Mis12 is a gene encoding a protein that plays crucial roles in cell division and cellular senescence. It is part of the Mis12 complex, which is a key component of the kinetochore, a structure essential for the attachment of chromosomes to spindle microtubules during mitosis [3,5,6]. Additionally, Mis12 is involved in regulating pathways related to cell cycle transitions and senescence, making it of great biological importance. Genetic models, such as mouse models, are valuable for studying its functions.

In mouse oocytes, depletion of Mis12 severely compromises germinal vesicle breakdown (GVBD) by impairing cyclin B1 accumulation, indicating its requirement for meiotic G2/M transition. However, it is dispensable for meiotic progression through meiosis I and II [1]. In prematurely senescent human mesenchymal stem cells, knockout of METTL3, which normally stabilizes MIS12 mRNA via m6A modifications, accelerates cellular senescence, suggesting that Mis12 is important in counteracting premature aging [2]. Also, in atherosclerotic plaque development, FTO stabilizes the MIS12 protein in vascular smooth muscle cells, inhibiting their senescence and thus slowing the progression of atherosclerotic plaques [4].

In conclusion, Mis12 is essential for cell cycle regulation during meiosis and in preventing cellular senescence. The gene knockout studies in mouse models and human cells have revealed its significance in diseases related to premature aging and atherosclerosis. Understanding Mis12's functions provides insights into the mechanisms underlying these biological processes and diseases, which may potentially lead to new therapeutic strategies.