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First published online 16 November 2005
doi: 10.1242/dev.02148


Development 132, 5411-5424 (2005)
Published by The Company of Biologists 2005


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Growth and cell survival are unevenly impaired in pixie mutant wing discs

Carmen M. A. Coelho1,2, Benjamin Kolevski1, Caroline Bunn1, Cherryl Walker1, Anupama Dahanukar3 and Sally J. Leevers1,*

1 Cancer Research UK London Research Institute, PO Box 123, 44 Lincolns Inn Fields, London WC2A 3PX, UK
2 National Centre for Biological Sciences, UAS-GKVK Campus, Bellary Road, Bangalore 560 065, India
3 Department of Genetics, Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA

* Author for correspondence (e-mail: sally.leevers{at}cancer.org.uk)

Accepted 4 October 2005

It is largely unknown how growth slows and then stops in vivo. Similar to most organs, Drosophila imaginal discs undergo a fast, near-exponential growth phase followed by a slow growth phase before final target size is reached. We have used a genetic approach to study the role of an ABC-E protein, Pixie, in wing disc growth. pixie mutants, like mutants in ribosomal proteins genes (known as Minutes), show severe developmental delay with relatively mild alterations in final body size. Intriguingly, pixie mutant wing imaginal discs show complex regional and temporal defects in growth and cell survival that are compensated to result in near-normal final size. In S2 cells, Pixie, like its yeast homolog RLI1, is required for translation. However, a comparison of the growth of eukaryotic translation initiation factor eIF4A and pixie mutant clones in wing discs suggests that only a subset of translation regulators, including pixie, mediate regional differences in growth and cell survival in wing discs. Interestingly, some of the regional effects on pixie mutant clone growth are enhanced in a Minute background. Our results suggest that the role of Pixie is not merely to allow growth, as might be expected for a translation regulator. Instead, Pixie also behaves as a target of putative constraining signals that slow disc growth during late larval life. We propose a model in which a balance of growth inhibitors and promoters determines tissue growth rates and cell survival. An alteration in this balance slows growth before final disc size is reached.

Key words: Cell growth, Ribosomal proteins, Drosophila




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