# MIM triggers formin to Arp2/3-based actin assembly in membrane remodeling in Drosophila embryos

## TL;DR

This study shows how the protein MIM helps reshape cell membranes during early fly embryo development by organizing actin networks.

## Contribution

The study identifies MIM as a key regulator of actin and endocytic dynamics during Drosophila syncytial divisions.

## Key findings

- MIM promotes branched actin networks and endocytosis during membrane remodeling in Drosophila embryos.
- MIM depletion disrupts furrow extension and increases apical protrusions with formin diaphanous.
- MIM balances actin networks with RhoGEF2 and diaphanous to enable cyclical membrane remodeling.

## Abstract

DMIM (also called MTSS1) promotes Rac1-mediated branched actin network formation and endocytosis to drive rapid, cyclical plasma membrane remodeling during embryonic syncytial divisions. Loss of DMIM leads to decreased branched actin networks and a coincident increase in bundled actin networks induced by RhoGEF2 and diaphanous.

BAR domain–containing proteins are key regulators of endocytosis and actin remodeling. Their function in morphogenesis remains to be investigated. We report that the I-BAR domain–containing protein, missing-in-metastasis (MIM) (also called MTSS1), promotes branched actin network formation and endocytosis to drive rapid, cyclical plasma membrane remodeling during syncytial divisions in Drosophila embryos. Actin-rich villous protrusions in the apical caps in interphase are depleted in metaphase, concurrent with furrow extension between adjacent nuclei. MIM depletion results in a loss of furrow extension and in longer, more abundant apical protrusions containing the formin diaphanous. Branched actin networks promoted by MIM are in balance with bundled actin networks induced by RhoGEF2 and diaphanous. Cyclical recruitment of MIM to the cortex promotes localization of active Rac, the WAVE regulatory complex, and the Arp2/3 complex to drive endocytic membrane remodeling. These findings identify MIM as an integrator of actin and endocytic dynamics that enables rapid membrane remodeling during Drosophila syncytial division cycles.