| First Author | Chi X | Year | 2021 |
| Journal | Cell Death Dis | Volume | 12 |
| Issue | 6 | Pages | 604 |
| PubMed ID | 34117213 | Mgi Jnum | J:307605 |
| Mgi Id | MGI:6721208 | Doi | 10.1038/s41419-021-03885-4 |
| Citation | Chi X, et al. (2021) Kindlin-2 in Sertoli cells is essential for testis development and male fertility in mice. Cell Death Dis 12(6):604 |
| abstractText | Kindlin-2 is known to play important roles in the development of mesoderm-derived tissues including myocardium, smooth muscle, cartilage and blood vessels. However, nothing is known for the role of Kindlin-2 in mesoderm-derived reproductive organs. Here, we report that loss of Kindlin-2 in Sertoli cells caused severe testis hypoplasia, abnormal germ cell development and complete infertility in male mice. Functionally, loss of Kindlin-2 inhibits proliferation, increases apoptosis, impairs phagocytosis in Sertoli cells and destroyed the integration of blood-testis barrier structure in testes. Mechanistically, Kindlin-2 interacts with LATS1 and YAP, the key components of Hippo pathway. Kindlin-2 impedes LATS1 interaction with YAP, and depletion of Kindlin-2 enhances LATS1 interaction with YAP, increases YAP phosphorylation and decreases its nuclear translocation. For clinical relevance, lower Kindlin-2 expression and decreased nucleus localization of YAP was found in SCOS patients. Collectively, we demonstrated that Kindlin-2 in Sertoli cells is essential for sperm development and male reproduction. |
