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Vol. 273, Issue 3, 1387-1392, January 16, 1998
From the During the endomitotic cell cycle of
megakaryocytic cell lines, the levels of cyclin B1 and the activity of
cyclin B1-dependent Cdc2 kinase, although detectable, are
reduced as compared with megakaryocytes undergoing a mitotic cell
cycle. The levels of cyclin A, however, are comparable during both cell
cycles. The expression of cyclin B1 mRNA is also equivalent in
proliferating and polyploidizing cells. In the current study, we found
that the rate of cyclin B1 protein degradation is enhanced in
polyploidizing megakaryocytes. This finding has led us to further
investigate whether the ubiquitin-proteosome pathway responsible for
cyclin B degradation is accelerated in these cells. Our data indicate that polyploidizing megakaryocytic cell lines and primary bone marrow
cells treated with the megakaryocyte proliferation- and ploidy-promoting factor, the c-Mpl ligand, display increased activities of the ubiquitin-proteosome pathway, which degrades cyclin B, as
compared with proliferating megakaryocytic cell lines or diploid bone
marrow cells, respectively. This degradation has all the hallmarks of a
ubiquitin pathway, including the dependence on ATP, the appearance of
high molecular weight conjugated forms of cyclin B, and inhibition of
the proteolytic process by a mutated form of the ubiquitin-conjugating
enzyme Ubc4. Our studies also indicate that the ability to degrade
cyclin A is equivalent in both the mitotic and endomitotic cell cycles.
The increased potential of polyploid megakaryocytes to degrade cyclin B
may be part of the cellular programming that leads to aborted
mitosis.
Ubiquitin-dependent Degradation of Cyclin B Is
Accelerated in Polyploid Megakaryocytes
,
,
Department of Biochemistry, Whitaker
Cardiovascular Institute, Boston University School of Medicine, Boston,
Massachusetts 02118 and § New York University Medical Center
and Kaplan Cancer Center, New York, New York 10016
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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