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doi: 10.1242/10.1242/dev.00168

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Development 129, 5719-5730 (2002)
Copyright © 2002 The Company of Biologists Limited

Shar-pei mediates cell proliferation arrest during imaginal disc growth in Drosophila

Madhuri Kango-Singh1, Riitta Nolo1, Chunyao Tao1, Patrik Verstreken3, P. Robin Hiesinger4, Hugo J. Bellen3,4,5 and Georg Halder1,2,3,*

1 Department of Biochemistry and Molecular Biology, M. D. Anderson Cancer Center, Houston, TX 77030, USA
2 Program in Genes and Development, M. D. Anderson Cancer Center, Houston, TX 77030, USA
3 Program in Developmental Biology, Baylor College of Medicine, Houston, TX 77030, USA
4 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA
5 Howard Hughes Medical Institute, Baylor College of Medicine, Houston, TX 77030, USA

* Author for correspondence (e-mail: ghalder{at}mdanderson.org)

Accepted 19 September 2002

During animal development, organ size is determined primarily by the amount of cell proliferation, which must be tightly regulated to ensure the generation of properly proportioned organs. However, little is known about the molecular pathways that direct cells to stop proliferating when an organ has attained its proper size. We have identified mutations in a novel gene, shar-pei, that is required for proper termination of cell proliferation during Drosophila imaginal disc development. Clones of shar-pei mutant cells in imaginal discs produce enlarged tissues containing more cells of normal size. We show that this phenotype is the result of both increased cell proliferation and reduced apoptosis. Hence, shar-pei restricts cell proliferation and promotes apoptosis. By contrast, shar-pei is not required for cell differentiation and pattern formation of adult tissue. Shar-pei is also not required for cell cycle exit during terminal differentiation, indicating that the mechanisms directing cell proliferation arrest during organ growth are distinct from those directing cell cycle exit during terminal differentiation. shar-pei encodes a WW-domain-containing protein that has homologs in worms, mice and humans, suggesting that mechanisms of organ growth control are evolutionarily conserved.

Key words: Drosophila, Imaginal discs, Cell proliferation, Apoptosis, WW domain-protein






© The Company of Biologists Ltd 2002