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doi:10.1534/genetics.106.065219
A more recent version of this article appeared on February 1, 2007.
REGULAR RESEARCH PAPERS |
Onset of the DNA Replication Checkpoint in the Early Drosophila Embryo
Justin Crest 1*, Nathan Oxnard 1, Jun-yuan Ji 2 and Gerold Schubiger 1
1 University of Washington
2 Massachusetts Generall Hospital Cancer Center
* To whom correspondence should be addressed. E-mail: jcrest{at}ucsc.edu.
Submitted on August 24, 2006
Revised on September 11, 2006
Accepted on 7 November 2006
The Drosophila embryo is a promising model for isolating gene products that coordinate S phase and mitosis. We have reported before that increasing maternal Cyclin B dosage to up to six copies (six cycB) increases Cdk1-CycB levels and activity in the embryo, delays nuclear migration at cycle 10, and produces abnormal nuclei at cycle 14. Here we show that the level of cycB in the embryo inversely correlates with the ability to lengthen interphase as the embryos transits from preblastoderm to blastoderm stages, and the onset of a checkpoint that regulates mitosis when DNA replication is blocked with Aphidicolin. A screen for modifiers of the six cycB phenotypes identified 10 new suppressor deficiencies. In addition, heterozygote dRPA2 mutant suppressed only the abnormal nuclear phenotype at cycle 14. Reduction of dRPA2 also restored interphase duration and checkpoint efficacy to control levels. We propose that lowered dRPA2 levels activate Grp/Chk1 to counteract excess Cdk1-CycB activity, restore interphase duration and the ability to block mitosis in response to aphidicolin. Our results suggest an antagonistic interaction between DNA replication checkpoint activation and Cdk1-CycB activity during the transition from preblastoderm to blastoderm cycles.
Key Words: Cdk1-CycB, Checkpoint, Drosophila, Replication protein A complex, embryo
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