Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA394676 | ENA |
REPOSITORIES: ENA
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Project description:NF-κB-mediated signaling is maintained silent by the action of IκB proteins, whose canonical role is to sequester NF-κB in the cytoplasm. An alternative chromatin role for IκB members have been shown to affect stemness and cell differentiation but the involvement of NF-κB in this function has not been excluded. NFKI-1 and IKB-1 are IκB homologs in Caenorhabditis elegans, which lacks NF-κB nuclear effectors. nfki-1 and ikb-1 mutants present developmental defects that phenocopy mutations in Polycomb genes and demethylases as utx-1. suggesting a role for C. elegans IKB proteins in chromatin regulation, which is supported by various lines of evidence:(i) we detected NFKI-1 in the nucleus; (ii) NFKI-1 and IKB-1 bind to histones and Polycomb proteins, (iii) NFKI-1 and IKB-1 bind to chromatin in vivo, and (iv) mutations in nfki-1 and ikb-1 alter chromatin marks . Thus, ancestral IκB inhibitors may exert nuclear functions regulating of gene expression and development.
2020-09-01 | GSE146652 | GEO
Project description:Our study focuses in undersatnding the chromatin-associated function of the c. elegans IKB homologues nfki-1 and ikb-1. We this objective, we have generated different worm mutant strains and then analyzed by ChIP-seq possible changes in H3K36me3 and H3K27me3 marks in the WT , nfki-1, ikb-1 and double c elegans mutants.
2020-06-27 | GSE101495 | GEO
Project description:NF-κB-mediated signaling is maintained silent by the action of IκB proteins, whose canonical role is to sequester NF-κB in the cytoplasm. An alternative chromatin role for IκB members have been shown to affect stemness and cell differentiation but the involvement of NF-κB in this function has not been excluded. NFKI-1 and IKB-1 are IκB homologs in Caenorhabditis elegans, which lacks NF-κB nuclear effectors. nfki-1 and ikb-1 mutants present developmental defects that phenocopy mutations in Polycomb genes and demethylases as utx-1. suggesting a role for C. elegans IKB proteins in chromatin regulation, which is supported by various lines of evidence:(i) we detected NFKI-1 in the nucleus; (ii) NFKI-1 and IKB-1 bind to histones and Polycomb proteins, (iii) NFKI-1 and IKB-1 bind to chromatin in vivo, and (iv) mutations in nfki-1 and ikb-1 alter chromatin marks . Thus, ancestral IκB inhibitors may exert nuclear functions regulating of gene expression and development.
2020-09-01 | GSE146654 | GEO
Project description:We applied a middle-down proteomics strategy for large scale protein analysis during in vivo development of Caenorhabditis elegans. We characterized post-translational modifications (PTMs) on histone H3 N-terminal tails at eight time points during the C. elegans lifecycle, including embryo, larval stages (L1 to L4), dauer and L1/L4 post dauer. Histones were analyzed by our optimized middle-down protein sequencing platform using high mass accuracy tandem mass spectrometry. This allows quantification of intact histone tails and detailed characterization of distinct histone tails carrying co-occurring PTMs. We measured temporally distinct combinatorial PTM profiles during C. elegans development. We show that the doubly modified form H3K23me3K27me3, which is rare or non-existent in mammals, is the most abundant PTM in all stages of C. elegans lifecycle. The abundance of H3K23me3 increased during development and it was mutually exclusive of the active marks H3K18ac, R26me1 and R40me1, suggesting a role for H3K23me3 in to silent chromatin. We observed distinct PTM profiles for normal L1 larvae and for L1-post dauer larvae, or L4 and L4 post-dauer, suggesting that histone PTMs mediate an epigenetic memory that is transmitted during dauer formation. Collectively, our data describe the dynamics of histone H3 combinatorial code during C. elegans lifecycle and demonstrate the feasibility of using middle-down proteomics to study in vivo development of multicellular organisms.
2015-11-02 | PXD002525 | Pride
Project description:O-GlcNAc Chromatin Marks from C. elegans L1 animals
| PRJNA123723 | ENA
Project description:mRNA Next Generation Sequencing of long-lived C. elegans mutants lacking the replication-independent histone variant H3.3
| PRJNA343462 | ENA
Project description:mRNA-seq analysis of C. elegans splicing factor mutants
| PRJDB10132 | ENA
Project description:Small RNA in wild type Caenorhabditis elegans and ADAR mutants
| PRJNA288070 | ENA
Project description:C. elegans daf-10(m79) mutants vs wild-type worms
| PRJNA178552 | ENA
Project description:Epigenetic modifications are thought to be important for gene expression changes during development and aging. However, besides the Sir2 histone deacetylase in somatic tissues and H3K4 trimethylation in germlines, there is scant evidence implicating epigenetic regulations in aging. The insulin/IGF-1 signaling (IIS) pathway is a major lifespan regulatory pathway. Here we show that progressive increases in gene expression and loss of H3K27me3 on IIS components are due, at least in part, to increased activity of the H3K27 demethylase UTX-1 during aging. RNAi of the utx-1 gene extended the mean lifespan of C. elegans by ~30%, dependent on DAF-16 activity and not additive in daf-2 mutants. The loss of utx-1 increased H3K27me3 on the Igf1r/daf-2 gene and decreased IIS activity leading to a more "naive" epigenetic state. Like stem cell reprogramming, our results suggest that reestablishing epigenetic marks lost during aging might help "reset" the developmental age of animal cells. Examination of H3K27me3 in young and old worms without or with Utx-1 RNAi.
2011-11-22 | E-GEOD-29896 | biostudies-arrayexpress