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SUMO and RNAPolII chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

ABSTRACT: Purpose: To determine SUMO1 and SUMO2 chromatin profile in a static and dynamic manner in BMDC before and after LPS stimulation, and to determine RNAPolII chromatin occupancy in sumoylation-deficient BMDC compared to wild-type cells. Methods: SUMO1, SUMO2 and RNAPolII chromatin profiles were determined by sequencing BMDC chromatin immunoprecipitated with antibodies specific for SUMO1, SUMO2 and RNAPolII before and after LPS stimulation. Results: We show dynamic occupancy of three distal sites upstream of Ifnb1 gene by SUMO1 and SUMO2, as well as increased RNAPolII recruitment on selected genes. Conclusions: SUMO acts as a regulator of inflammatory and anti-viral gene programs.

ORGANISM(S): Mus musculus

PROVIDER: GSE66315 | GEO | 2015/12/14

SECONDARY ACCESSION(S): PRJNA276507

REPOSITORIES: GEO

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SUMO and RNAPolII chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

Project description:Purpose: To determine SUMO1 and SUMO2 chromatin profile in a static and dynamic manner in BMDC before and after LPS stimulation, and to determine RNAPolII chromatin occupancy in sumoylation-deficient BMDC compared to wild-type cells. Methods: SUMO1, SUMO2 and RNAPolII chromatin profiles were determined by sequencing BMDC chromatin immunoprecipitated with antibodies specific for SUMO1, SUMO2 and RNAPolII before and after LPS stimulation. Results: We show dynamic occupancy of three distal sites upstream of Ifnb1 gene by SUMO1 and SUMO2, as well as increased RNAPolII recruitment on selected genes. Conclusions: SUMO acts as a regulator of inflammatory and anti-viral gene programs. A study of SUMO and RNAPolII chromatin profile in Bone Marrow derived Dendritic Cells.

2015-12-14 | E-GEOD-66315 | biostudies-arrayexpress

Transcriptomics analysis of SUMO1 and SUMO2 U2OS knockout (KO) cell lines

Project description:CRISPR-Cas9 was used to individually knock out SUMO1 and SUMO2 expression in U2OS cells. The transcriptomes of SUMO1 and SUMO2 knockout (KO) cell lines were analyzed using RNA-sequencing.

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Genome wide occupancy of SUMO machinery in proliferative and Ras-induced senescent human primary fibroblasts

Project description:Transcription factors represent one of the largest groups of proteins regulated by SUMO, and their modification has generally been correlated with transcriptional repression. However, as most of the studies focus on specific sumoylated transcriptional regulators, the distribution and global role of SUMO on chromatin in relation to transcription regulation remain largely unknown. To investigate this role, we determined the occupancy of SUMO machinery proteins on chromatin by ChIP coupled to sequencing in human primary cells. Examination of 3 histone modifications, Polymerase II, SUMO1, SUMO2, Ubc9 and PIASy in proliferative and Ras-induced senescent fibroblasts.

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Gene expression analysis in the hippocampus of SUMO1 and SUMO2 transgenic mice

Project description:Transgenic mouse lines that express His6-SUMO1 and His6-SUMO2 under the control of the neuron specific Thy1.2 promoter were generated and characterized. The effect of increased levels of SUMO1 and -2 at the level of gene expression in the hippocampus was studied. Pooled (left and right) hippocampi were dissected from adult littermate wild-type control (WT1) and SUMO1 and WT2 and SUMO2 transgenic animals (n=3) and subjected to RNA expression analysis.

2013-12-31 | E-GEOD-47951 | biostudies-arrayexpress

H3K4me3 chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

Project description:Purpose: To determine H3K4me3 chromatin profile in UBC9WT and UBC9KO BMDC before and after LPS stimulation. Methods: H3K4me3 chromatin profile was determined by sequencing UBC9 WT and UBC9 KO BMDC chromatin immunoprecipitated with antibody specific for H3K4me3. Results: We show differential chromatin profile for H3K4me3 on the ifnb1 locus between UBC9 KO cells and UBC9 WT. Conclusions: Loss of SUMOylation causes a deregulation of ifnb1 transcription activation mark. A study of H3K4me3 chromatin profile in UBC9 WT and UBC9 KO Bone Marrow derived Dendritic Cells.

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H3K4me3 chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

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2011-10-17 | E-GEOD-31896 | biostudies-arrayexpress

RNAPolII ChIP to find differences between third instar salivary glands of WT and SuUR

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Ubc9 overexpression and SUMO1 deficiency blunt inflammation after intestinal ischemia/reperfusion.

Project description:The intestinal epithelium constitutes a crucial defense to the potentially life-threatening effects of gut microbiota. However, due to a complex underlying vasculature, hypoperfusion and resultant tissue ischemia pose a particular risk to function and integrity of the epithelium. The small ubiquitin-like modifier (SUMO) conjugation pathway critically regulates adaptive responses to metabolic stress and is of particular significance in the gut, as inducible knockout of the SUMO-conjugating enzyme Ubc9 results in rapid intestinal epithelial disintegration. Here we analyzed the pattern of individual SUMO isoforms in intestinal epithelium and investigated their roles in intestinal ischemia/reperfusion (I/R) damage. Immunostaining revealed that epithelial SUMO2/3 expression was almost exclusively limited to crypt epithelial nuclei in unchallenged mice. However, intestinal I/R or overexpression of Ubc9 caused a remarkable enhancement of epithelial SUMO2/3 staining along the crypt-villus axis. Unexpectedly, a similar pattern was found in SUMO1 knockout mice. Ubc9 transgenic mice, but also SUMO1 knockout mice were protected from I/R injury as evidenced by better preserved barrier function and blunted inflammatory responses. PCR array analysis of microdissected villus-tip epithelia revealed a specific epithelial contribution to reduced inflammatory responses in Ubc9 transgenic mice, as key chemotactic signaling molecules such as IL17A were significantly downregulated. Together, our data indicate a critical role particularly of the SUMO2/3 isoforms in modulating responses to I/R and provide the first evidence that SUMO1 deletion activates a compensatory process that protects from ischemic damage.

2018-11-07 | GSE96733 | GEO

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