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Background  Spindle assembly checkpoint components BubR1 and Sgo1 play a key role in the maintenance of chromosomal instability during cell division. These proteins function to block the anaphase entry until all condensed chromosomes have been attached by the microtubules emanating from both spindle poles. Haplo-insufficiency of either  BubR1  or  SGO1  results in enhanced chromosomal instability and tumor development in the intestine. Recent studies show that spindle checkpoint proteins also have a role in slowing down the ageing process. Therefore, we want to study whether haplo-insufficiency of both  BubR1  and  SGO1  accelerates cellular senescence in mice.    Methods  We took advantage of the availability of  BubR1  and  SGO1  knockout mice and generated primary murine embryonic fibroblasts (MEFs) with mutations in either  BubR1 ,  SGO1 , or both and analyzed cellular senescence of the MEFs of various genetic backgrounds.    Results  We observed that  BubR1   +/−   SGO   +/−   MEFs had an accelerated cellular senescence characterized by morphological changes and expressed senescence-associated β-galactosidase. In addition, compared with wild-type MEFs or MEFs with a single gene deficiency,  BubR1   +/−   SGO1   +/−   MEFs expressed enhanced levels of p21 but not p16.    Conclusions  Taken together, our observations suggest that combined deficiency of  BubR1  and  Sgo1  accelerates cellular senescence.

Haplo-insufficiency of both BubR1 and SGO1 accelerates cellular senescence