Gap junction (GJ) proteins, the primary constituents of GJ channels, are conserved determinants of patterning. Canonically, a GJ channel, made up of two hemi-channels contributed by the neighboring cells, facilitates transport of metabolites/ions. Here we demonstrate the involvement of GJ proteins during cuboidal to squamous epithelial transition displayed by the anterior follicle cells (AFCs) from Drosophila ovaries. Somatically derived AFCs stretch and flatten when the adjacent germline cells start increasing in size. GJ proteins, Innexin2 (Inx2) and Innexin4 (Inx4), functioning in the AFCs and germline respectively, promote the shape transformation by modulating calcium levels in the AFCs. Our observations suggest that alterations in calcium flux potentiate STAT activity to influence actomyosin-based cytoskeleton, possibly resulting in disassembly of adherens junctions. Our data have uncovered sequential molecular events underlying the cuboidal to squamous shape transition and offer unique insight into how GJ proteins expressed in the neighboring cells contribute to morphogenetic processes.

Specification of migratory cell fate from a stationary population is complex and indispensable both for metazoan development as well for the progression of the pathological condition like tumor metastasis. Though this cell fate transformation is widely prevalent, the molecular understanding of this phenomenon remains largely elusive. We have employed the model of border cells (BC) in Drosophila oogenesis and identified germline activity of an RNA binding protein, Cup that limits acquisition of migratory cell fate from the neighbouring follicle epithelial cells. As activation of JAK-STAT in the follicle cells is critical for BC specification, our data suggest that Cup, non-cell autonomously restricts the domain of JAK-STAT by activating Notch in the follicle cells. Employing genetics and Delta endocytosis assay, we demonstrate that Cup regulates Delta recycling in the nurse cells through Rab11GTPase thus facilitating Notch activation in the adjacent follicle cells. Since Notch and JAK-STAT are antagonistic, we propose that germline Cup functions through Notch and JAK-STAT to modulate BC fate specification from their static epithelial progenitors.

Attaining migratory fate from a stationary cell population is complex and indispensable both for the multicellular organism development as well for the pathological condition like tumor metastasis. Though widely prevalent in the metazoans, the molecular understanding of this phenomenon remains elusive. Specification of migratory border cells from the follicular epithelium during Drosophila oogenesis has emerged as one of the excellent model systems to study motile cell fate transitions. JAK-STAT activation in the 6-10 anterior most follicle cells of the Drosophila egg chamber transforms them to a migratory cluster called the border cells. We show that a nurse cell protein, Cup, non-cell autonomously restricts the domain of JAK-STAT activation in the anterior follicle cells. Further examination suggests that Cup functions through Rab11GTPase to regulate Delta trafficking in the nurse cells potentiating Notch activation in the anterior follicle cells. Since Notch activity in the follicle cells modulates the JAK-STAT, any perturbation in Notch activation affects the border cell fate. Altogether, we propose that germline Cup affects the border cell fate through appropriate activation of Notch and JAK-STAT signaling in the follicle cells.

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