Glutamine 5 serotonylation on histone H3 is a permissive modification that functions combinatorialy with H3K4me3 to potentiate TFIID interactions
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PROVIDER: PRJNA417049 | ENA |
REPOSITORIES: ENA
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Project description:Chemical modifications of histone proteins, along with the ?writers,? ?erasers? and ?readers? of these modifications, are capable of mediating a diverse set of DNA-templated processes including gene transcription1-7. Here, we provide evidence for a new class of histone posttranslational modification (PTM), serotonylation of glutamine, which occurs at position 5 (Q5ser) on histone H3 in serotonin (5-hydroxytryptamine, 5-HT) producing organisms. We demonstrate that the tissue Transglutaminase 2 (TGM2) enzyme, a transamidase that is both necessary and sufficient to deposit the mark, can serotonylate H3 on lysine 4 tri-methylated (H3K4me3) nucleosomes resulting in the presence of combinatorial H3K4me3Q5ser in vivo. H3K4me3Q5ser displays a ubiquitous pattern of tissue expression in mammals, with predicted enrichment observed in brain and gut, two organ systems responsible for the bulk of 5-HT production. Genome-wide analyses of its enrichment in human serotonergic neurons, developing mouse brain and cultured serotonergic cells, using an H3K4me3Q5ser specific antibody, indicate that the mark is enriched in euchromatin, is sensitive to cellular differentiation and correlates with permissive gene expression, phenomena that are linked to the mark?s potentiation of TFIID8-10 interactions with H3K4me3. Cells ectopically expressing an H3 mutant that cannot be serotonylated display significantly altered expression of H3K4me3Q5ser target loci leading to deficits in differentiation. Taken together, these data identify a direct role for 5-HT, independent from its contributions to neurotransmission and cellular signaling, in the mediation of permissive gene expression in mammalian cells, and further define its biophysical activities as a putative co-regulator of TFIID recruitment to H3K4me3 marked chromatin.
2018-12-18 | GSE106495 | GEO
Project description: Not available
| S-EPMC6557285 | biostudies-literature
Project description:Expression analysis of Saccharomyces cerevisiae TAF5 and taf5 temperature conditional mutants grown at permissive and non-permissive temperature. Investigation of whole genome gene expression level changes in Saccharomyces cerevisae taf5-17, taf5-45, taf5-408 and taf5-10.4 mutants, compared to the wild-type strain. The mutations engineered into the strains confer temperature conditional growth. The mutants analyzed in this study are further described in Layer et. al., 2010. Direct Transactivator-Transcription Factor IID (TFIID) Contacts Drive Yeast Ribosomal Protein Gene Transcription. Journal of Biological Chemistry.
2010-03-06 | GSE20444 | GEO
Project description:Expression analysis of Saccharomyces cerevisiae TAF5 and taf5 temperature conditional mutants grown at permissive and non-permissive temperature. Investigation of whole genome gene expression level changes in Saccharomyces cerevisae taf5-17, taf5-45, taf5-408 and taf5-10.4 mutants, compared to the wild-type strain. The mutations engineered into the strains confer temperature conditional growth. The mutants analyzed in this study are further described in Layer et. al., 2010. Direct Transactivator-Transcription Factor IID (TFIID) Contacts Drive Yeast Ribosomal Protein Gene Transcription. Journal of Biological Chemistry. A twenty chip study using total RNA recovered from four separate wild-type cultures of Saccharomyces cerevisiae and four separate cultures for each of four taf5 temperature conditional mutants (16 mutant cultures). Each chip measures the expression level of 5,777 genes from Saccharomyces S288C with eight 60-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.
2010-05-06 | E-GEOD-20444 | biostudies-arrayexpress
Project description:we provide evidence for a new class of histone posttranslational modification (PTM): serotonylation.
2018-12-19 | PXD008106 | Pride
Project description:TFIID and SAGA share a common set of TAFs, regulate chromatin, and deliver TBP to promoters. Here we examine their relationship within the context of the Saccharomyces cerevisiae genome-wide regulatory network. We find that while TFIID and SAGA make overlapping contributions to the expression of all genes, TFIID function predominates at ~90% and SAGA at ~10% of the measurable genome. Strikingly, SAGA-dominated genes are largely stress-induced and TAF-independent, and are down-regulated by the coordinate action of a variety of chromatin, TBP, and RNA polymerase II regulators. In contrast, the TFIID-dominated class is less regulated, but is highly dependent upon TAFs including those shared between TFIID and SAGA. These two distinct modes of transcription regulation might reflect the need to balance inducible stress responses with the steady output of housekeeping genes. Keywords = Taf1 Keywords = Spt3 Keywords = Gcn5
2004-02-26 | E-GEOD-885 | biostudies-arrayexpress
Project description:TFIID and SAGA share a common set of TAFs, regulate chromatin, and deliver TBP to promoters. Here we examine their relationship within the context of the Saccharomyces cerevisiae genome-wide regulatory network. We find that while TFIID and SAGA make overlapping contributions to the expression of all genes, TFIID function predominates at ~90% and SAGA at ~10% of the measurable genome. Strikingly, SAGA-dominated genes are largely stress-induced and TAF-independent, and are down-regulated by the coordinate action of a variety of chromatin, TBP, and RNA polymerase II regulators. In contrast, the TFIID-dominated class is less regulated, but is highly dependent upon TAFs including those shared between TFIID and SAGA. These two distinct modes of transcription regulation might reflect the need to balance inducible stress responses with the steady output of housekeeping genes. Keywords = Taf1 Keywords = Spt3 Keywords = Gcn5 Keywords: other
2004-02-27 | GSE885 | GEO
Project description:The multisubunit TFIID plays a direct role in transcription initiation by binding to core promoter elements and directing preinitiation complex assembly. Although TFIID may also function as a coactivator through direct interactions with promoter-bound activators, mechanistic aspects of this poorly defined function remain unclear. Here biochemical studies show a direct TFIID-E protein interaction that (i) is mediated through interaction of a novel E protein activation domain (AD3) with the TAF homology (TAFH) domain of TAF4, (ii) is critical for activation of a natural target gene by an E protein and (iii) mechanistically, acts by enhancing TFIID binding to the core promoter. Complementary assays establish a gene-specific role for the TAFH domain in TFIID recruitment and gene activation in vivo. These results firmly establish TAF4 as a bona fide E protein coactivator, as well as a mechanism involving facilitated TFIID binding through direct interaction with an E protein activation domain. Genome-wide profiling of mRNA levels in MEF lines with Taf4 loxp/- (ctrl), Taf4 -/- (ko), Taf4 -/- Tg:hTAF4 wt, and Taf4 -/- Tg: hTAF4 ? (TAFH-deleted).
2013-06-06 | E-GEOD-46807 | biostudies-arrayexpress
Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states. Three iPS lines, iPS#1, iPS#4, and iPS#5 were used in duplicate for microarray analysis against a pool of RNA from ES-cells.
2013-03-21 | E-GEOD-33645 | biostudies-arrayexpress
Project description:Pluripotent stem cells can be isolated from early embryos or induced by cell fusion, somatic nuclear transfer, or expression of a selected set of transcription factors. Embryonic stem (ES) cells are characterized by an open chromatin configuration and high transcription levels achieved via autoregulatory and feed-forward transcription factor loops. How the general transcription machinery is involved in pluripotency is unclear. Here, we show that TFIID knockdown affected the pluripotent circuitry in ES cells and inhibited reprogramming of fibroblasts. TFIID and pluripotency factors form a feed-forward loop to induce and maintain a stable transcription state. Strikingly, transient expression of TFIID subunits greatly enhanced reprogramming by Oct4, Sox2, Klf4 and c-Myc reaching efficiencies upto 50%. These results show that TFIID is a critical and selective component for transcription factor-mediated reprogramming. We anticipate that by creating plasticity in gene expression programs, basal transcription complexes such as TFIID assist reprogramming into different cellular states. Two Taf5 knockdown cell lines and two control knockdown lines were each grown in duplicate and analysed on microarray against a pool of RNA from the parental ES-cells
2013-03-21 | E-GEOD-33644 | biostudies-arrayexpress