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(Received for publication, August 16, 1994; and in revised form, January 13, 1995) From the
Earlier work demonstrated that cyclins A1, B1, and B2 are not
associated with Cdk2 from unfertilized Xenopus eggs. As a
potential Cdk2 partner during meiosis, a cyclin E homolog was cloned
from a Xenopus oocyte cDNA library and found to be 60%
identical at the amino acid level to human cyclin E. Cyclin E1 protein
was detected in resting oocytes, and the level increased severalfold in
meiosis II, concomitant with the appearance of forms with decreased
electrophoretic mobility. During oocyte maturation, the patterns of
cyclin E1-associated kinase activity and Cdk2 activity were identical,
with activity low until after germinal vesicle breakdown, peaking
during meiosis II. Cyclin E1 complexes immunoprecipitated from
unfertilized Xenopus eggs contained Cdk2 but not Cdc2. In
cycling egg extracts Cdk2-cyclin E1-associated kinase activity
oscillated, but the level of cyclin E1 protein and its association with
Cdk2 did not vary appreciably; complex activity appeared to be
regulated neither by the synthesis and destruction of the cyclin
subunit nor by association/disassociation of the two subunits. During
the early cleavage divisions in embryos, cyclin E1 and Cdk2 remained
associated. The data indicate that the Cdk2-cyclin E complex functions
during meiotic and embryonic cell cycles in addition to performing its
established role during G
The nucleotide
sequence(s) reported in this paper has been submitted to the
GenBank(TM)/EMBL Data Bank with accession number(s)
L23857[GenBank].
Volume 270,
Number 12,
Issue of March 24, 1995 pp. 6843-6855
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
Phase (*)
in somatic cells.
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)
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)
We thank Brad Lattes and Andrea Lewellyn for technical
assistance, Olivier Haccard for help with computerized sequence
analysis, Rebecca Hartley for assistance with embryo staging, and
Eleanor Erikson for a critical reading of the manuscript.
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
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