SET-9 and SET-26 are H3K4me3 readers and play critical roles in germline development and longevity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA428937 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6493980.fastq.gz | Fastqsanger.gz | |||
| SRR6493990.fastq.gz | Fastqsanger.gz | |||
| SRR6494000.fastq.gz | Fastqsanger.gz | |||
| SRR6493981.fastq.gz | Fastqsanger.gz | |||
| SRR6493991.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 32 |
Similar Datasets
Project description:SET-9 and SET-26 are highly homologous paralogs that share redundant function in germline development, but SET-26 alone plays a key role in longevity and heat stress response. SET-26 is broadly expressed, but SET-9 is only detectable in the germline, which likely account for their different biological roles. SET-9 and SET-26 bind to H3K4me3 in vitro and in vivo, and their loss results in broadening of H3K4me3 domains. SET-9 and SET-26 also regulate the RNA expression of a subset of their target genes, irrespective of their H3K4me3 status. We propose that SET-9 and SET-26 function to organize local chromatin environment and to regulate the expression of specific target genes, and these activities together contribute to their critical roles in germline development, stress response, and longevity. SET-9 and SET-26 are highly homologous to human MLL5, a factor implicated in leukemia and glioblastoma, and our findings help to provide new insights into MLL5.
2018-05-31 | GSE108848 | GEO
Project description:C. elegans SET-9 and SET-26 are highly homologous paralogs that share redundant functions in germline development, but SET-26 alone plays a key role in longevity and heat stress response. Whereas SET-26 is broadly expressed, SET-9 is only detectable in the germline, which likely accounts for their different biological roles. SET-9 and SET-26 bind to H3K4me3 with adjacent acetylation marks in vitro and in vivo. In the soma, SET-26 acts through DAF-16 to modulate longevity. In the germline, SET-9 and SET-26 restrict H3K4me3 domains around SET-9 and SET-26 binding sites, and regulate the expression of specific target genes, with critical consequence on germline development. SET-9 and SET-26 are highly conserved and our findings provide new insights into the functions of these H3K4me3 readers in germline development and longevity.
| S-EPMC6010342 | biostudies-literature
Project description:SET-9 and SET-26 are highly homologous paralogs that share redundant function in germline development, but SET-26 alone plays a key role in longevity and heat stress response. SET-26 is broadly expressed, but SET-9 is only detectable in the germline, which likely account for their different biological roles. SET-9 and SET-26 bind to H3K4me3 in vitro and in vivo, and their loss results in broadening of H3K4me3 domains. SET-9 and SET-26 also regulate the RNA expression of a subset of their target genes, irrespective of their H3K4me3 status. We propose that SET-9 and SET-26 function to organize local chromatin environment and to regulate the expression of specific target genes, and these activities together contribute to their critical roles in germline development, stress response, and longevity. SET-9 and SET-26 are highly homologous to human MLL5, a factor implicated in leukemia and glioblastoma, and our findings help to provide new insights into MLL5.
2018-05-31 | GSE100623 | GEO
Project description:SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. HDA-1 opposes SET-26 and HCF-1 on the regulation of a subset of their common target genes and in longevity. Our findings suggest that SET-26, HCF-1, and HDA-1 comprise a mechanism to fine-tune gene expression and longevity and likely have important implications for the mechanistic understanding of how these factors function in diverse organisms, particularly in aging biology.
2024-01-29 | GSE224076 | GEO
Project description:SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. HDA-1 opposes SET-26 and HCF-1 on the regulation of a subset of their common target genes and in longevity. Our findings suggest that SET-26, HCF-1, and HDA-1 comprise a mechanism to fine-tune gene expression and longevity and likely have important implications for the mechanistic understanding of how these factors function in diverse organisms, particularly in aging biology.
2024-01-29 | GSE224075 | GEO
Project description:We performed multilevel proteomics to identify mono-ADPr readers. Pulldowns using ADPribosylated peptides and nucleosomes, analysis of the chromatin proteome using targeted modulations of the ADPr system (H2O2 treatment, ARH3 KO, HPF1 KO). We reveal multiple mono-ADPr readers, including RNF114, a ubiquitin ligase recruited to DNA lesions through a zinc finger domain.
2023-04-28 | PXD037026 | Pride
Project description:Transgenerational epigenetic inheritance (TEI), the transmission of epigenetic states between generations, has been observed in complex organisms ranging from plants to nematode worms, insects and mammals. One form of TEI that has been robustly studied is the inheritance of gene silencing. In Caenorhabditis elegans transgenerational gene silencing can be partitioned into three phases: the initiation of silencing, establishment of a heritable silencing signal within the parent individuals, and maintenance of this silencing signal within subsequent generations. Silencing involves nuclear and cytoplasmic components, and most genes involved in the process are linked to small RNA processing pathways. To date, two predicted histone methyltransferases have been implicated in the establishment of TEI, set-25 and set-32. Here, we demonstrate that the closely related paralogues set-9 and set-26 function in establishment and maintenance of TEI. We also identify a third related gene that lacks any predicted ordered domains; we name this gene intrinsically disordered protein-1 (idp-1). Strikingly, idp-1 also plays a role in establishment of TEI. SET-9 and SET-26 each contain a PHD finger and a SET domain. We show that the SET domains of SET-9 and SET-26 likely have no histone lysine methyltransferase activity, but that the PHD fingers bind trimethylated histone 3 lysine 4 (H3K4me3) in the absence of adjacent histone marks. We demonstrate that despite modelling data that suggests that set-9 and set-26 lack histone lysine methyltransferase activity, the function of both genes in TEI requires their PHD finger and SET domains. Our data confirm that the SET domain is functional and identifies three new chromatin factors required for epigenetic inheritance.
2024-12-31 | GSE245980 | GEO
Project description:Transgenerational epigenetic inheritance (TEI), the transmission of epigenetic states between generations, has been observed in complex organisms ranging from plants to nematode worms, insects and mammals. One form of TEI that has been robustly studied is the inheritance of gene silencing. In Caenorhabditis elegans transgenerational gene silencing can be partitioned into three phases: the initiation of silencing, establishment of a heritable silencing signal within the parent individuals, and maintenance of this silencing signal within subsequent generations. Silencing involves nuclear and cytoplasmic components, and most genes involved in the process are linked to small RNA processing pathways. To date, two predicted histone methyltransferases have been implicated in the establishment of TEI, set-25 and set-32. Here, we demonstrate that the closely related paralogues set-9 and set-26 function in establishment and maintenance of TEI. We also identify a third related gene that lacks any predicted ordered domains; we name this gene intrinsically disordered protein-1 (idp-1). Strikingly, idp-1 also plays a role in establishment of TEI. SET-9 and SET-26 each contain a PHD finger and a SET domain. We show that the SET domains of SET-9 and SET-26 likely have no histone lysine methyltransferase activity, but that the PHD fingers bind trimethylated histone 3 lysine 4 (H3K4me3) in the absence of adjacent histone marks. We demonstrate that despite modelling data that suggests that set-9 and set-26 lack histone lysine methyltransferase activity, the function of both genes in TEI requires their PHD finger and SET domains. Our data confirm that the SET domain is functional and identifies three new chromatin factors required for epigenetic inheritance.
2024-12-31 | GSE245981 | GEO
Project description:YTH domain family proteins Ythdf1, Ythdf2, Ythdf3 are three readers with highly similar structure, which were shown to have different roles in the cell. However, their similarity and the fact that they tend to bind the same targets suggest that in some cases they may have an overlapping role. In this paper, we systematically knocked-out (KO) each of the three readers and the three together (triple-KO), and estimated the effect in-vitro in mouse embryonic stem cells (mESCs), and in-vivo, in viability and gametogenesis. We show that in mESCs there is a compensation between the three readers, with a dramatic hyper-pluripotent phenotype only in the triple-KO. However, in-vivo, Ythdf2 has a dominant role that cannot be compensated by Ythdf1 or Ythdf3, both in viability of the mouse pups and in gametogenesis. We suggest that compensation is dosage-dependent, and in-vivo we cannot detect it due to difference in the readers’ expression, both in level and in spatial location. In addition, we found that Ythdf1 and Ythdf3 specifically down-regulate 2-cell genes, that Ythdf2-KO in gametogenesis affects microtubuline related genes, and that Mettl3-KO severity is increased as the deletion occurs earlier in gametogenesis.
2020-06-04 | GSE151788 | GEO
Project description:EML histone readers prevent seed development without fertilization
| PRJNA454261 | ENA