Meiotic arrest of oocytes depends on cell-to-cell communication in the ovarian follicle.

The source of the inhibitory levels of cAMP that maintain oocytes meiotically arrested is under controversy. A model for regulation of the meiotic division that suggests the transfer of a somatic follicular cells-derived cAMP into the oocyte via gap junctions was first proposed by us in 1978. Later studies provide strong evidence that established gap-junctional communication within the ovarian follicle is indispensable for maintenance of meiotic arrest.

Disruption of gap junctional communication within the ovarian follicle induces oocyte maturation.

Meiotically arrested mammalian oocytes are stimulated to resume meiosis by LH. This response, which can be reversed by elevation of intraoocyte cAMP levels, is associated with interruption of gap junctional communication (GJC) within the ovarian follicle. In the present study, we examined the hypothesis that disruption of GJC within the ovarian follicle is sufficient for induction of oocyte maturation.

Glucose and nitrogen regulate the switch from histone deacetylation to acetylation for expression of early meiosis-specific genes in budding yeast.

In eukaryotes, the switch between alternative developmental pathways is mainly attributed to a switch in transcriptional programs. A major mode in this switch is the transition between histone deacetylation and acetylation. In budding yeast, early meiosis-specific genes (EMGs) are repressed in the mitotic cell cycle by active deacetylation of their histones.