| First Author | Matsumoto M | Year | 2016 |
| Journal | Genes Cells | Volume | 21 |
| Issue | 6 | Pages | 553-67 |
| PubMed ID | 27030212 | Mgi Jnum | J:318621 |
| Mgi Id | MGI:6851459 | Doi | 10.1111/gtc.12365 |
| Citation | Matsumoto M, et al. (2016) Genomewide approaches for BACH1 target genes in mouse embryonic fibroblasts showed BACH1-Pparg pathway in adipogenesis. Genes Cells 21(6):553-67 |
| abstractText | The transcription repressor BTB and CNC homology 1 (BACH1) represses genes involved in heme metabolism and oxidative stress response. BACH1 also suppresses the p53-dependent cellar senescence in primary mouse embryonic fibroblasts (MEFs). To investigate the role of BACH1 in MEF other than its known functions, we carried out a genomewide mapping of binding site for BACH1 and its heterodimer partner MAFK in immortalized MEFs (iMEFs) using chromatin immunoprecipitation and next-generation sequencing technology (ChIP-sequence). The comparative analysis of the ChIP-sequence data and DNA microarray data from Bach1-deficient and wild-type (WT) iMEF showed 35 novel candidate target genes of BACH1. Among these genes, five genes (Pparg, Nfia, Ptplad2, Adcy1 and Ror1) were related with lipid metabolism. Bach1-deficient iMEFs showed increased expression of mRNA and protein of PPARgamma, which is the key factor of adipogenesis. These cells also showed a concomitant increase in ligand-dependent activation of PPARgamma target genes compared with wild-type iMEFs. Moreover, Bach1-deficient iMEFs efficiently differentiated to adipocyte compared with wild-type cells in the presence of PPARgamma ligands. Our results suggest that BACH1 regulates expression of adipocyte-related genes including Pparg and potentiates adipocyte differentiation capacity. |
