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Med23 deletion causes decreased H3K9me2 occupancy among the promoter of Ccl5 and Cxcl10.

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posted on 2019-12-05, 19:01 authored by Zhichao Wang, Dan Cao, Chonghui Li, Lihua Min, Gang Wang

(A, B) ChIP analysis of MED23 and Pol II occupancy in AML12 cells (n = 3 per group) (A) as well as H3K4me3 and H3K9me2 occupancy in med23f/f and med23Δli mouse livers after acute administration of CCl4 (med23f/f, n = 3; med23Δli, n = 4) (B). IgG was used as a negative control. The precipitated DNA was analyzed by qRT-PCR with primers targeting the promoter regions of Ccl5 and Cxcl10. The relative binding level of each factor was calculated by normalization to the input DNA. (C) qRT-PCR analysis of proinflammatory cytokines and chemokines in AML12 cells after G9a transient transfection (n = 3 per group). (D) A proposed model for the role of MED23 in hepatocyte after CCl4 challenge. MED23 modulates RORα transcriptional activity possibly via G9a-mediated H3K9me2 modification to the target promoters for transcriptional repression. Data are presented as means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001. For underlying data, see S1 Data file. AML12, alpha mouse liver 12; Ccl, C-C motif chemokine ligand; CCl4, carbon tetrachloride; ChIP, chromatin immunoprecipitation; Cxcl, C-X-C motif chemokine ligand; IgG, immunoglobulin G; KO, knockout; MED23, Mediator complex subunit 23; med23Δli, liver-specific knockout of Med23; med23f/f, med23-floxed; Pol II, RNA polymerase II; qRT-PCR, quantitative real-time PCR; RORα, RAR-related orphan receptor alpha; WT, wild-type.

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