PLK1 is required for chromosome compaction and microtubule organization in mouse oocytes.

Errors during meiotic resumption in oocytes can result in chromosome missegregation and infertility. Several cell cycle kinases have been linked with roles in coordinating events during meiotic resumption, including polo-like kinases (PLKs). Mammals express four kinase-proficient PLKs (PLK1-4). Previous studies assessing the role of PLK1 have relied on RNA knockdown and kinase inhibition approaches, as null mutations are embryonically lethal. To further assess the roles of PLK1 during meiotic resumption, we developed a conditional knockout (cKO) mouse to specifically mutate in oocytes. Despite normal oocyte numbers and follicle maturation, cKO mice were infertile. From analysis of meiotic resumption, cKO oocytes underwent nuclear envelope breakdown with the same timing as control oocytes. However, cKO oocytes failed to form compact bivalent chromosomes, and localization of cohesin and condensin were defective. Furthermore, cKO oocytes either failed to organize α-tubulin or developed an abnormally small bipolar spindle. These abnormalities were attributed to aberrant release of the microtubule organizing center (MTOC) linker protein, C-NAP1, and the failure to recruit MTOC components and liquid-like spindle domain (LISD) factors. Ultimately, these defects result in meiosis I arrest before homologous chromosome segregation.