A. Hampl et Jj. Eppig, TRANSLATIONAL REGULATION OF THE GRADUAL INCREASE IN HISTONE H1 KINASE-ACTIVITY IN MATURING MOUSE OOCYTES, Molecular reproduction and development, 40(1), 1995, pp. 9-15
In maturing mouse oocytes, p34(cdc2)-associated histone H1 kinase acti
vity gradually increases until it reaches its maximum at metaphase I (
Choi et al., 1991: Development 113:789-795). In this study, treatment
of oocytes with cycloheximide resulted in a failure to increase the le
vel of histone H1 activity above that detected at approximately the ti
me of germinal vesicle breakdown (GVB), which is similar to 20-30% of
the level normally achieved at metaphase I. Cyclin B was detected in G
V-stage oocytes, but there was a 2-2.5-fold increase in the amount of
cyclin B in maturing oocytes from GV-stage to metaphase I and a burst
of cyclin B synthesis during the first 3 hr of maturation. Okadaic aci
d-treatment of mouse oocytes did not accelerate activation of histone
H1 kinase but rather arrested its activity at the same level observed
in cycloheximide-treated oocytes. Thus the components of the p34(cdc2)
kinase activating system in mouse oocytes are apparently not present
in GV-stage oocytes in an amount or configuration that would allow max
imum kinase activation when meiosis is reinitiated by okadaic acid. Im
portantly, okadaic acid-treatment dramatically inhibited protein synth
esis. Therefore, the inhibition of protein synthesis by okadaic acid p
robably abrogates the possibility of de novo synthesis of the regulato
rs of p34(cdc2) kinase required to drive its activity to the maximum l
evel normally achieved by metaphase I. It is concluded that there is a
critical point in driving the continued activation of histone H1 kina
se that occurs at approximately the time of GVB. Progression beyond th
is point requires de novo protein synthesis. Since newly synthesized c
yclin B is immediately complexed with the p34(cdc2) kinase in maturing
mouse oocytes, cyclin B is a candidate for one of the proteins whose
synthesis is required to drive the continued increase in histone H1 ki
nase activity after the time of GVB. (C) 1995 Wiley-Liss, Inc.