Bmal1-deficient mouse fibroblast cells do not provide premature cellular senescence in vitro.

Bmal1 is a core circadian clock gene. Bmal1 mice show disruption of the clock and premature aging phenotypes with a short lifespan. However, little is known whether disruption of Bmal1 leads to premature aging at cellular level. Here, we established primary mouse embryonic fibroblast (MEF) cells derived from Bmal1 mice and investigated its effects on cellular senescence. Unexpectedly, Bmal1 primary MEFs that showed disrupted circadian oscillation underwent neither premature replicative nor stress-induced cellular senescence. Our results therefore uncover that Bmal1 is not required for in vitro cellular senescence, suggesting that circadian clock does not control in vitro cellular senescence.