Affiliation:
1. Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan 48201; and
2. Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, Detroit, Michigan 48201
Abstract
Abstract
The Drosophila gene CG14939 encodes a member of a highly conserved family of cyclins, the Y-type cyclins, which have not been functionally characterized in any organism. Here we report the generation and phenotypic characterization of a null mutant of CG14939, which we rename CyclinY (CycY). We show that the null mutant, CycYE8, is homozygous lethal with most mutant animals arresting during pupal development. The mutant exhibits delayed larval growth and major developmental defects during metamorphosis, including impaired gas bubble translocation, head eversion, leg elongation, and adult tissue growth. Heat-shock-induced expression of CycY at different times during development resulted in variable levels of rescue, the timing of which suggests a key function for zygotic CycY during the transition from third instar larvae to prepupae. CycY also plays an essential role during embryogenesis since zygotic null embryos from null mothers fail to hatch into first instar larvae. We provide evidence that the CycY protein (CycY) interacts with Eip63E, a cyclin-dependent kinase (Cdk) for which no cyclin partner had previously been identified. Like CycY, the Eip63E gene has essential functions during embryogenesis, larval development, and metamorphosis. Our data suggest that CycY/Eip63E form a cyclin/Cdk complex that is essential for several developmental processes.
Publisher
Oxford University Press (OUP)
Cited by
34 articles.
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