal reprogramming and conserved chromatin repressor complexes act synergistically to repress germline transcription in somatic tissues, ensuring proper somatic development and preventing soma-to-germline transformation.
2025-07-19 | GSE303062 | GEO
Project description:The Dream and MEC Complexes reinforce SPR-5 MET-2 maternal reprogramming to maintain the Germline-Soma distinction [lin-35 RNAseq]
| PRJNA1293434 | ENA
Project description:Mutations in the DREAM complex induce germline-like gene expression patterns including the increase of multiple mechanisms of DNA repair in the soma of Caenorhabditis elegans. This confers mutants of the DREAM complex resistance to a wide range of DNA damage types during development and aging.
2023-01-31 | PXD033836 | Pride
Project description:The highly conserved DREAM transcriptional repressor complex contains an RB-like pocket protein, an E2F-DP transcription factor heterodimer, and the 5-subunit MuvB complex. Using CRISPR/Cas9 targeted mutagenesis, we disrupted the interaction between the sole Caenorhabditis elegans pocket protein LIN-35 and the MuvB subunit LIN-52. A triple alanine substitution of LIN-52's LxCxE motif (3A) severed LIN-35-MuvB association and caused classical DREAM mutant phenotypes, including synthetic multiple vulvae, high-temperature arrest, and ectopic expression of germline genes in the soma. We performed RNA-seq in lin-52(3A) mutant late embryos (4 replicates) compared to lin-52(WT) wild-type late embryos (4 replicates) to assess the genome-wide effects on gene expression that result from severing LIN-35-MuvB association.
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2015-11-01 | GSE68943 | GEO
Project description:Expression data from Caenorhabditis elegans let-418(RNAi), mep-1(RNAi) and gfp(RNAi) L1 larvae. The C. elegans genome encodes two homologs of the human protein Mi-2, namely LET-418 and CHD-3. LET-418 plays an essential role during development; its depletion leads to a pleiotropic and lethal phenotype that includes larval arrest, an everted vulva and sterility. Without maternal contribution, let-418 mutants stop their development at the L1 larval stage (von Zelewsky et al., 2000). We further characterized this arrest and showed that it is very similar to the L1 diapause induced by starvation; both germline and somatic cells remain in a quiescent state in let-418 L1 arrested larvae, indicating that LET-418 activity is required to bypass the L1 arrest in presence of food. The let-418 L1 larvae express ectopically the P granule component PGL-1 in somatic cells (Unhavaithaya et al., 2002). Interestingly, the phenotype of mep-1 mutants is remarkably similar to that of let-418: RNAi targeting mep-1 also induced an L1 arrest phenotype; furthermore, MEP-1 and LET-418 have been shown to physically interact (Unhavaithaya et al., 2002 and M. Passannante). The null allele mep-1(q660) is temperature sensitive and shows a more severe phenotype at higher temperatures. At 20°C, about 10% of mep-1 homozygotes derived from heterozygous mothers arrest as young larvae, whereas the remaining 90% develop into sterile adults (Belfiore et al., 2002). Later in development, the somatic gonad is affected in mep-1(q660) mutants. This results in an abnormal and disorganized gonad, a phenotype also observed in let-418(s1617) mutants. Both let-418 and mep-1 mutants produce a very limited number of oocytes and have pseudovulvae derived from P8.p (Belfiore et al., 2002; von Zelewsky et al., 2000 and C. Wicky, personal communication). Preliminary quantitative real-time PCR revealed that the expression of genes coding for P granule components was deregulated in both mep-1(RNAi) and let-418(RNAi) L1 larvae (data not shown). To further investigate this issue, we performed a complete gene expression analysis. Given the fact that mep-1(q660) mutants are sterile, we used RNA interference to generate mep-1 depleted worms. Bacteria expressing gfp dsRNA (pPE128.110 in HT115) were used as reference, since RNA interference may induce gene expression changes by itself.
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2008-06-10 | GSE10593 | GEO
Project description:PSU mouse MEP RNA 100 cells RNA-seq For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2016-03-18 | GSE78654 | GEO