First published online May 1, 2006
Development 133, 1001e (2006)
© The Company of Biologists Limited
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.
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]
