Chemical proteomic profiling of protein dopaminylation in colorectal cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Qingfei Zheng
PROVIDER: PXD052426 | iProX | Tue May 21 00:00:00 BST 2024
REPOSITORIES: iProX
Similar Datasets
Project description:Vulnerability to relapse during periods of attempted abstinence from cocaine use is hypothesized to result from rewiring of brain reward circuitries, particularly ventral tegmental area (VTA) dopamine neurons. How cocaine exposures act on midbrain dopamine neurons to precipitate addiction-relevant changes in gene expression is unclear. We found that histone H3 glutamine 5 dopaminylation (H3Q5dop) plays a critical role in cocaine-induced transcriptional plasticity in midbrain. Rats undergoing withdrawal from cocaine showed an accumulation of H3Q5dop in VTA. By reducing H3Q5dop in VTA during withdrawal, we reversed cocaine-mediated gene expression changes, attenuated cue-induced dopamine release in nucleus accumbens and reduced cocaine-seeking behavior. These findings establish a neurotransmission-independent role for nuclear dopamine in relapse-related transcriptional plasticity in VTA.
2020-05-19 | GSE124055 | GEO
Project description:This model is described in the article:
Kinetics of histone gene expression during early development of Xenopus laevis.
Koster JG, Destrée OH and Westerhoff HV. J Theor Biol.
1988 Nov 21;135(2):139-67. PMID: 3267765
Abstract:
Using literature data for transcriptional and translational rate constants, gene copy numbers, DNA concentrations, and stability constants, we have calculated the expected concentrations of histones and histone mRNA during embryogenesis of Xenopus laevis. The results led us to conclude that: (i) for X. laevis the gene copy number of the histone genes is too low to ensure the synthesis of sufficient histones during very early development, inheritance from the oocyte of either histone protein or histone mRNA (but not necessarily both) is necessary; (ii) from the known storage of histones in the oocyte and the rates of histone synthesis determined by Adamson and Woodland (1977), there would be sufficient histones to structure the newly synthesized DNA up to gastrulation but not thereafter (these empirical rates of histone synthesis may be underestimates); (iii) on the other hand, the amount of H3 mRNA recently observed during early embryogenesis (Koster, 1987, Koster et al., 1988) could direct a higher and sufficient synthesis of H3 protein, also after gastrulation. We present a quantitative model that accounts both for the observed H3 mRNA concentration as a function of time during embryogenesis and for the synthesis of sufficient histones to structure the DNA throughout early embryogenesis. The model suggests that X. laevis exhibits a major (i.e. some 14-fold) reduction in transcription of histone genes approximately 11 hours after fertilization. This reduction could be due to a decrease in the number of transcribed histone genes, a decreased rate constant of transcription with continued transcription of all the histone genes, and/or a reduction in the time during the cell cycle in which histone mRNA synthesis takes place. Alternatively, the histone mRNA stability might decrease approximately 16-fold 11 hours after fertilization.
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL5954483266 | BioModels
Project description:Dopaminylation, the covalent attachment of dopamine to the side chain of glutamine (Gln, Q) in proteins, has been identified as a class of posttranslational modification. Due to the limited number of substrates, the functions and underlying molecular mechanisms of dopaminylation are not fully characterized. Utilizing an alkyne-functionalized dopamine probe, we have developed a method to selectively enrich dopaminylated proteins in the whole-cell context. We identified 4133 proteins potentially modified with dopamine and validated the modification of histone H4 glutamine 27 by dopamine (H4Q27dop). H4Q27dop can inhibit cell proliferation through downregulating cyclin D1 gene CCND1 transcription, a classical well-known proliferation promoter. Our study provides a valuable resource of putative substrate proteins modified with dopamine and reveals a novel mechanism of dopamine regulating cell growth in a neuroblastoma cancer model.
2024-07-10 | GSE271454 | GEO
Project description:Replication-independent deposition of histone variant H3.3 into chromatin is essential for many biological processes, including development, oogenesis and nuclear reprogramming. Unlike replication-dependent H3.1/2 isoforms, H3.3 is expressed throughout the cell cycle and becomes enriched in postmitotic cells with age. However, lifelong dynamics of H3 variant replacement and the impact of this process on chromatin organization remain largely undefined. To address this, we investigated genome-wide changes in histone H3 variants composition and H3 modification abundances throughout the lifespan in mice using quantitative mass spectrometry (MS) – based middle-down proteomics strategy. Using middle-down MS we demonstrate that H3.3 accumulates in the chromatin of various somatic mouse tissues throughout life, resulting in near complete replacement of H3.1/2 isoforms by the late adulthood. Accumulation of H3.3 is associated with profound changes in the global level of H3 methylation. H3.3-containing chromatin exhibits distinct stable levels of H3R17me2 and H3K36me2, different from those on H3.1/H3.2-containing chromatin, indicating a direct link between H3 variant exchange and histone methylation dynamics with age. In summary, our study provides the first time comprehensive characterization of dynamic changes in the H3 modification landscape during mouse lifespan and links these changes to the age-dependent accumulation of histone variant H3.3.
2017-07-28 | PXD005300 | Pride
Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5M-bM-^@M-^Y and 3M-bM-^@M-^Y ends of genes, accelerating H3 replacement at the 5M-bM-^@M-^Y ends of genes while protecting the 3M-bM-^@M-^Y ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1M-bM-^@M-^Ys effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3M-bM-^@M-^Y ends of genes. ChIP on chip experiments, compares IP of newly expressed, Flag-tagged histone H3 to total histone H3.
2012-06-07 | E-GEOD-38491 | biostudies-arrayexpress
Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5M-bM-^@M-^Y and 3M-bM-^@M-^Y ends of genes, accelerating H3 replacement at the 5M-bM-^@M-^Y ends of genes while protecting the 3M-bM-^@M-^Y ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1M-bM-^@M-^Ys effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3M-bM-^@M-^Y ends of genes. ChIP on chip experiments, comparing IP to input.
2012-06-07 | E-GEOD-38492 | biostudies-arrayexpress
Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5M-bM-^@M-^Y and 3M-bM-^@M-^Y ends of genes, accelerating H3 replacement at the 5M-bM-^@M-^Y ends of genes while protecting the 3M-bM-^@M-^Y ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1M-bM-^@M-^Ys effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3M-bM-^@M-^Y ends of genes. ChIP on chip experiments, compare IP to input, with dye-flips, comparing distribution of RNA polymerase II in chd1 deletion to wild type cells.
2012-06-07 | E-GEOD-38493 | biostudies-arrayexpress
Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5M-bM-^@M-^Y and 3M-bM-^@M-^Y ends of genes, accelerating H3 replacement at the 5M-bM-^@M-^Y ends of genes while protecting the 3M-bM-^@M-^Y ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1M-bM-^@M-^Ys effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3M-bM-^@M-^Y ends of genes. This series compares gene expession in wild type to that in chd1 mutant cells. Two biological replicates with dye swaps.
2012-06-07 | E-GEOD-38496 | biostudies-arrayexpress
Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5’ and 3’ ends of genes, accelerating H3 replacement at the 5’ ends of genes while protecting the 3’ ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1’s effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3’ ends of genes.
2012-06-08 | GSE38491 | GEO
Project description:Chd proteins are ATP-dependent chromatin remodeling enzymes implicated in biological functions from transcriptional elongation to control of pluripotency. Here, we examine roles of Chd1 in replication- independent dynamics of histone H3 in yeast. Using genome-wide ChIP on chip analysis, we find that Chd1 influences histone turnover at the 5’ and 3’ ends of genes, accelerating H3 replacement at the 5’ ends of genes while protecting the 3’ ends of genes from excessive H3 turnover. Although consistent with a direct role for Chd1 in exchange, these results may indicate that Chd1 stabilizes nucleosomes perturbed by transcription. Curiously, we observe a strong effect of gene length on Chd1’s effects on H3 turnover. Finally, we show that Chd1 also affects histone H3K4 and H3K36 methylation patterns over genes, likely as a consequence of its effects on histone replacement. In control experiments, we measure effects of deletion of CHD1 on RNA polymerase II distribution across the genome and on gene expression. We also examine the effect of deleting the TOP1 gene, alone and in combination with deletion of CHD1, on histone replacement. Taken together, our results emphasize a role for Chd1 in histone replacement in both budding yeast and Drosophila, and surprisingly show that the major effects of Chd1 on turnover occur at the 3’ ends of genes.
2012-06-08 | GSE38493 | GEO