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Genome-wide maps of chromatin state in renal tubular epithelial cells

ABSTRACT: To further understand the underlying mechanisms and identify genes directly regulated by SETD2 and H3K36me3 on a genome-wide scale, we performed chromatin immunoprecipitation using a H3K36me3 specific antibody followed by next-generation sequencing (ChIP-seq) assays using the renal tubules isolated from SETD2FL/FL KSPCRE/+ and its control SETD2fl/fl mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE125528 | GEO | 2020/12/31

REPOSITORIES: GEO

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Genome-wide maps of H3K36me3 in metastatic renal cell carcinoma and isogenic renal cell carcinoma cell lines

Project description:We report the application of H3K36me3 ChIP sequencing in SETD2 genotyped samples Examination of H3K36me3 in SETD2 wild-type, mutant renal cell carcinoma and SETD2 isogenic cell lines

2015-06-19 | E-GEOD-66884 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of MYC+ and MYC+; SETD2-/- Renal Tubular Cells Transcriptomes

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Chromatin landscape analysis of murine renal tubular epithelial cells upon SETD2 knockout [ATACseq_RTE]

Project description:SETD2, a H3K36 trimethyltransferase, is frequently mutated in human cancers with the highest prevalence (13%) in clear cell renal cell carcinoma (ccRCC). Genomic profiling of primary ccRCC tumors reveals a positive correlation between SETD2 mutations and metastasis. However, whether and how SETD2-loss promotes metastasis remains unclear. Here, we detected SETD2 mutations in 24 of 51 (47%) metastatic ccRCC tumors. Using SETD2-mutant metastatic ccRCC patient-derived cell line and xenograft models, we showed that H3K36me3 restoration greatly reduced distant metastases of ccRCC in mice. An integrated ATAC-seq, ChIP-seq, and transcriptome analysis concluded a tumor suppressor model in which loss of SETD2-mediated H3K36me3 activates enhancers to drive oncogenic transcription through dysregulating histone chaperone recruitment, enhancing histone exchange, and expanding chromatin accessibility. Furthermore, we uncovered mechanism-based therapeutic strategies for SETD2-deficient cancer through inhibition of histone chaperones. Overall, SETD2-loss creates a permissive epigenetic landscape for cooperating oncogenic drivers to amplify transcriptional output, providing unique therapeutic opportunities.

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Dynamic Reprogramming of DNA Methylation in SETD2-Deregulated Renal Cell Carcinoma

Project description:Clear cell renal cell carcinomas (ccRCCs) harbor frequent mutations in epigenetic modifiers including SETD2, the writer for H3K36me3. We profiles DNA methylation across cell line models of SETD2 inactivation and SETD2 mutated primary tumors as this epigenetic mark is linked to H3K36me3 and is a targetable mark for cancer therapy. SETD2 depleted cell line models (long-term and acute) exhibited a hypermethylation phenotype coinciding with ectopic gains in H3K36me3 centered across intergenic regions adjacent to low expression genes that became upregulated with dysregulation of the epigenome. Poised enhancers of developmental genes demonstrated enrichment for the hypermethylation phenotype. Deregulation of the epigenome observed in the cell line models was recapitulated in SETD2 mutated primary ccRCC, papillary renal cell carcinomas, and lung adenocarcinomas.

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Immunohistochemical Investigation for Renal Tubules in Adaptive and Maladaptive Repair Process after Renal Tubular Injury in the Kidney of Rats

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Project description:The endocytic receptor megalin constitutes the main pathway for clearance of plasma proteins from the glomerular filtrate in the proximal tubules. However, little is know about the mechanisms that control receptor activity. A widely discussed hypothesis states that the intracellular domain (ICD) of megalin, released upon ligand binding, acts as a transcription regulator to suppress receptor expression - a mechanism proposed to safeguard the proximal tubules from protein overload. Here, we have put this hypothesis to the test by generating a mouse model co-expressing the soluble ICD and the full-length receptor. Despite pronounced expression in the proximal tubules, the ICD failed to exert any effects on renal proximal tubular function such as megalin expression, protein retrieval, or renal gene transcription. Thus, our data argue that the ICD does not play a role in regulation of megalin activity in vivo in the proximal tubules. We used microarrays to compare gene expression profile in adult kidney from a new mouse model expressing the intracellular domain of megalin with wildtype. 10 week old mice were collected for RNA extraction and hybridization on Affymetrix microarrays. Three individuals for each genotype were analyzed comparing heterozygous animals for the intracellular domain of megalin with littermates controls.

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