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Cyclin Y-like 1  ( Ccnyl1 ) is a newly-identified member of the cyclin family and is highly similar in protein sequences to  Cyclin Y  ( Ccny ). However, the function of  Ccnyl1  is poorly characterized in any organism. Here we found that  Ccnyl1  was most abundantly expressed in the testis of mice and was about seven times higher than the level of  Ccny . Male  Ccnyl1 -/- mice were infertile, whereas both male and female  Ccny -/- mice displayed normal fertility. These results suggest that  Ccnyl1 , but not  Ccny , is indispensable for male fertility. Spermatozoa obtained from  Ccnyl1 -/- mice displayed significantly impaired motility, and represented a thinned annulus region and/or a bent head. We found that the protein, but not the mRNA, level of cyclin-dependent kinase 16 (CDK16) was decreased in the testis of  Ccnyl1 -/- mice. Further study demonstrated that CCNYL1 interacted with CDK16 and this interaction mutually increased the stability of these two proteins. Moreover, the interaction increased the kinase activity of CDK16. In addition, we observed an alteration of phosphorylation levels of CDK16 in the presence of CCNYL1. We identified the phosphorylation sites of CDK16 by mass spectrometry and revealed that several phosphorylation modifications on the N-terminal region of CDK16 were indispensable for the CCNYL1 binding and the modulation of CDK16 kinase activity. Our results therefore reveal a previously unrecognized role of CCNYL1 in regulating spermatogenesis through the interaction and modulation of CDK16.

CCNYL1, but Not CCNY, Cooperates with CDK16 to Regulate Spermatogenesis in Mouse