Title: Regulation of inositol 1,4,5-trisphosphate receptor function during mouse oocyte maturation
Authors: Wakai, Takuya
Vanderheyden, Veerle
Yoon, Sook-Young
Cheon, Banyoon
Zhang, Nan
Parys, Jan
Fissore, Rafael A # ×
Issue Date: Feb-2012
Publisher: Wiley Subscription Services, Inc.
Series Title: Journal of Cellular Physiology vol:227 issue:2 pages:705-17
Article number: 10.1002/jcp.22778
Abstract: At the time of fertilization, an increase in the intracellular Ca(2+) concentration ([Ca(2+) ](i) ) underlies egg activation and initiation of development in all species studied to date. The inositol 1,4,5-trisphosphate receptor (IP(3) R1), which is mostly located in the endoplasmic reticulum (ER) mediates the majority of this Ca(2+) release. The sensitivity of IP(3) R1, i.e. its Ca(2+) releasing capability, is increased during oocyte maturation so that the optimum [Ca(2+) ](i) response concurs with fertilization, which in mammals occurs at metaphase of second meiosis. Multiple IP(3) R1 modifications affect its sensitivity, including phosphorylation, sub-cellular localization and ER Ca(2+) concentration ([Ca(2+) ](ER) ). Here we evaluated using mouse oocytes how each of these factors affected IP(3) R1 sensitivity. The capacity for IP(3) -induced Ca(2+) release markedly increased at the germinal vesicle breakdown stage, although oocytes only acquire the ability to initiate fertilization-like oscillations at later stages of maturation. The increase in IP(3) R1 sensitivity was underpinned by an increase in [Ca(2+) ](ER) and receptor phosphorylation(s) but not by changes in IP(3) R1 cellular distribution, as inhibition of the former factors reduced Ca(2+) release, whereas inhibition of the latter had no impact. Therefore, the results suggest that the regulation of [Ca(2+) ](ER) and IP(3) R1 phosphorylation during maturation enhance IP(3) R1 sensitivity rendering oocytes competent to initiate oscillations at the expected time of fertilization. The temporal discrepancy between the initiation of changes in IP(3) R1 sensitivity and acquisition of mature oscillatory capacity suggest that other mechanisms that regulate Ca(2+) homeostasis also shape the pattern of oscillations in mammalian eggs. © 2011 Wiley Periodicals, Inc.
ISSN: 0021-9541
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Molecular and Cellular Signaling
× corresponding author
# (joint) last author

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