Cellular senescence is one of the key strategies to suppress expansion of cells 
with mutations. Senescence is induced in response to genotoxic and oxidative 
stress. Here we show that the transcription factor Bach1 (BTB and CNC homology 
1, basic leucine zipper transcription factor 1), which inhibits oxidative 
stress-inducible genes, is a crucial negative regulator of oxidative 
stress-induced cellular senescence. Bach1-deficient murine embryonic fibroblasts 
showed a propensity to undergo more rapid and profound p53-dependent premature 
senescence than control wild-type cells in response to oxidative stress. Bach1 
formed a complex that contained p53, histone deacetylase 1 and nuclear 
co-repressor N-coR. Bach1 was recruited to a subset of p53 target genes and 
contributed to impeding p53 action by promoting histone deacetylation. Because 
Bach1 is regulated by oxidative stress and heme, our data show that Bach1 
connects oxygen metabolism and cellular senescence as a negative regulator of 
p53.