Abstract
Each follicle represents the basic functional unit of the ovary. From its very initial stage of development, the follicle consists of an oocyte surrounded by somatic cells. The oocyte grows and matures to become fertilizable and the somatic cells proliferate and differentiate into the major suppliers of steroid sex hormones as well as generators of other local regulators. The process by which a follicle forms, proceeds through several growing stages, develops to eventually release the mature oocyte, and turns into a corpus luteum (CL) is known as “folliculogenesis”. The task of this review is to define the different stages of folliculogenesis culminating at ovulation and CL formation, and to summarize the most recent information regarding the newly identified factors that regulate the specific stages of this highly intricated process. This information comprises of either novel regulators involved in ovarian biology, such as Ube2i, Phoenixin/GPR73, C1QTNF, and α-SNAP, or recently identified members of signaling pathways previously reported in this context, namely PKB/Akt, HIPPO, and Notch.
Highlights
A large fraction of these growing follicles is destined to go through another massive death wave, defined as oocyte degeneration, with only a minority activated to transform into primary follicles [6]
Activation of the Hippo pathway starts with a sequential phosphorylation of serine threonine kinase 3 (STK3) and STK4, triggering phosphorylation of the large tumor suppressor 1/2 (LATS1/2) kinases, that in turn phosphorylate the transcriptional co-activators, Yes-associated protein1 (YAP1) and WW domain-containing transcription regulator protein 1 (WWTR1, known as TAZ)
The reciprocal effect, manifested by a reduced number of primordial follicles and elevation in secondary follicles, is obtained upon YAP1 overexpression [47,52]. These findings are supported by another study, in which a specific deletion of YAP1 in granulosa cells (GCs) of primordial follicles resulted in subfertility which was subsequent to increased cell apoptosis, reduced number of corpus luteum (CL) and a decline in ovarian size [48]
Summary
The information presented has been published during the past five years (2016 and on), not including regulators, such as FIGLA, Forkhead box L2 (FOXL2), and Transforming growth factor β (TGFβ) family members, KITL/KIT signaling, PI3K/Akt, Leukemia inhibitory factor (>LIF), Notch signaling, cAMP, cGMP, and their corresponding phosphodiesterases (PDEs), Epidermal growth factor receptors (EGFR) and ligands, etc. These regulators have been discussed in detail previously [3]
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