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First published online May 1, 2006

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Vps25 sorts it out

An imbalance in cell-cell signalling can cause over-proliferation or apoptosis. Endocytosis - which involves sorting ligand-bound receptors into vesicles for degradation - keeps cell-cell signalling in check. Protein sorting requires the vacuolar protein sorting (Vps) proteins, and vps25 mutant mosaics in the Drosophila eye have three distinct phenotypes: non-autonomous cell proliferation, non-autonomous resistance to apoptosis and cell-autonomous cell death. Bergmann and colleagues (p. 1871) have investigated the mechanisms behind these phenotypes by making detailed observations of vps25 mosaics, so extending recent published findings on this gene. They report that non-autonomous proliferation in vps25 mutant mosaics is caused by inappropriate Notch signalling via JAK/STAT, and that cells surrounding vps25 clones are resistant to apoptosis due to increased Diap1 (Drosophila inhibitor of apoptosis protein 1) levels. As for cell-autonomous cell death, this is caused not only by Dronc-mediated apoptosis (clones lacking both vps25 and Ark can die), but probably involves JNK and Hippo. In light of this, the authors discuss the possibilities of using vps25 mosaics for modelling cancer.

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Related articles in Development:

vps25 mosaics display non-autonomous cell survival and overgrowth, and autonomous apoptosis

Hans-Martin Herz, Zhihong Chen, Heather Scherr, Melinda Lackey, Clare Bolduc, and Andreas Bergmann
Development 2006 133: 1871-1880. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?