Vp1524, a Vibrio parahaemolyticus NAD+ dependent deacetylase, regulates host response during infection by induction of histone deacetylation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE158369 | GEO | 2021/09/22
REPOSITORIES: GEO
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Project description:Vibrio parahaemolyticus is a Gram-negative marine bacterium. A limited population of the organisms causes acute gastroenteritis in humans. Almost all of the clinical V. parahaemolyticus isolates exhibit a beta-type hemolysis on Wagatsuma agar, known as the Kanagawa phenomenon (KP). KP is induced by the thermostable direct hemolysin (TDH) produced by the organism, and has been considered a crucial marker to distinguish pathogenic strains from non-pathogenic ones. Since 1996, so-called “pandemic clones”, the majority of which belong to serotype O3:K6, have caused worldwide outbreaks of gastroenteritis. In this study, we used a DNA microarray constructed based on the genome sequence of a pandemic V. parahaemolyticus strain RIMD2210633 to examin the genomic composition of 22 strains of V. parahaemolyticus, including both pathogenic (pandemic as well as non-pandemic) and non-pathogenic strains. Over 85% of the RIMD2210633 genes were conserved in all the strains tested. Many of variably present genes formed gene clusters on the genome of RIMD2210633 and were probably acquired through lateral gene transfer. At least 70 genes over 10 loci were specifically present in the pandemic strains when compared with any of the non-pandemic strains, suggesting that the difference between pandemic and non-pandemic strains is not due to a simple genetic event. Only the genes in the 80-kb pathogenicity island (Vp-PAI) on chromosome II, including two tdh genes and a set of genes for the Type III secretion system, were detected only in the KP-positive pathogenic strains. These results strongly suggest that acquisition of this Vp-PAI was crucial for the emergence of V. parahaemolyticus strains that are pathogenic for humans. Keywords: comparative genomic hybridization, CGH
2008-03-31 | GSE10020 | GEO
Project description:Vibrio parahaemolyticus is a Gram-negative marine bacterium. A limited population of the organisms causes acute gastroenteritis in humans. Almost all of the clinical V. parahaemolyticus isolates exhibit a beta-type hemolysis on Wagatsuma agar, known as the Kanagawa phenomenon (KP). KP is induced by the thermostable direct hemolysin (TDH) produced by the organism, and has been considered a crucial marker to distinguish pathogenic strains from non-pathogenic ones. Since 1996, so-called âpandemic clonesâ, the majority of which belong to serotype O3:K6, have caused worldwide outbreaks of gastroenteritis. In this study, we used a DNA microarray constructed based on the genome sequence of a pandemic V. parahaemolyticus strain RIMD2210633 to examin the genomic composition of 22 strains of V. parahaemolyticus, including both pathogenic (pandemic as well as non-pandemic) and non-pathogenic strains. Over 85% of the RIMD2210633 genes were conserved in all the strains tested. Many of variably present genes formed gene clusters on the genome of RIMD2210633 and were probably acquired through lateral gene transfer. At least 70 genes over 10 loci were specifically present in the pandemic strains when compared with any of the non-pandemic strains, suggesting that the difference between pandemic and non-pandemic strains is not due to a simple genetic event. Only the genes in the 80-kb pathogenicity island (Vp-PAI) on chromosome II, including two tdh genes and a set of genes for the Type III secretion system, were detected only in the KP-positive pathogenic strains. These results strongly suggest that acquisition of this Vp-PAI was crucial for the emergence of V. parahaemolyticus strains that are pathogenic for humans. Keywords: comparative genomic hybridization, CGH Total 66 test samples were analyzed. Genomic DNA from each test strain and a reference strain (RIMD2210633) were labeled with Cy3 and Cy5, respectively, and were cohybridized on a single array. Labeling and hybridization were performed three times independently.
2010-05-25 | E-GEOD-10020 | biostudies-arrayexpress
Project description:Using bioinformatics analysis, we found that VP0057 may be a potential Ser/Thr protein kinase with phosphorylation activity. Thus, we constructed the vp0057-deletion mutant (∆vp0057) from the wild-type V. parahaemolyticus serotype O3:K6 and employed a mass spectrometry-based proteomic strategy to characterize proteome-wide changes in response to vp0057 deletion. One hundred ninety-seven differentially expressed proteins were identified in the ∆vp0057 strain compared with the wild-type strain, among which 135 proteins were upregulated and 62 proteins were downregulated.
2020-09-30 | PXD021775 |
Project description:H3K56 deacetylation and H2A.Z deposition are required for aberrant heterochromatin spreading
| PRJNA794749 | ENA
Project description:Vp1524, a Vibrio parahaemolyticus NAD+ dependent deacetylase, regulates host response during infection by induction of histone deacetylation
| PRJNA665029 | ENA
Project description:Pericentric heterochromatin silencing at mammalian centromeres is essential for mitotic fidelity and genomic stability. Defective pericentric silencing is observed in senescent cells, aging tissues, and mammalian tumors, but the underlying mechanisms and functional consequences of these defects are unclear. Here, we uncover a pivotal role of the human SIRT6 enzyme in pericentric transcriptional silencing, and this function protects against mitotic defects, genomic instability, and cellular senescence. At pericentric heterochromatin, SIRT6 promotes deacetylation of a new substrate, histone H3 lysine K18 (H3K18), and inactivation of SIRT6 in cells leads to H3K18 hyperacetylation and aberrant accumulation of pericentric transcripts. Strikingly, RNAi-depletion of these transcripts rescues the mitotic and senescence phenotypes of SIRT6-deficient cells. Together, our findings reveal a new function for SIRT6 and H3K18Ac regulation at heterochromatin, and demonstrate the pathogenic role of de-regulated pericentric transcription in aging- and cancer- related cellular dysfunction. H3K18ac, H3K9ac, H3K9me3, H3K56ac and Input ChIP-seq for U2OS cell
2016-04-04 | E-GEOD-69809 | biostudies-arrayexpress
Project description:The data provide information of Gcn5 enrichment, H3K18 and H4K16 acetylation level and Histone H3 density for 5 different physioloigcal conditions during stress adpatation and stress recovery (normal growth, during stress adaptation, after stress adaptation, under stress recovery, after stress recovery) in yeast. The purpose of the study is to understand how histone acetyltransferase HATs (Gcn5) apply it is function in gene regulation by changing global or local histone acetylation level under different physiological conditions. Gcn5 enrichment, H3K18 and H4K16 acetylation level and Histone H3 density are mearured and compared to input signal for 5 different physioloigcal conditions (normal growth, during stress adaptation, after stress adaptation, under stress recovery, after stress recovery). Replicates are used.
2013-07-22 | E-GEOD-36600 | biostudies-arrayexpress
Project description:Crucial mechanisms are required to restrict self-propagating heterochromatin spreading within defined boundaries and prevent euchromatic gene silencing. In the filamentous fungus Neurospora crassa, the JmjC domain protein DNA METHYLATION MODULATOR-1 (DMM-1) prevents aberrant spreading of heterochromatin, but the molecular details remain unknown. Here, we revealed that DMM-1 is highly enriched in a well-defined 5-kb heterochromatin domain and constrained its aberrant spreading. Interestingly, aberrant spreading of the 5-kb heterochromatin domain observed in the dmm-1KO strain is accompanied by the sharp deposition of histone variant H2A.Z, and deletion of H2A.Z abolishes aberrant spreading of the 5-kb heterochromatin domain into adjacent euchromatin. Furthermore, lysine 56 of histone H3 is deacetylated at the expanded heterochromatin regions, and mimicking H3K56 acetylation with an H3K56Q mutation effectively blocks H2A.Z-mediated aberrant spreading of the 5-kb heterochromatin domain. More importantly, genome-wide analyses demonstrated the general roles of H3K56 deacetylation and H2A.Z deposition in aberrant spreading of heterochromatin. Altogether, our results illustrate a previously unappreciated regulatory process that mediates aberrant heterochromatin spreading.
2022-01-25 | GSE193075 | GEO
Project description:Vibrio parahaemolyticus is a Gram-negative marine bacterium. Strain RIMD 2210633, the wild type strain of the organism, causes acute gastroenteritis in humans. Human intestinal factor bile often affects the global gene regulation in some species of enteropathogenic bacteria. To determine the genes in V. parahaemolyticus that respond to bile, we investigated the differences in the transcriptomes of the wild type strain and the vtrA-null strain grown in Luria-Bertani medium cultivated with or without 0.04% crude bile. The vtrA gene encodes the previously identified T3SS2 regulator. Our goal is to demonstrate bile regulon controlled by VtrA in V. parahaemolyticus.
2010-10-10 | GSE21666 | GEO