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Regulation of inositol 1,4,5‐trisphosphate receptor function during mouse oocyte maturation
Author(s) -
Wakai Takuya,
Vanderheyden Veerle,
Yoon SookYoung,
Cheon Banyoon,
Zhang Nan,
Parys Jan B.,
Fissore Rafael A.
Publication year - 2012
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22778
Subject(s) - germinal vesicle , oocyte , endoplasmic reticulum , inositol , phosphorylation , microbiology and biotechnology , human fertilization , oocyte activation , receptor , inositol trisphosphate receptor , biology , chemistry , endocrinology , medicine , biochemistry , anatomy , embryo
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, that is, 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. J. Cell. Physiol. 227: 705–717, 2012. © 2011 Wiley Periodicals, Inc.