Similar Datasets
Project description:scRNAseq of spr-5 met-2 mutant embryos
| PRJNA1139204 | ENA
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: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:In C. elegans, the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2, are maternally deposited into the oocyte where they reprogram histone methylation to prevent somatic expression of germline genes. Here, we show that the progeny of spr-5; met-2 mutants display a severe developmental delay that is associated with the ectopic expression of germline genes targeted by the H3K36me2/3 methyltransferase, MES-4. Maternally deposited MES-4 maintains H3K36me2/3 at a subset of germline genes (hereafter referred to as MES-4 germline genes) in a transcription-independent manner, and this is required for germline proliferation in the subsequent generation. By performing ChIP-seq on L1 progeny from spr-5; met-2 mutants, we find that MES-4 germline genes ectopically accumulate H3K36me3 in somatic tissues. Additionally, knocking down MES-4 suppresses the ectopic expression of MES-4 germline genes and rescues the developmental delay. These data suggest a model where SPR-5, MET-2 and MES-4 carefully balance the inheritance of histone methylation from the parental germline to ensure the proper specification of germline versus soma in the progeny. Without SPR-5; MET-2 maternal reprogramming, somatic cells struggle to specify their proper cell fate amongst the background noise of inappropriate germline gene transcription, leading to a severe developmental delay.
2020-05-29 | GSE151340 | GEO
Project description:In C. elegans, the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2, are maternally deposited into the oocyte where they reprogram histone methylation to prevent somatic expression of germline genes. Here, we show that the progeny of spr-5; met-2 mutants display a severe developmental delay that is associated with the ectopic expression of germline genes targeted by the H3K36me2/3 methyltransferase, MES-4. Maternally deposited MES-4 maintains H3K36me2/3 at a subset of germline genes (hereafter referred to as MES-4 germline genes) in a transcription-independent manner, and this is required for germline proliferation in the subsequent generation. By performing ChIP-seq on L1 progeny from spr-5; met-2 mutants, we find that MES-4 germline genes ectopically accumulate H3K36me3 in somatic tissues. Additionally, knocking down MES-4 suppresses the ectopic expression of MES-4 germline genes and rescues the developmental delay. These data suggest a model where SPR-5, MET-2 and MES-4 carefully balance the inheritance of histone methylation from the parental germline to ensure the proper specification of germline versus soma in the progeny. Without SPR-5; MET-2 maternal reprogramming, somatic cells struggle to specify their proper cell fate amongst the background noise of inappropriate germline gene transcription, leading to a severe developmental delay.
2020-01-17 | GSE143838 | GEO
Project description:In C. elegans, the H3K4me2 demethylase, SPR-5, and the H3K9 methyltransferase, MET-2, are maternally deposited into the oocyte where they reprogram histone methylation to prevent somatic expression of germline genes. Here, we show that the progeny of spr-5; met-2 mutants display a severe developmental delay that is associated with the ectopic expression of germline genes targeted by the H3K36me2/3 methyltransferase, MES-4. Maternally deposited MES-4 maintains H3K36me2/3 at a subset of germline genes (hereafter referred to as MES-4 germline genes) in a transcription-independent manner, and this is required for germline proliferation in the subsequent generation. By performing ChIP-seq on L1 progeny from spr-5; met-2 mutants, we find that MES-4 germline genes ectopically accumulate H3K36me3 in somatic tissues. Additionally, knocking down MES-4 suppresses the ectopic expression of MES-4 germline genes and rescues the developmental delay. These data suggest a model where SPR-5, MET-2 and MES-4 carefully balance the inheritance of histone methylation from the parental germline to ensure the proper specification of germline versus soma in the progeny. Without SPR-5; MET-2 maternal reprogramming, somatic cells struggle to specify their proper cell fate amongst the background noise of inappropriate germline gene transcription, leading to a severe developmental delay.
2020-01-17 | GSE143837 | GEO
Project description:How epigenetic information is transmitted from generation to generation remains largely unknown. Deletion of the C. elegans Histone H3 lysine 4 dimethyl (H3K4me2) demethylase spr-5 leads to inherited accumulation of the euchromatic H3K4me2 mark and progressive decline in fertility. Here we identified a genetic network of chromatin-modifying factors, including the H3K4me1/me2 methyltransferases SET-17 and SET-30, the H3K9me1/me2 methyltransferase MET-2, an H3K9me3 methyltransferase, SET-26, the H3K9me3 demethylase JMJD-2, and an H3K9me reader EAP-1, which regulate the trans-generational flow of epigenetic information. Importantly, genetic ablation of set-17, set-30, jmjd-2, or eap-1 suppresses the progressive transgenerational phenotypes, while loss of SET-26 or MET-2 accelerates the infertility of spr-5 mutant worms. We further show that loss of spr-5 also causes a trans-generational increase in lifespan, which is dependent on these chromatin regulators as well as DAF-36 and DAF-12, which control a germline to soma longevity signaling pathway. These findings suggest that the balance between the euchromatic H3K4 and the heterochromatic H3K9 methylation regulates trans-generational effects on longevity and fertility. EAP-1 binding ChIPseq libraries were prepared from 50 ul of packed young adult worms which were maintained at 16 degrees until the appropriate generation and then shifted to 25 degrees after birth. Two biological repeats were generated for wildtype and generation 20 spr-5(by101) mutant worms and a single repeat for generation 10. There were four input samples and eap-1 null mutant worms were also analyzed.
2014-04-08 | E-GEOD-52102 | biostudies-arrayexpress
Project description:Since the germline mortality phenotype of met-2; spr-1 mutants lie between spr-5; met-2 mutants and single mutants, it raises the possibility that maternal SPR-5 reprogramming may be partially dependent upon the SPR-5 interacting partner SPR-1. If mutating spr-1 partially compromises SPR-5 maternal reprogramming, we would expect that the gene expression changes in met-2; spr-1 mutants would be similar to spr-5; met-2 mutants, but that the changes would be less severe in met-2; spr-1 mutants. To test this possibility, we performed RNA-seq on spr-1, met-2, and met-2; spr-1 mutant L1 progeny compared to N2 L1 progeny.
2021-03-03 | GSE168081 | GEO
Project description:How epigenetic information is transmitted from generation to generation remains largely unknown. Deletion of the C. elegans Histone H3 lysine 4 dimethyl (H3K4me2) demethylase spr-5 leads to inherited accumulation of the euchromatic H3K4me2 mark and progressive decline in fertility. Here we identified a genetic network of chromatin-modifying factors, including the H3K4me1/me2 methyltransferases SET-17 and SET-30, the H3K9me1/me2 methyltransferase MET-2, an H3K9me3 methyltransferase, SET-26, the H3K9me3 demethylase JMJD-2, and an H3K9me reader EAP-1, which regulate the trans-generational flow of epigenetic information. Importantly, genetic ablation of set-17, set-30, jmjd-2, or eap-1 suppresses the progressive transgenerational phenotypes, while loss of SET-26 or MET-2 accelerates the infertility of spr-5 mutant worms. We further show that loss of spr-5 also causes a trans-generational increase in lifespan, which is dependent on these chromatin regulators as well as DAF-36 and DAF-12, which control a germline to soma longevity signaling pathway. These findings suggest that the balance between the euchromatic H3K4 and the heterochromatic H3K9 methylation regulates trans-generational effects on longevity and fertility.
2014-04-08 | GSE52102 | GEO
Project description:The goal of this study is to identify differentially expressed genes in Cbr-spr-4(gu163)/Cbr-ivp-1(gu163) and Cbr-htz-1(gu167)/Cbr-ivp-2(gu167) mutant compare to AF16 wild-type (WT). Our study represents the first analysis of Cbr-spr-4/Cbr-ivp-1 and Cbr-htz-1/Cbr-ivp-2 transcriptomes in C. briggsae and facilitates investigations of Cbr-spr-4/Cbr-ivp-1 and Cbr-htz-1/Cbr-ivp-2 mediated processes
2020-06-24 | GSE133769 | GEO