Abstract: Polarity is an important aspect of oogenesis and early development for many animal groups, but only recently it has become relevant to the study of mammals. Mammalian oocyte development occurs through tight coordination and interaction between all ovarian structures. In fact, bi-directional communication between the oocyte and its companion granulosa cells (GC) in the ovarian follicle seems essential for GC proliferation, differentiation, and production of a functional female gamete. The transzonal projections (TZP), which are specialized extensions from granulosa cells that terminate on the oolema after crossing the zona pellucida, are major structural components necessary for oocyte-GC interaction. Granulosa cell polarity seems to be a necessary requisite for appropriate function of TZP, and the role of FSH as modulator of a polarized phenotype on GC is discussed. This article also discusses oocyte polarity with special reference to the partial loss of polarity that occurs during in-vitro oocyte maturation and possible implications in the modulation of oocyte competencies. Cytoskeletal markers that may account for oocyte quality were defined and found to be distinct in in-vivo and in-vitro matured oocytes. Implications of partial loss of oocyte polarity during in-vitro maturation, reflected by distinct distribution of these markers, are further discussed. It is also proposed that expression of both somatic and germ cell polarity in the ovarian follicle will ultimately determine acquisition of meiotic, fertilization and developmental competences by the oocyte.

Abstract: We have previously demonstrated that initiation of intracellular calcium ([Ca21]i) oscillations in mouse eggs signals activation or apoptotic death depending on the age of the eggs in which the oscillations are induced. To extend these studies, mouse eggs were aged in vitro to 24, 32, and 40 h post-hCG and injected with sperm cytosolic factor (SF), adenophostin A, or sperm (intracytoplasmic sperm injection), and the times at which signs of apoptosis first appeared were examined. These treatments, which induced [Ca21]i oscillations, caused fragmentation and other signs of programmed cell death in eggs as early as 32 h post-hCG. The susceptibility of aged eggs to apoptosis appeared to be due to cytoplasmic deficiencies, because fusion of recently ovulated eggs with aged, SF-injected eggs prevented fragmentation. Evaluation of mRNA and protein levels of the apoptotic regulatory proteins Bcl-2 and Bax showed a prominent decrease in the amounts of Bcl-2 mRNA and protein in aged eggs, whereas Bax mRNA levels did not appear to be changed. Lastly, the Ca21 responses induced by the aforementioned Ca21 agonists ceased in advance in aged eggs. Together, these results suggest that one or several critical cytosolic molecules involved in the regulation of Ca21 homeostasis, and in maintaining the equilibrium between anti- and proapoptotic proteins, is either lost or inactivated during postovulatory egg aging, rendering the fertilizing Ca21 signal into an apoptosis-inducing signal.