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Chromosome association of minichromosome maintenance proteins in Drosophila mitotic cycles.

Su TT, O'Farrell PH - J. Cell Biol. (1997)

Bottom Line: Arrest of mitosis by induced expression of nondegradable forms of cyclins A and/or B showed that reassociation of MCMs to chromatin requires cyclin A destruction but not cyclin B destruction.In contrast to the earlier mitoses, mitosis 16 (M16) is followed by G1, and MCMs do not reassociate with chromatin at the end of M16. dacapo mutant embryos lack an inhibitor of cyclin E, do not enter G1 quiescence after M16, and show mitotic reassociation of MCM proteins.We propose that cyclin E, inhibited by Dacapo in M16, promotes chromosome binding of MCMs. We suggest that cyclins have both positive and negative roles in controlling MCM-chromatin association.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Biophysics, University of California San Francisco 94143-0448, USA.

ABSTRACT
Minichromosome maintenance (MCM) proteins are essential DNA replication factors conserved among eukaryotes. MCMs cycle between chromatin bound and dissociated states during each cell cycle. Their absence on chromatin is thought to contribute to the inability of a G2 nucleus to replicate DNA. Passage through mitosis restores the ability of MCMs to bind chromatin and the ability to replicate DNA. In Drosophila early embryonic cell cycles, which lack a G1 phase, MCMs reassociate with condensed chromosomes toward the end of mitosis. To explore the coupling between mitosis and MCM-chromatin interaction, we tested whether this reassociation requires mitotic degradation of cyclins. Arrest of mitosis by induced expression of nondegradable forms of cyclins A and/or B showed that reassociation of MCMs to chromatin requires cyclin A destruction but not cyclin B destruction. In contrast to the earlier mitoses, mitosis 16 (M16) is followed by G1, and MCMs do not reassociate with chromatin at the end of M16. dacapo mutant embryos lack an inhibitor of cyclin E, do not enter G1 quiescence after M16, and show mitotic reassociation of MCM proteins. We propose that cyclin E, inhibited by Dacapo in M16, promotes chromosome binding of MCMs. We suggest that cyclins have both positive and negative roles in controlling MCM-chromatin association.

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A summary of cyclin profiles and  MCM–chromosome association. (A) In wild-type embryonic cycles in which S phase follows  M, cyclin E (dashed line) is present continuously,  and association of MCMs (dots) with chromosomes (bars) occurs as mitotic cyclins (solid  lines) are degraded during mitosis. (B) In M16,  cyclin E–associated activity is down regulated as  dacapo is expressed (arrow), and MCMs fail to  associate with chromosomes, even when mitotic  cyclins are degraded (Lehner and O'Farrell,  1989). (C) In dap mutants, cyclin E–associated  activity persists, MCMs associate with chromosomes as described in A, and M16 is followed by  S phase. We propose that cyclin:cdk activity is coupled to MCM–chromosome association in the following manner: a cyclin A–associated activity inhibits chromosome association of MCMs. After the loss of cyclin A in mitosis, chromosome association of MCMs requires a second cyclin-dependent activity that is provided by cyclin E:cdk2. The diagrams are not drawn to scale.
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Figure 6: A summary of cyclin profiles and MCM–chromosome association. (A) In wild-type embryonic cycles in which S phase follows M, cyclin E (dashed line) is present continuously, and association of MCMs (dots) with chromosomes (bars) occurs as mitotic cyclins (solid lines) are degraded during mitosis. (B) In M16, cyclin E–associated activity is down regulated as dacapo is expressed (arrow), and MCMs fail to associate with chromosomes, even when mitotic cyclins are degraded (Lehner and O'Farrell, 1989). (C) In dap mutants, cyclin E–associated activity persists, MCMs associate with chromosomes as described in A, and M16 is followed by S phase. We propose that cyclin:cdk activity is coupled to MCM–chromosome association in the following manner: a cyclin A–associated activity inhibits chromosome association of MCMs. After the loss of cyclin A in mitosis, chromosome association of MCMs requires a second cyclin-dependent activity that is provided by cyclin E:cdk2. The diagrams are not drawn to scale.

Mentions: A summary of data on MCM–chromosome interactions is shown schematically in Fig. 6 and described below.


Chromosome association of minichromosome maintenance proteins in Drosophila mitotic cycles.

Su TT, O'Farrell PH - J. Cell Biol. (1997)

A summary of cyclin profiles and  MCM–chromosome association. (A) In wild-type embryonic cycles in which S phase follows  M, cyclin E (dashed line) is present continuously,  and association of MCMs (dots) with chromosomes (bars) occurs as mitotic cyclins (solid  lines) are degraded during mitosis. (B) In M16,  cyclin E–associated activity is down regulated as  dacapo is expressed (arrow), and MCMs fail to  associate with chromosomes, even when mitotic  cyclins are degraded (Lehner and O'Farrell,  1989). (C) In dap mutants, cyclin E–associated  activity persists, MCMs associate with chromosomes as described in A, and M16 is followed by  S phase. We propose that cyclin:cdk activity is coupled to MCM–chromosome association in the following manner: a cyclin A–associated activity inhibits chromosome association of MCMs. After the loss of cyclin A in mitosis, chromosome association of MCMs requires a second cyclin-dependent activity that is provided by cyclin E:cdk2. The diagrams are not drawn to scale.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2139827&req=5

Figure 6: A summary of cyclin profiles and MCM–chromosome association. (A) In wild-type embryonic cycles in which S phase follows M, cyclin E (dashed line) is present continuously, and association of MCMs (dots) with chromosomes (bars) occurs as mitotic cyclins (solid lines) are degraded during mitosis. (B) In M16, cyclin E–associated activity is down regulated as dacapo is expressed (arrow), and MCMs fail to associate with chromosomes, even when mitotic cyclins are degraded (Lehner and O'Farrell, 1989). (C) In dap mutants, cyclin E–associated activity persists, MCMs associate with chromosomes as described in A, and M16 is followed by S phase. We propose that cyclin:cdk activity is coupled to MCM–chromosome association in the following manner: a cyclin A–associated activity inhibits chromosome association of MCMs. After the loss of cyclin A in mitosis, chromosome association of MCMs requires a second cyclin-dependent activity that is provided by cyclin E:cdk2. The diagrams are not drawn to scale.
Mentions: A summary of data on MCM–chromosome interactions is shown schematically in Fig. 6 and described below.

Bottom Line: Arrest of mitosis by induced expression of nondegradable forms of cyclins A and/or B showed that reassociation of MCMs to chromatin requires cyclin A destruction but not cyclin B destruction.In contrast to the earlier mitoses, mitosis 16 (M16) is followed by G1, and MCMs do not reassociate with chromatin at the end of M16. dacapo mutant embryos lack an inhibitor of cyclin E, do not enter G1 quiescence after M16, and show mitotic reassociation of MCM proteins.We propose that cyclin E, inhibited by Dacapo in M16, promotes chromosome binding of MCMs. We suggest that cyclins have both positive and negative roles in controlling MCM-chromatin association.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Biophysics, University of California San Francisco 94143-0448, USA.

ABSTRACT
Minichromosome maintenance (MCM) proteins are essential DNA replication factors conserved among eukaryotes. MCMs cycle between chromatin bound and dissociated states during each cell cycle. Their absence on chromatin is thought to contribute to the inability of a G2 nucleus to replicate DNA. Passage through mitosis restores the ability of MCMs to bind chromatin and the ability to replicate DNA. In Drosophila early embryonic cell cycles, which lack a G1 phase, MCMs reassociate with condensed chromosomes toward the end of mitosis. To explore the coupling between mitosis and MCM-chromatin interaction, we tested whether this reassociation requires mitotic degradation of cyclins. Arrest of mitosis by induced expression of nondegradable forms of cyclins A and/or B showed that reassociation of MCMs to chromatin requires cyclin A destruction but not cyclin B destruction. In contrast to the earlier mitoses, mitosis 16 (M16) is followed by G1, and MCMs do not reassociate with chromatin at the end of M16. dacapo mutant embryos lack an inhibitor of cyclin E, do not enter G1 quiescence after M16, and show mitotic reassociation of MCM proteins. We propose that cyclin E, inhibited by Dacapo in M16, promotes chromosome binding of MCMs. We suggest that cyclins have both positive and negative roles in controlling MCM-chromatin association.

Show MeSH
Related in: MedlinePlus