TY - JOUR
T1 - The role of Src family kinases in egg activation
AU - Reut, Tomashov Matar
AU - Mattan, Levi
AU - Dafna, Tchetchik
AU - Ruth, Kaplan Kraicer
AU - Ruth, Shalgi
N1 - Funding Information:
This work is in partial fulfillment of the requirements for the Ph.D. degree of R. Tomashov-Matar at the Sackler Faculty of Medicine, Tel-Aviv University. This work was partially supported by grants from the Israel Science Foundation (695/05) and from the Ministry of Health to RS.
PY - 2007/12/1
Y1 - 2007/12/1
N2 - The Src family kinases (SFKs) are believed to mediate some of the early events of egg activation at fertilization - intracellular Ca2+ increase and resumption of the second meiotic division (RMII). SFKs are both necessary and sufficient for triggering intracellular Ca2+ increase in eggs of sea urchin, sea star, Xenopus etc, but their role in mammalian eggs is not entirely determined. In this study we examined the involvement of SFKs in the events leading to Ca2+ increase in rat eggs and demonstrated their involvement in RMII. Microinjecting mRNAs of active forms of Fyn or c-Yes but not of c-Src, into ovulated eggs, triggered RMII without evoking Ca2+ increase. A specific SFKs inhibitor (SU6656) or dominant-negative (DN) forms of Fyn or c-Yes were unable to block Ca2+ oscillations rather, modulated them, in fertilized eggs or in parthenogenetically activated eggs. Moreover, inhibiting SFKs activity blocked RMII and decreased the level of cyclin B1 degradation. Our results imply participation of SFKs in the signal transduction pathway leading to egg activation, but not in the one leading to Ca2+ increase. We propose that SFKs act downstream to Ca2+ increase at the level of M-phase promoting factor (MPF).
AB - The Src family kinases (SFKs) are believed to mediate some of the early events of egg activation at fertilization - intracellular Ca2+ increase and resumption of the second meiotic division (RMII). SFKs are both necessary and sufficient for triggering intracellular Ca2+ increase in eggs of sea urchin, sea star, Xenopus etc, but their role in mammalian eggs is not entirely determined. In this study we examined the involvement of SFKs in the events leading to Ca2+ increase in rat eggs and demonstrated their involvement in RMII. Microinjecting mRNAs of active forms of Fyn or c-Yes but not of c-Src, into ovulated eggs, triggered RMII without evoking Ca2+ increase. A specific SFKs inhibitor (SU6656) or dominant-negative (DN) forms of Fyn or c-Yes were unable to block Ca2+ oscillations rather, modulated them, in fertilized eggs or in parthenogenetically activated eggs. Moreover, inhibiting SFKs activity blocked RMII and decreased the level of cyclin B1 degradation. Our results imply participation of SFKs in the signal transduction pathway leading to egg activation, but not in the one leading to Ca2+ increase. We propose that SFKs act downstream to Ca2+ increase at the level of M-phase promoting factor (MPF).
KW - Ca rise
KW - Fertilization
KW - Fyn
KW - MPF
KW - Src family kinase inhibition
KW - c-Src
KW - c-Yes
UR - http://www.scopus.com/inward/record.url?scp=36549072580&partnerID=8YFLogxK
U2 - 10.1016/j.ydbio.2007.09.010
DO - 10.1016/j.ydbio.2007.09.010
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C2 - 17949706
AN - SCOPUS:36549072580
SN - 0012-1606
VL - 312
SP - 77
EP - 89
JO - Developmental Biology
JF - Developmental Biology
IS - 1
ER -