The large Maf factor Traffic jam functions to repress hub cell fate in the developing germline stem cell niche. Lindsey Wingert, Steve DiNardo. Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA.

   The Drosophila testis is an excellent system for studying stem cell-niche interactions. The hub (niche) cells residing at the apical tip of the testis provide germline stem cells (GSCs) and cyst stem cells (CySCs) with signals promoting self-renewal and attachment. The somatic component of the testis is derived from a pool of somatic gonadal precursors (SGPs). SGPs facilitate the coalescence and compaction of the gonad through Ecadherin-mediated adhesion (Jenkins et al., 2003). Hub cell specification among SGPs is dependent on interaction with two additional cell populations. Notch activation by endodermal gut cells acts to positively specify hub cell fate while EGFR activation by germ cells acts to repress hub cell fate (Kitadate et al., 2007; Kitadate and Kobayash, 2010; Okegbe and DiNardo, 2011). Positively-specified hub cells undergo a mesenchymal to epithelial transition (MET) as they sort away from germ cells toward the periphery at the anterior pole of the gonad. During this process, they maximize attachments to each other via adherens and septate junctions and anchor via integrins (Le Bras and Van Doren, 2006; Tanentzapf et al., 2007). The remaining non-hub SGPs maintain their mesenchymal identity and encystment of germ cells. We are investigating Traffic jam (Tj), a transcription factor expressed in SGPs then downregulated in hub cells, for its role in MET. Tj mutant gonads display ectopic, epithelialized cells by septate and adherens junctional markers. These ectopic cells also express unpaired which encodes one of the self-renewal factors secreted by hub cells. We suspect that Tj functions in non-hub SGPs to maintain their preferential adhesion for germ cells in order to prevent them from becoming hub (Li et al., 2007).