A persistent intracellular bridge and cell cycle misregulation enable polar body cell divisions and tumor formation in <i>Mos</i>-deficient eggs.

ABSTRACT: Mammalian female meiosis is uniquely regulated to produce a developmentally competent egg capable of supporting embryogenesis. During meiosis I, homologous chromosomes segregate, with half extruded into the first polar body. The egg then arrests at metaphase II and only resumes meiosis and extrudes the second polar body following fertilization. The MOS/MAPK signaling pathway is important for maintaining the metaphase II arrest; in mos ^-/- mutants, a subset of eggs undergo spontaneous parthenogenetic activation and exhibit additional abnormal cell divisions. To further understand the cell cycle mis-regulation in activated mos ^-/- eggs, we used time-lapse microscopy to monitor the abnormal divisions. We discovered that, following parthenogene

SUBMITTER: Cairo G 

PROVIDER: S-EPMC12407848 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature