Caenorhabditis elegans
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PROVIDER: PRJNA260212 | ENA |
REPOSITORIES: ENA
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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:Deposition of histone H3 lysine 4 (H3K4) methylation at promoter regions by the SET1/COMPASS complex is associated with context-dependent effects on gene expression. Transcription-independent functions have also been attributed to this highly conserved complex, but whether these contribute to higher-order chromosome organization has not been explored. Using a quantitative FRET (Förster resonance energy transfer)-based fluorescence lifetime imaging microscopy (FLIM) approach to assay nanometer scale chromatin compaction in live animals, we reveal an unexpected role for SET1/COMPASS in structuring meiotic chromosomes in the germline of C. elegans. Inactivation of SET-2, the C. elegans homologue of the catalytic subunit SET1, strongly enhanced chromosome organization defects and loss of fertility resulting from partial depletion of condensin-II. Loss of CFP-1, the chromatin targeting subunit of COMPASS, similarly affected germline chromatin compaction measured by FLIM-FRET and enhanced condensin-II knock-down phenotypes. Defects in chromosome morphology following conditional inactivation of topoisomerase II, another structural component of chromosomes, were also aggravated in the absence of set-2. Our results are consistent with a role of SET1/COMPASS in shaping meiotic chromosomes in the C. elegans germline, and have important implications for how chromatin-modifying complexes and histone modifications may cooperate with non histone-proteins to achieve proper chromosome organization, not only in meiosis, but also in mitosis.
2020-09-03 | GSE146932 | GEO
Project description:The plasticity of ageing suggests that longevity may be controlled epigenetically by specific alterations in chromatin state. The link between chromatin and ageing has mostly focused on histone deacetylation by the Sir2 family1, 2, but less is known about the role of other histone modifications in longevity. Histone methylation has a crucial role in development and in maintaining stem cell pluripotency in mammals3. Regulators of histone methylation have been associated with ageing in worms4, 5, 6, 7 and flies8, but characterization of their role and mechanism of action has been limited. Here we identify the ASH-2 trithorax complex9, which trimethylates histone H3 at lysine 4 (H3K4), as a regulator of lifespan in Caenorhabditis elegans in a directed RNA interference (RNAi) screen in fertile worms. Deficiencies in members of the ASH-2 complex—ASH-2 itself, WDR-5 and the H3K4 methyltransferase SET-2—extend worm lifespan. Conversely, the H3K4 demethylase RBR-2 is required for normal lifespan, consistent with the idea that an excess of H3K4 trimethylation—a mark associated with active chromatin—is detrimental for longevity. Lifespan extension induced by ASH-2 complex deficiency requires the presence of an intact adult germline and the continuous production of mature eggs. ASH-2 and RBR-2 act in the germline, at least in part, to regulate lifespan and to control a set of genes involved in lifespan determination. These results indicate that the longevity of the soma is regulated by an H3K4 methyltransferase/demethylase complex acting in the C. elegans germline. There are 23 samples in total. ASH-2 knock-down increases lifespan in a germline dependent manner. We examined ASH-2 regulated genes that are dependent on the presence of an intact germline using WT or glp-1(e2141ts) mutant worms which develop only 5-15 meiotic germ cells treated with either empty vector (EV) or ash-2 RNAi. We examined gene expression at the L3 stage (when we observe changes in H3K4me3) and at a mid life stage (day 8). The majority of ASH-2 controlled genes were regulated in a germline dependent manner. Samples were collected in triplicate for each condition (but Day 8 N2 (WT) E.V. #3 was excluded from all analysis due to quality issues).
2011-07-08 | E-GEOD-30505 | biostudies-arrayexpress
Project description:The plasticity of ageing suggests that longevity may be controlled epigenetically by specific alterations in chromatin state. The link between chromatin and ageing has mostly focused on histone deacetylation by the Sir2 family1, 2, but less is known about the role of other histone modifications in longevity. Histone methylation has a crucial role in development and in maintaining stem cell pluripotency in mammals3. Regulators of histone methylation have been associated with ageing in worms4, 5, 6, 7 and flies8, but characterization of their role and mechanism of action has been limited. Here we identify the ASH-2 trithorax complex9, which trimethylates histone H3 at lysine 4 (H3K4), as a regulator of lifespan in Caenorhabditis elegans in a directed RNA interference (RNAi) screen in fertile worms. Deficiencies in members of the ASH-2 complex—ASH-2 itself, WDR-5 and the H3K4 methyltransferase SET-2—extend worm lifespan. Conversely, the H3K4 demethylase RBR-2 is required for normal lifespan, consistent with the idea that an excess of H3K4 trimethylation—a mark associated with active chromatin—is detrimental for longevity. Lifespan extension induced by ASH-2 complex deficiency requires the presence of an intact adult germline and the continuous production of mature eggs. ASH-2 and RBR-2 act in the germline, at least in part, to regulate lifespan and to control a set of genes involved in lifespan determination. These results indicate that the longevity of the soma is regulated by an H3K4 methyltransferase/demethylase complex acting in the C. elegans germline.
2011-07-08 | GSE30505 | GEO
Project description:Caenorhabditis elegans LITE-Seq germline 3'UTR sequencing
| PRJNA360979 | ENA