Journal
GENES TO CELLS
Volume 21, Issue 6, Pages 553-567Publisher
WILEY
DOI: 10.1111/gtc.12365
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Funding
- JSBi
- Ministry of Education Science, Sports and Culture, Japan [22700869, 23659168, 23590324, 15H02506]
- GCOE Program Special Research Grant (Tohoku University) from the Ministry of Education Science, Sports and Culture, Japan
- Grants-in-Aid for Scientific Research [15H02506, 23659168, 22700869, 26830064, 23590324] Funding Source: KAKEN
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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 PPAR gamma, which is the key factor of adipogenesis. These cells also showed a concomitant increase in ligand-dependent activation of PPAR gamma target genes compared with wild-type iMEFs. Moreover, Bach1-deficient iMEFs efficiently differentiated to adipocyte compared with wild-type cells in the presence of PPAR gamma ligands. Our results suggest that BACH1 regulates expression of adipocyte-related genes including Pparg and potentiates adipocyte differentiation capacity.
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