Caenorhabditis elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA371645 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5235990.fastq.gz | Fastqsanger.gz | |||
| SRR5235991.fastq.gz | Fastqsanger.gz | |||
| SRR5235992.fastq.gz | Fastqsanger.gz | |||
| SRR5235993.fastq.gz | Fastqsanger.gz | |||
| SRR5235994.fastq.gz | Fastqsanger.gz |
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Project description:Background:Histone H3 lysine 4 methylation (H3K4me) is generally associated with active transcription and bivalent chromatin, but can also contribute to repression. In metazoans, H3K4 methylation is catalysed by KMT2 methyltransferases assembled with the core scaffolding proteins WDR5, ASH2L, and RBBP5. RBBP5 mediates complex assembly and nucleosome binding, whilst WDR5 stabilises interactions to promote tri-methylation. However, WDR5 also exhibits additional ‘moonlighting’ functions, leaving its specific roles in H3K4 methylation and transcription regulation unclear. Using C. elegans embryos, spike-in ChIP-seq, and null alleles of wdr-5(-) and rbbp-5(-), we dissected the contributions of these scaffolds towards H3K4 mono-, di-, and tri-methylation as well as gene expression during C. elegans embryogenesis. Results:We show that C. elegans RBBP-5 is essential for both mono- and multi-methylated H3K4 deposition. On the other hand, WDR-5 is primarily required for H3K4me3, but can influence H3K4me2 and H3K4me1 deposition either positively or negatively depending on the genomic feature involved. We additionally performed RNA-seq on these mutants and found that rbbp-5 deletion was largely tolerated with mis-regulation of ~ 700 genes, whereas the wdr-5 deletion led to widespread transcriptomic disruption (~ 3000 genes). We initially hypothesised that these broad changes were driven by the altered H3K4me1 and H3K4me2 landscapes in the wdr-5(-) mutant. However, transcriptomic profiling of the wdr-5(-); rbbp-5(-) double mutant, which lacks H3K4 methylation, revealed a high degree of similarity to the wdr-5(-) single mutant. This refuted our initial hypothesis and indicates that the changes in H3K4 methylation are unlikely to underlie the transcriptional effects of the wdr-5 deletion. Conclusions:Our findings strongly indicate that WDR-5 profoundly shapes gene expression through mechanisms beyond H3K4 methylation. Distinguishing between H3K4me-dependent and independent functions of WDR-5 will further understanding of its roles in development and disease.
2019-02-08 | GSE94639 | GEO
Project description:WDR-5 exhibits H3K4 methylation-independent activity, whereas RBBP-5 is essential for H3K4 methylation during embryonic development in C. elegans
| PRJEB88882 | ENA
Project description:Histone H3 Lys 4 methylation (H3K4me) is deposited by the conserved SET1/MLL methyltransferases acting in multiprotein complexes including Ash2 and Wdr5. While individual subunits contribute to complex activity, how they influence gene expression in a specific tissue remains largely unknown. In caenorhabditis elegans, SET-2/SET1, WDR-5.1 and ASH-2 are differentially required for germline H3K4 methylation. Using expression profiling on germlines from animals lacking set-2, ash-2 or wdr-5.1, we show that these subunits play unique and redundant functions to promote expression of germline genes and repress somatic genes. We further show that in set-2 and wdr-5.1 deficient germlines, somatic gene misexpression is associated with conversion of germ cells into somatic cells, and that nuclear RNAi acts in parallel with SET-2 and WDR-5.1 to maintain germline identity. These findings uncover a unique role for SET-2 and WDR-5.1 in preserving germline pluripotency, and underline the complexity of the cellular network regulating this process. Gene misregulation in SET1/set-2, wdr-5.1 and ash-2 defective germlines
2014-09-04 | E-GEOD-61094 | biostudies-arrayexpress
Project description:Histone H3 Lys 4 methylation (H3K4me) is deposited by the conserved SET1/MLL methyltransferases acting in multiprotein complexes including Ash2 and Wdr5. While individual subunits contribute to complex activity, how they influence gene expression in a specific tissue remains largely unknown. In caenorhabditis elegans, SET-2/SET1, WDR-5.1 and ASH-2 are differentially required for germline H3K4 methylation. Using expression profiling on germlines from animals lacking set-2, ash-2 or wdr-5.1, we show that these subunits play unique and redundant functions to promote expression of germline genes and repress somatic genes. We further show that in set-2 and wdr-5.1 deficient germlines, somatic gene misexpression is associated with conversion of germ cells into somatic cells, and that nuclear RNAi acts in parallel with SET-2 and WDR-5.1 to maintain germline identity. These findings uncover a unique role for SET-2 and WDR-5.1 in preserving germline pluripotency, and underline the complexity of the cellular network regulating this process.
2014-09-04 | GSE61094 | GEO
Project description:Changes in histone post-translational modifications are associated with aging through poorly defined mechanisms. Histone 3 lysine 4 (H3K4) methylation at promoters is deposited by SET1 family methyltransferases acting within conserved multiprotein complexes known as COMPASS. Using co-immunopurification coupled to mass spectrometry-based proteomics, we characterized complex members and binding partners in various genetic contexts, using WDR-5 or CFP-1 proteins as baits.
2021-12-08 | PXD029904 | Pride
Project description:Expression data from C. elegans wdr-23 mutants
| PRJNA296035 | ENA
Project description:Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents. There are 35 samples in total. We found that genetically WT descendents from mutants of the H3K4me3 modifying complex had extended longevity up until the F4 generation. Their lifespan returned to WT levels in the F5 generation. We performed microarrays to examine what gene expression differences there were between N2(WT) worms, +/+ (from wdr-5 mutant) worms, and wdr-5/wdr-5 in the F4 and the F5 generation. We analyzed L3 samples from the first and second days of egg laying in triplicate each. Samples consist of ~1000 worms each.
2011-10-18 | E-GEOD-31043 | biostudies-arrayexpress
Project description:Chromatin modifiers regulate lifespan in several organisms, raising the question of whether changes in chromatin states in the parental generation could be incompletely reprogrammed in the next generation and thereby affect the lifespan of descendents. The histone H3 lysine 4 trimethylation (H3K4me3) complex composed of ASH-2, WDR-5, and the histone methyltransferase SET-2 regulates C. elegans lifespan. Here we show that deficiencies in the H3K4me3 chromatin modifiers ASH-2, WDR-5, or SET-2 in the parental generation extend the lifespan of descendents up until the third generation. The transgenerational inheritance of lifespan extension by members of the ASH-2 complex is dependent on the H3K4me3 demethylase RBR-2, and requires the presence of a functioning germline in the descendents. Transgenerational inheritance of lifespan is specific for the H3K4me3 methylation complex and is associated with epigenetic changes in gene expression. Thus, manipulation of specific chromatin modifiers only in parents can induce an epigenetic memory of longevity in descendents.
2011-10-19 | GSE31043 | GEO
Project description:The WDR-23 protein regulates the transcription factor SKN-1 directly. C. elegans wdr-23 mutants have highly active SKN-1 and are stress resistant, long-lived, small, and reproduce poorly. We used microarrays to measure global gene expression in wdr-23 mutants and to indentify genes regulated by SKN-1.
2020-09-01 | GSE73101 | GEO
Project description:The embryonic muscle transcriptome of Caenorhabditis elegans
| PRJNA101543 | ENA