Transformation of epithelial cells to migratory fate is quite prevalent in the metazoans. It is integral to gastrulation, organ morphogenesis, tissue repair and unfortunately disease progression like tumor cell metastasis. We are employing the genetic model of border cell migration in Drosophila oogenesis as to understand how intercellular communication modulates transformation of epithelial follicle cells to migratory fate. In this regard, we are specifically examining how intercellular communication among the Somatic follicle cells and between the Somatic follicle cells-Germline nurse cells regulate border cell fate specification. 

We proposed novel function of gap junction protein Innexin2 in border cell fate specification. Specifically we demostrated that Inx2 regulates interfollicular cells communication through  calcium fluxes thus modulating JAK-STAT signaling and border cell fate specification (Sahu et al. 2017). 

Our recent data suggests that germline nurse cell also plays a non-autonomous role in modulating the number of follicle cells that acquire migratory border cell fate. Here we are characterizing the role of RNA binding protein Cup in border cell fate specification. (Saha et al.2023)

Group cell movement that retain intercellular adhesion is commonly referred to as collective cell migration.  This kind of cellular movement is context dependent and is critical for various physiological processes including morphogenesis (mammary gland development), angiogenesis (vascular sprouting), nervous system development (neural crest migration), wound healing (sheet migration) and tumor cell movement (cluster movement). Though collective cell movement is physiologically very relevant, it has been studied less extensively than single cell movement. 

We are exploiting the powerful combination of sophisticated genetic analysis together with live-imaging to elucidate the molecular and cellular mechanisms that govern the collective migration  employing the model of border cell migration in Drosophila oogenesis. 

Specifically we have demonstrated the p21 activated kinase 3 functions downstream of guidance signal to regulate the asymmetric distribution of polarity proteins thus enabling efficient cluster movement (Felix et al 2015). 

In addition, we have shown that Drosophila Insulin signaling (InS) modulate border cell movement. Our results suggest that InS likely influences Par-1 activity to engineer border cell detachment and subsequent movement via Drosophila Myosin (Sharma et al 2018).