A model for the response of the GSC niche to low levels of Hh signalling.

<p>(A) In wild-type niches En regulates Hh production in CpCs, which is then delivered to the neighbouring ECs via short, thin cytoplasmic extensions. Upon binding to the Ptc receptor, thus releasing Smo from inhibition, the Hh signal is transduced in ECs to regulate Dpp and Gbb production, which in turn act as survival factors to maintain the GSC population within the niche. (B) Mosaic niche containing <i>en</i> mutant CpCs unable to produce the Hh ligand. As a result, the transcription of the <i>dpp</i> and <i>gbb</i> genes in the adjacent ECs is compromised, resulting in GSC loss. Wild-type CpCs respond to this deficiency in Hh levels by directing Hh-rich long cytonemes towards the Hh-deprived ECs. (C) Blocking <i>smo</i> function prevents target gene activation and causes GSC depletion. Wild-type CpCs react to this deficient readout of Hh signalling by projecting Hh-coated long cytonemes towards the <i>smo</i> mutant ECs.