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

Small 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.