8 pages, 5 figures.-- PMID: 18171682 [PubMed].-- Printed version published Feb 2008.-- Supporting information (Suppl. table S1, figure S1) available at: http://dev.biologists.org/cgi/content/full/135/3/533/DC1The existence of specialised regulatory microenvironments or niches that sustain stable stem cell populations is well documented in many tissues. However, the specific mechanisms by which niche support (or stromal) cells govern stem cell maintenance remain largely unknown. Here we demonstrate that removal of the Jak/Stat pathway in support cells of the Drosophila ovarian niche leads to germline stem cell loss by differentiation. Conversely, ectopic Jak/Stat activation in support cells induces stem cell tumours, implying the presence of a signal relay between the stromal compartment and the stem cell population. We further show that ectopic Jak/Stat signalling in support cells augments dpp mRNA levels and increases the range of Dpp signalling, a Bmp2 orthologue known to act as a niche extrinsic factor required for female germline stem cell survival and division. Our results provide strong evidence for a model in which Jak/Stat signalling in somatic support cells regulates dpp transcription to define niche size and to maintain the adjacent germline stem cells in an undifferentiated state.[To be completed upon receiving the author full-text version of the paper]Peer reviewed