Similar Datasets
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: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:scRNAseq of spr-5 met-2 mutant embryos
| PRJNA1139204 | ENA
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. 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: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:In animals with germ plasm, specification of the germline involves “germ granules”, cytoplasmic condensates that enrich maternal transcripts in the germline founder cells. In C. elegans embryos, P granules enrich maternal transcripts, but surprisingly P granules are not essential for germ cell fate specification. Here we have described a second condensate in the C. elegans germ plasm. Like canonical P-bodies found in somatic cells, “germline P-bodies” contain regulators of mRNA decapping and deadenylation and, in addition, the intrinsically-disordered proteins MEG-1 and MEG-2 and the TIS11-family RNA-binding protein POS-1. Embryos lacking meg-1 and meg-2 do not stabilize P-body components, miss-regulate POS-1 targets, miss-specify the germline founder cell, and do not develop a germline. Our findings suggest that specification of the germ line involves at least two distinct condensates that independently enrich and regulate maternal mRNAs in the germline founder cells.
2022-10-05 | PXD036610 | Pride
Project description:To investigate the expression patterns driven by hyperactivated MET in MET-dependent cells, we employed LoVo colon adenocarcinoma cell line, harbouring a post-translational modification of MET that leads to its constitutive activation. We then silenced MET in LoVo cells using CRISPR/Cas9 knock-out (KO) protocol, and performed gene expression profiling analysis using data obtained from RNA-seq of cells with hyperactivated-MET versus MET-KO.
2023-10-14 | GSE212835 | GEO
Project description:Chromatin diminution is the programmed elimination of specific DNA sequences during development. It occurs in diverse species, but the function(s) of diminution and the specificity of sequence loss remain largely unknown. Diminution in the nematode Ascaris suum occurs during early embryonic cleavages and leads to the loss of germline genome sequences and the formation of a distinct genome in somatic cells. We found that M-bM-^HM-<43 Mb (M-bM-^HM-<13%) of genome sequence is eliminated in A. suum somatic cells, including M-bM-^HM-<12.7 Mb of unique sequence. The eliminated sequences and location of the DNA breaks are the same in all somatic lineages from a single individual and between different individuals. At least 685 genes are eliminated. These genes are preferentially expressed in the germline and during early embryogenesis. We propose that diminution is a mechanism of germline gene regulation that specifically removes a large number of genes involved in gametogenesis and early embryogenesis. To profile the tissue expression of all A. suum genes, we used 8 different developmental stages/tissues of A. suum, including testis, ovary, embryo, larvae, intestine, muscle, male carcass and female carcass. In this submission there are 10 samples: 3 for early embryos (24hr, 46hr and 64hr) and the other 7 for testis, ovary, larvae, intestine, muscle, male carcass and female carcass. For each sample, 200 ug of total RNA was used for poly(A) selection and 200 ng of poly(A)+ RNA was used to make the cDNA libraries using standard Illumina protocol.
2012-11-13 | E-GEOD-38470 | biostudies-arrayexpress