Format

Send to

Choose Destination
PLoS One. 2014 Aug 26;9(8):e106211. doi: 10.1371/journal.pone.0106211. eCollection 2014.

Notch inhibits Yorkie activity in Drosophila wing discs.

Author information

1
Department of Physiology Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; IRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France; INSERM, U896, Montpellier, France; Université Montpellier1, Montpellier, France; Institut régional du Cancer Montpellier, Montpellier, France.
2
IRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France; INSERM, U896, Montpellier, France; Université Montpellier1, Montpellier, France; Institut régional du Cancer Montpellier, Montpellier, France.
3
Department of Physiology Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom.

Abstract

During development, tissues and organs must coordinate growth and patterning so they reach the right size and shape. During larval stages, a dramatic increase in size and cell number of Drosophila wing imaginal discs is controlled by the action of several signaling pathways. Complex cross-talk between these pathways also pattern these discs to specify different regions with different fates and growth potentials. We show that the Notch signaling pathway is both required and sufficient to inhibit the activity of Yorkie (Yki), the Salvador/Warts/Hippo (SWH) pathway terminal transcription activator, but only in the central regions of the wing disc, where the TEAD factor and Yki partner Scalloped (Sd) is expressed. We show that this cross-talk between the Notch and SWH pathways is mediated, at least in part, by the Notch target and Sd partner Vestigial (Vg). We propose that, by altering the ratios between Yki, Sd and Vg, Notch pathway activation restricts the effects of Yki mediated transcription, therefore contributing to define a zone of low proliferation in the central wing discs.

PMID:
25157415
PMCID:
PMC4144958
DOI:
10.1371/journal.pone.0106211
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center