Format

Send to

Choose Destination
Curr Biol. 2010 Mar 9;20(5):458-63. doi: 10.1016/j.cub.2010.01.038.

Retinoids regulate a developmental checkpoint for tissue regeneration in Drosophila.

Author information

1
Department of Molecular and Cell Biology, University of California, Berkeley, 365 LSA, MC 3200, Berkeley, CA 94720, USA.

Abstract

Damage to Drosophila imaginal discs elicits a robust regenerative response from the surviving tissue [1-4]. However, as in other organisms, developmental progression and differentiation can restrict the regenerative capacity of Drosophila tissues. Experiments in Drosophila and other holometabolous insects have demonstrated that either damage to imaginal tissues [5, 6] or transplantation of a damaged imaginal disc [7, 8] delays the onset of metamorphosis. Therefore, in Drosophila there appears to be a mechanism that senses tissue damage and extends the larval phase to coordinate tissue regeneration with the overall developmental program of the organism. However, how such a pathway functions remains unknown. Here we demonstrate that a developmental checkpoint extends larval growth after imaginal disc damage by inhibiting the transcription of the gene encoding PTTH, a neuropeptide that promotes the release of the steroid hormone ecdysone. Using a genetic screen, we identify a previously unsuspected role for retinoid biosynthesis in regulating PTTH expression and delaying development in response to tissue damage. Retinoid signaling plays an important but poorly defined role in several vertebrate regeneration models [9-11]. Our findings demonstrate that retinoid biosynthesis in Drosophila is important for the maintenance of a condition that is permissive for regenerative growth.

PMID:
20189388
PMCID:
PMC2847081
DOI:
10.1016/j.cub.2010.01.038
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center