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p16  Ink4a  /CDKN2A is a tumor suppressor that critically regulates the cell cycle. Indeed, p16  Ink4a   deficiency promotes tumor formation in various tissues. We now report that p16  Ink4a   deficiency in female mice, but not male mice, induces leanness especially in old age, as indicated by lower body weight and smaller white adipose tissue, although other major organs are unaffected. Unexpectedly, the integrity, number, and sizes of adipocytes in white adipose tissue were unaffected, as was macrophage infiltration. Hence, hypermobility appeared to be accountable for the phenotype, since food consumption was not altered. Histological analysis of the cerebellum and deep cerebellar nuclei, a vital sensorimotor control center, revealed increased proliferation of neuronal cells and improved cerebellum integrity. Expression of estrogen receptor β (ERβ) and PCNA also increased in deep cerebellar nuclei, implying crosstalk between p16  Ink4a   and ERβ. Furthermore, p16  Ink4a   deficiency expands LC3B +  cells and GFAP +  astrocytes in response to estrogen. Collectively, the data suggest that loss of  p16   INK4a   induces sexually dimorphic leanness in female mice, which appears to be due to protection against cerebellar senescence by promoting neuronal proliferation and homeostasis via ERβ.

Sexually dimorphic leanness and hypermobility in p16Ink4a/CDKN2A-deficient mice coincides with phenotypic changes in the cerebellum