Tissue stem cells are dependent on their local microenvironment – the niche – for regulation of self-renewal and differentiation. In the Drosophila male germline, the niche comprises a set of 8-10 somatic cells called hub cells, which are located in a cluster at the anterior of the gonad. Specification of the niche is known to require Notch signalling and the transcription factor Bowl, but is not fully understood. Lindsey Wingert and Stephen DiNardo (p. ) now find that the Maf transcription factor Traffic jam (Tj) plays a key role in repressing hub cell development. In tj mutants, the number of somatic gonadal cells expressing hub markers increases. Tj is downregulated in hub cells in a Notch-dependent manner, and mutation of tj can rescue hub cell formation in Notch mutants. However, while Tj depletion can induce hub cell fate, it does not promote hub cell morphology or clustering. Instead, this requires Bowl activity – also probably acting downstream of Notch. Thus, Notch signalling regulates hub cell specification and hub assembly via different downstream effectors. Intriguingly, Maf factors are expressed in the mammalian gonad, where Notch also plays a role, raising the possibility that this mechanism is conserved.
