Tetraspanins and Mouse Oocyte Microvilli Related to Fertilizing Ability

Abstract

Our electron microscopy observations demonstrate for the first time that the number of microvilli on the mice oocyte membrane decreases when meiosis progresses from prophase I to metaphase II (MII) stage, and the morphology of the microvilli also changes. Microvilli are significantly shorter and larger on the ovulated oocyte membrane than at the previous stages. Although clathrin vesicles clearly disappear during oocyte maturation, exosome-like vesicles begin to be secreted at the metaphase I stage, more strongly at the MII stage. Multivesicular bodies are visible only at the MII stage. Since several oocyte tetraspanins are involved in the gamete interaction, Cd9 being congregated on the MII oocyte microvilli, we analyzed the effect of tetraspanin deletion on oocyte membrane morphology. The Cd9 and Cd9 Cd81 deletions are associated with a decreased microvilli density on the MII oocyte surface. Microvilli thickness is significantly increased whatever the deleted tetraspanin gene be. Only Cd9 deletion clearly disturbs the vesicular traffic, increasing the number of clathrin and exosome vesicles. Additional investigations are necessary to elucidate how tetraspanins modulate the microvilli morphology, likely in relation with cytoskeleton. The role of oocyte exosomes in gamete adhesion/fusion remains to be further studied.

Anchoring cortical granules in the cortex ensures trafficking to the plasma membrane for post-fertilization exocytosis

“…To validate these protocols, we imaged zona-free eggs from Cd9 Null female mice. CD9 is a tetraspanin protein that localizes to microvilli of membranes 53 and Cd9 Null eggs have an altered membrane due to varied length, thickness and density of their microvilli 54 . Projected confocal images detected a >1.5-fold reduction in the fluorescent intensity of Cd9 Null compared to wild-type eggs (Supplementary Fig.…”

Placenta‐specific 1 regulates oocyte meiosis and fertilization through furin

“…Similarly, in our study, Plac1 enriched on the cell membrane, presumably via its ZP-like domain, and Plac1 knockdown caused the abnormal distribution of cortical microvillus. As an irregular microvillar shape and organization contribute to the abnormal fertilization of mouse oocytes (20)(21)(22), this could account, in part, for the decreased fertilization after Plac1 knockdown. In contrast, Plac1 knockdown significantly decreased Akt phosphorylation, as Akt is well known to play an important role in the mitotic cell cycle and in meiosis (23,24), and we also showed that Akt inhibition significantly perturbed meiosis progression (reduced MII rate).…”

Review: Sperm–oocyte interactions and their implications for bull fertility, with emphasis on the ubiquitin–proteasome system

“…Gene knock-out studies demonstrated that these molecules are either non-essential or compensable in mouse fertilization (Primakoff and Myles, 2007). Alternatively proposed sperm receptors on the oollema, tetraspanins CD9 and CD81 were knocked out, resulting in reduced fertility of single gene knock-out and complete infertility of double knock-out (Benammar et al 2016). The most convincing evidence for gamete adhesion receptors came with the discovery of the sperm-specific immunoglobulin family cell adhesion protein IZUMO (Inoue et al, 2005) and its oocyte-binding partner, the folate-binding receptor JUNO (Bianchi et al, 2014).…”