Fully grown mouse oocytes are normally competent to progress from prop
hase I to metaphase II without interruption. However, growing mouse oo
cytes initially become only partially competent to undergo meiotic mat
uration. Meiotic maturation in these oocytes does not progress beyond
metaphase I. In contrast to the oocytes of most strains of mice, most
oocytes of strain LT/Sv mice become arrested at metaphase I even when
they are fully grown. The initiation of oocyte maturation is correlate
d with an increase in p34(cdc2) kinase activity that continues to rise
until metaphase I. The transition into anaphase I is normally correla
ted with a decrease in p34(cdc2) kinase activity. This study demonstra
ted that metaphase I arrest in both partially competent growing oocyte
s and fully grown LT/Sv oocytes is correlated with a sustained elevati
on of p34(cdc2) kinase activity. In fact, p34(cdc2) activity continued
to increase during the time when activity normally decreased. In norm
ally maturing oocytes, some, but not all, of the cyclin B, the regulat
ory protein associated with p34(cdc2), became degraded in oocytes that
entered anaphase I. In contrast, the amount of cyclin B present in th
e metaphase I-arrested oocytes continued to increase at the time when
it was being degraded in normal oocytes progressing to metaphase II. T
hese results suggest that the progression of meiosis is arrested at me
taphase I in both groups of oocytes because of continued p34(cdc2) kin
ase activity sustained, at least in part, by restricted degradation of
cyclin B. Finally, metaphase I arrest in these oocytes is sustained b
y a mechanism that differs from that maintaining metaphase II arrest,
since an inhibitor of protein phosphorylation, 6-DMAP, induced a drama
tic decline in p34(cdc2) kinase activity and the resumption of meiosis
in metaphase I-arrested oocytes but not in metaphase II-arrested oocy
tes. Moreover, without 6-DMAP treatment, cyclin B was more stable in t
he metaphase I-arrested oocytes than in metaphase II-arrested oocytes.