Cell cycle control of chorion gene amplification.
Over-replication of two clusters of chorion genes in Drosophila ovarian follicle cells is essential for rapid eggshell biosynthesis. The relationship of this amplification to the follicle cell cycles has remained unclear. To investigate the regulation of amplification, we developed a technique to detect amplifying chorion genes in individual follicle cells using BrdU incorporation and FISH. Amplification occurs in two developmental phases. One of the gene clusters begins to amplify periodically during S phases of follicle cell endocycles. Subsequently, after endocycles have ceased, both clusters amplify continuously during the remainder of oogenesis. In contrast to the early phase, late amplification commences synchronously among follicle cells. The pattern of Cyclin E expression mirrors these two phases. We present evidence that Cyclin E is required positively for amplification. We suggest that Cyclin E also acts negatively to inhibit refiring of most origins within a cycle, and that specific factors at chorion origins allow them to escape this negative rereplication control. Our findings suggest that chorion amplification is a model for understanding metazoan replicons and the controls that restrict replication to once per cell cycle.
Calvi
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Howard Hughes Medical Institute Research Laboratories, Carnegie Institution of Washington, Baltimore, Maryland 21210, USA.
Lilly
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MA
Spradling
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AC
D000818:Animals; D002453:Cell Cycle / Q000235:genetics*; D002823:Chorion / Q000502:physiology*; D019927:Cyclin E / Q000235:genetics / Q000378:metabolism*; D004261:DNA Replication; D004330:Drosophila / Q000196:embryology / Q000235:genetics*; D004625:Embryo, Nonmammalian; D005260:Female; D005784:Gene Amplification; D006080:Ovarian Follicle / Q000502:physiology
D019927:Cyclin E