Abstract:
Stages 8, 9, and 10 of Drosophila oogenesis are critical for border cell (BC) migration. During stage 8, migration initiation occurs, while stage 9 sees BCs traversing nurse cells toward the oocyte. By stage 10, BCs reach the oocyte, necessitating close contact. In collective cell migration (CCM), the leading cells in the cohort generate forward protrusions, and lagging cells make backward retractions in a harmonized and concerted manner. Effectively, the actin cytoskeleton stands as the leading driver of protrusion formation and retractions. Using Drosophila melanogaster as a model, we study collective cell migration (CCM) in border cells (BCs). Singed (the vertebrate homolog of fascin) and the Arp2/3 complex genetically interact to regulate F-actin architecture in BCs. Depletion of both hindered migrations, leading to a substantial cell migration defect. Both collaborate to regulate F-actin density in border cell clusters. The consequence of F-actin alteration is manifested upon cluster shape and area as clusters become large and rounded. As the BC cluster’s shape depends on mechanical and physiological behavior of the individual border cell, we can predict a relationship between shape increase and border cell number. Our experiment focuses on three signaling pathways governing migration: a global steroid-hormone signal coordinating migration timing, a localized cytokine signal activating the Jak-Stat pathway for migration induction, and a growth factor guiding cells to their destination. We have made an experimental setup to observe each of the individual cells of the cluster and count their number through fixed imaging for both control and double knockdown. Furthermore, we are trying to find the correlation of stat92E and slbo with singed and arp2 during border cell migrations through genetic interaction studies.
