ScRNAseq of spr-5 met-2 mutant embryos
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1139204 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29932102_1.fastq.gz | Fastqsanger.gz | |||
| SRR29932102_2.fastq.gz | Fastqsanger.gz | |||
| SRR29932103_1.fastq.gz | Fastqsanger.gz | |||
| SRR29932103_2.fastq.gz | Fastqsanger.gz |
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Project description:Germline genes are ectopically expressed in the somatic lineages of spr-5; met-2 mutant 100-200 cell embryos
2024-07-24 | GSE272897 | 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: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.
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Project description:We asked if the perinuclear position of chromosome arms in C. elegans depends on the histone methyltransferases MET-2 and SET-25. To this end, we performed LMN-1-DamID in wild-type (N2) and mutant (set-25 met-2) strains. LMN-1-DamID signal on chromosome arms was significantly reduced in the mutant.
2012-09-04 | GSE37226 | 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
Project description:We asked if the perinuclear position of chromosome arms in C. elegans depends on the histone methyltransferases MET-2 and SET-25. To this end, we performed LMN-1-DamID in wild-type (N2) and mutant (set-25 met-2) strains. LMN-1-DamID signal on chromosome arms was significantly reduced in the mutant. Three biological replicas were performed for each genotype. For one replica dyes were swapped. For each replica methylated DNA amplified from a strain expressing LMN-1-Dam was competitively hybridized against DNA amplified from a strain expressing GFP-Dam.
2012-09-04 | E-GEOD-37226 | biostudies-arrayexpress
Project description:Tyrosine kinase-activating mutations in Met have been observed in hereditary papillary renal carcinomas as well as in other cancers. These mutations have been examined in several in vitro systems, where they cause constitutive Met activation, focus formation, and cell motility, and are tumorigenic in xenografts. To determine the influence of these mutations on tumorigenesis in vivo, we generated mice with targeted mutations in the murine met locus. Five mouse lines with mutant Met were created: wt, D1226N, Y1228C, M1248T, and M1248T/L1193V. These mouse lines develop a wide range of sarcomas, lymphomas, and carcinomas. To determine if mutationally activated forms of Met have altered signaling specificity we utilized gene expression analysis. Mouse embryonic fibroblasts (MEFs) were isolated from the mutant Met lines and here we present data for wild type and M1248T (M833). Our results indicate that Met activating mutations have unique gene expression signatures. Keywords: mutant analysis
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Project description:Tyrosine kinase-activating mutations in Met have been observed in hereditary papillary renal carcinomas as well as in other cancers. These mutations have been examined in several in vitro systems, where they cause constitutive Met activation, focus formation, and cell motility, and are tumorigenic in xenografts. To determine the influence of these mutations on tumorigenesis in vivo, we generated mice with targeted mutations in the murine met locus. Five mouse lines with mutant Met were created: wt, D1226N, Y1228C, M1248T, and M1248T/L1193V. These mouse lines develop a wide range of sarcomas, lymphomas, and carcinomas. To determine if mutationally activated forms of Met have altered signaling specificity we utilized gene expression analysis. Mouse embryonic fibroblasts (MEFs) were isolated from the mutant Met lines and here we present data for wild type and M1248T (M833). Our results indicate that Met activating mutations have unique gene expression signatures. Keywords: mutant analysis Color swapped replicates with common reference
2011-11-20 | E-GEOD-11319 | biostudies-arrayexpress