Glutamine 5 serotonylation on histone H3 is a permissive modification that functions combinatorialy with H3K4me3 to potentiate TFIID interactions
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA417049 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6253220.fastq.gz | Fastqsanger.gz | |||
| SRR6253221.fastq.gz | Fastqsanger.gz | |||
| SRR6253202.fastq.gz | Fastqsanger.gz | |||
| SRR6253222.fastq.gz | Fastqsanger.gz | |||
| SRR6253232_1.fastq.gz | Fastqsanger.gz |
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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:we provide evidence for a new class of histone posttranslational modification (PTM): serotonylation.
2018-12-19 | PXD008106 | Pride
Project description:we provide evidence for a new class of histone posttranslational modification (PTM): serotonylation.
2023-12-04 | MSV000093567 | MassIVE
Project description:Chemical modifications of histones can mediate diverse DNA-templated processes, including gene transcription1-3. Here we provide evidence for a class of histone post-translational modification, serotonylation of glutamine, which occurs at position 5 (Q5ser) on histone H3 in organisms that produce serotonin (also known as 5-hydroxytryptamine (5-HT)). We demonstrate that tissue transglutaminase 2 can serotonylate histone H3 tri-methylated lysine 4 (H3K4me3)-marked nucleosomes, resulting in the presence of combinatorial H3K4me3Q5ser in vivo. H3K4me3Q5ser displays a ubiquitous pattern of tissue expression in mammals, with enrichment observed in brain and gut, two organ systems responsible for the bulk of 5-HT production. Genome-wide analyses of human serotonergic neurons, developing mouse brain and cultured serotonergic cells indicate that H3K4me3Q5ser nucleosomes are enriched in euchromatin, are sensitive to cellular differentiation and correlate with permissive gene expression, phenomena that are linked to the potentiation of TFIID4-6 interactions with H3K4me3. Cells that ectopically express a H3 mutant that cannot be serotonylated display significantly altered expression of H3K4me3Q5ser-target loci, which leads to deficits in differentiation. Taken together, these data identify a direct role for 5-HT, independent from its contributions to neurotransmission and cellular signalling, in the mediation of permissive gene expression.
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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:Brain development requires appropriate regulation of serotonin (5-HT) signaling from distinct tissue sources across embryogenesis. At the maternal-fetal interface, the placenta is thought to be an important contributor of offspring brain 5-HT and is critical to overall fetal health. Yet, how placental 5-HT is acquired, and the mechanisms through which 5-HT influences placental functions, are not well understood. Recently, our group identified a novel epigenetic role for 5-HT, in which 5-HT can be added to histone proteins to regulate transcription, a process called H3 serotonylation. Here, we show that H3 serotonylation undergoes dynamic regulation during placental development, corresponding to gene expression changes that are known to influence key metabolic processes. Using transgenic mice, we demonstrate that placental H3 serotonylation largely depends on 5-HT uptake by the serotonin transporter (Sert/Slc6a4). Sert deletion robustly reduces enrichment of H3 serotonylation across the placental genome, and disrupts neurodevelopmental gene networks in offspring brain tissues. Thus, these findings suggest a novel role for H3 serotonylation in coordinating placental transcription at the intersection of maternal physiology and offspring brain development.
2024-01-23 | GSE246539 | GEO
Project description:Brain development requires appropriate regulation of serotonin (5-HT) signaling from distinct tissue sources across embryogenesis. At the maternal-fetal interface, the placenta is thought to be an important contributor of offspring brain 5-HT and is critical to overall fetal health. Yet, how placental 5-HT is acquired, and the mechanisms through which 5-HT influences placental functions, are not well understood. Recently, our group identified a novel epigenetic role for 5-HT, in which 5-HT can be added to histone proteins to regulate transcription, a process called H3 serotonylation. Here, we show that H3 serotonylation undergoes dynamic regulation during placental development, corresponding to gene expression changes that are known to influence key metabolic processes. Using transgenic mice, we demonstrate that placental H3 serotonylation largely depends on 5-HT uptake by the serotonin transporter (Sert/Slc6a4). Sert deletion robustly reduces enrichment of H3 serotonylation across the placental genome, and disrupts neurodevelopmental gene networks in offspring brain tissues. Thus, these findings suggest a novel role for H3 serotonylation in coordinating placental transcription at the intersection of maternal physiology and offspring brain development.
2024-01-23 | GSE246538 | GEO
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
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Project description:Bidirectional communication between tumors and neurons has emerged as a key facet of the tumor microenvironment that drives malignancy. Another hallmark feature of cancer is epigenomic dysregulation, where alterations in gene expression influences cell states and interactions with the tumor microenvironment. Using the pediatric brain tumor ependymoma (EPN) as a model, we found that inhibition of histone serotonylation blocks EPN tumorigenesis and regulates expression of a core set of developmental transcription factors (TFs). High-throughput, in vivo screening of these TFs revealed that ETV5 promotes EPN tumorigenesis and functions by enhancing repressive chromatin states. Neuropeptide Y (NPY) is amongst the genes repressed by ETV5 and its overexpression suppresses EPN tumor progression and tumor-associated network hyperactivity via synaptic remodeling. Collectively, these studies identify histone serotonylation as a key driver of EPN tumorigenesis, while further revealing how neuronal signaling, neuro-epigenomics, and developmental programs are intertwined to drive malignancy in brain cancer.
2024-09-09 | PXD048170 | Pride