Fig. 8. Model for Hh signaling in border cells.

Upd signaling from the polar cells activates JAK/STAT in surrounding border cells (reviewed in Montell et al., 2012). JAK/STAT triggers expression of slbo and other genes required for border cell fate and motility. Hh is a downstream target of JAK/STAT but is independent of Slbo. Hh may be upstream (1) of active Rac (Rac-GTP), for example if it regulates the expression of genes required for Rac regulation such as a guanine-nucleotide exchange factor (GEF). Alternatively, the genetic data are consistent with Hh functioning with (2, 3), or in parallel to (4) Rac-GTP, possibly through Par-1 (for simplicity not shown). Hh could upregulate Rac levels in border cells (2), act downstream of Rac on presently unknown targets (3) and/or regulate E-cad/p-Tyr localization in parallel to Rac (4). Together, the border cell signaling pathways converge to direct collective border cell migration in response to a gradient of guidance signals secreted from the oocyte via the RTKs, PVR/EGFR. Hh is active in each border cell and likely received by the same cell, although autocrine signaling between cells in the cluster could also occur (arrows, border cell schematic). See text for additional details.