c-jun N-terminal kinase activation in Xenopus laevis eggs and embryos - A possible non-genomic role for the JNK signaling pathway

The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated pr otein kinase family that play critical roles in stress responses and apopto sis, We have discovered that JNK is present in Xenopus oocytes, an experime ntal system that offers a variety of powerful experimental approaches to qu estions of protein function and regulation. Like ERK2/p42 MAPK, JNK is acti vated just prior to germinal vesicle breakdown during Xenopus oocyte matura tion and remains active throughout meiosis I and II. However, unlike p42 MA PK which is inactivated about 30 min after eggs are fertilized or parthenog enetically activated, JNK stays constitutively active until the early gastr ula stage of embryogenesis, These findings suggest that the JNK pathway may play a role in oocyte maturation and embryogenesis, JNK was activated by m icroinjection of Mos, by activation of an estrogen-inducible form of Raf, a nd by a constitutively active MEK-1 (MEK R4F), indicating that the p42 MAPK cascade can trigger JNK activation. However, the MEK inhibitor U0126 block ed progesterone-induced p42 MAPK activation but not progesterone-induced JN K activation, Thus, progesterone can stimulate JNK activation both through the MEK/p42 MAPK pathway and through MEK/p42 MAPK-independent pathways. Man y of the key substrates of JNKs identified to date are transcriptional regu lators. However, since transcription is not required for germinal vesicle b reakdown in progesterone-treated oocytes or for the early embryonic cell cy cles, our findings suggest that in these contexts the JNK pathway exerts no ngenomic effects.