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The kinetochore is the crucial apparatus regulating chromosome segregation in mitosis and meiosis. Particularly in meiosis I, unlike in mitosis, sister kinetochores are captured by microtubules emanating from the same spindle pole (mono-orientation) and centromeric cohesion mediated by cohesin is protected in the following anaphase. Although meiotic kinetochore factors have been identified only in budding and fission yeasts, these molecules and their functions are thought to have diverged earlier. Therefore, a conserved mechanism for meiotic kinetochore regulation remains elusive. Here we have identified in mouse a meiosis-specific kinetochore factor that we termed MEIKIN, which functions in meiosis I but not in meiosis II or mitosis. MEIKIN plays a crucial role in both mono-orientation and centromeric cohesion protection, partly by stabilizing the localization of the cohesin protector shugoshin. These functions are mediated mainly by the activity of Polo-like kinase PLK1, which is enriched to kinetochores in a MEIKIN-dependent manner. Our integrative analysis indicates that the long-awaited key regulator of meiotic kinetochore function is Meikin, which is conserved from yeasts to humans., In mitosis, the establishment of sister chromatid cohesion is dependent on cohesin in S phase and maintained until metaphase when the sister chromatids are captured by spindle microtubules from opposite [...]

Mutant mice embryos in which the focal adhesion kinase (FAK), a protein tyrosine kinase, is absent show poor development of mesoderm because of retarded motility of cells. The anteroposterior axis, notochord and somite are not formed while the head mesenchyme becomes involuted. However, formation of the head, lateral, and extra-embryonic mesenchyme remains normal. The absence of FAK also increases the formation of focal adhesions which causes rise in tyrosine phosphorylation in many proteins.

The c-mos proto-oncogene product (Mos) is vital for the inhibition of the second meiotic metaphase in mice and for the oocyte maturation mechanism in Xenopus. Mos inhibits parthenogenetic stimulation in Xenopus, explains oogenetic and teratogenic processes in mammals and infertility in women. Mos is not essential for the induction of oocyte maturation, spermatogenesis or somatic cell cycle in mice.