z-logo
open-access-imgOpen Access
Insulin signaling modulates border cell movement in Drosophila oogenesis
Author(s) -
Aditi Sharma,
Sudipta Halder,
Martina Felix,
Khairun Nisaa,
Girish Deshpande,
Mohit Prasad
Publication year - 2018
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.15
H-Index - 36
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.166165
Subject(s) - biology , oocyte , microbiology and biotechnology , drosophila (subgenus) , nurse cell , border cells , insulin , oogenesis , cell , genetics , embryo , endocrinology , gene
As collective cell migration is intimately involved in different aspects of metazoan development, molecular mechanisms underlying this process are being explored in a variety of developmental contexts. Border cell (BC) migration during Drosophila oogenesis has emerged as an excellent genetic model for studying collective cell migration. BCs are of epithelial origin but acquire partial mesenchymal characteristics before migrating as a group towards the oocyte. Here we report that insulin signalling modulates collective BC movement during Drosophila oogenesis. Supporting the involvement of Insulin pathway, we demonstrate that compromising Insulin-like Receptor (dInR) levels in BCs, inhibits their migration. Furthermore, we show that canonical Insulin signalling pathway components participate in this process. Interestingly, visualization of dInR-depleted BC clusters, using time-lapse imaging, revealed a delay in detachment of BC clusters from the surrounding anterior follicle cells and altered protrusion dynamics. Lastly, based on genetic interactions between dInR, the polarity determinant, dPAR-1 and a regulatory subunit of Drosophila Myosin, (Spaghetti squash) we propose that Insulin signalling likely influences dPAR-1 activity to engineer border cell detachment and subsequent movement via Drosophila Myosin.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here