Role of Polarity and BAR domain proteins in plasma membrane re-modelling in syncytial Drosophila embryos

Abstract

Extensive plasma membrane remodelling is a hallmark of epithelial cells during their division. The syncytial stage of early Drosophila embryogenesis is an excellent model for studying mechanisms involved in epithelial-like plasma membrane remodelling. The apical microvilli present in the pseudo-epithelial cells in interphase get reduced in the metaphase stage of each cortical nuclear division cycle. This is also concurrent with the extension of the lateral plasma membrane in between adjacent nuclei. Effective remodelling requires the interaction of adhesion, polarity, cytoskeletal remodelling and membrane trafficking proteins. BAR domain containing proteins link cytoskeletal and plasma membrane dynamics. We find that polarity protein Bazooka and cytoskeletal regulator septin, Peanut are essential for the establishment of hexagon dominance in the polygonal array of cells at metaphase of nuclear cycle 12. Bazooka and Peanut are present on the lateral membrane at the edges and vertices, respectively and regulate efficient endocytosis of the DE-cadherin. I-BAR domain containing protein Missing-in-metastasis in the syncytial embryos of Drosophila melanogaster (DMIM) have a role in microvilli remodelling from interphase to metaphase. Microvilli remain long and abundant in both interphase and metaphase of the syncytial division cycle 12 in DMIM depleted embryos. DMIM is present on the apical membrane from interphase to prometaphase during the time period of villi remodelling. There is a loss of furrow extension and the epithelial-like polygonal array is unstable here as well. DMIM allows for the proper recruitment of actin-regulatory proteins and membrane trafficking at the cortex to promote the remodelling of villi and the formation of furrows in the syncytial division cycle. We found that the Rac-GTP pathway regulates the recruitment of DMIM for villi remodelling and a decrease in activated Rac leads to aberrant association of MIM during villi remodelling. Our studies find an essential role for DMIM recruitment at a precise time to affect villi remodelling during embryogenesis in early Drosophila embryogenesis.