The Mos-MAPK signaling pathway involving the Mos-MEK1/2-ERK1/2-RSK1/2/3 or MSK1-EMI2 cascade is directly linked to metaphase-II arrest of vertebrate oocytes. In this study, we examined whether p38, a member of the MAPK subfamily, is regulated under the control of Mos and contributes to metaphase-II arrest in the mouse oocyte. Morpholino oligonucleotide-mediated depletion of Mos revealed a remarkable decrease in phosphorylation of p38. Simultaneous treatment of oocytes with two chemical inhibitors of p38 and MEK1/2 induced both release from metaphase II and degradation of cyclin B1, whereas the treatment with each of these two inhibitors had little effect. Moreover, phosphorylation of EMI2 was dramatically abolished by addition of the two inhibitors. Indeed, MNK1, a kinase downstream of p38, exhibited the ability to phosphorylate EMI2. These results suggest that in addition to the Mos-MEK1/2 pathway, the Mos-mediated p38 pathway may be implicated in metaphase-II arrest.
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11 June 2014
Possible Role of p38 MAPK-MNK1-EMI2 Cascade in Metaphase-II Arrest of Mouse Oocytes
Yu Miyagaki,
Yoshinori Kanemori,
Fumi Tanaka,
Tadashi Baba
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Biology of Reproduction
Vol. 91 • No. 2
August 2014
Vol. 91 • No. 2
August 2014
EMI2
ERK1/2 MAPK
meiosis
MOS
oocyte
p38 MAPK