Memo–RhoA–mDia1 signaling controls microtubules, the actin network, and adhesion site formation in migrating cells

• DOI: 10.1083/jcb.200805107
• Publication Date: 2008-10-28T15:53:15Z
• Authors: Kossay Zaoui; Stéphane Honoré; Daniel Isnardon; Diane Braguer; Ali Badache
• Keywords: Lamellipodium; Formins; MDia1; Pseudopodia; Cell polarity; Filopodia; Actin remodeling

Actin assembly at the cell front drives membrane protrusion and initiates migration cycle. Microtubules (MTs) extend within forward protrusions to sustain polarity promote adhesion site turnover. Memo is an effector of ErbB2 receptor tyrosine kinase involved in breast carcinoma migration. However, its mechanism action remained unknown. We report this study that controls ErbB2-regulated MT dynamics by altering transition frequency between growth shortening phases. Moreover, although Memo-depleted cells can assemble Rac1-dependent actin meshwork form lamellipodia, they show defective localization lamellipodial markers such as α-actinin-1 a reduced number short-lived sites underlying advancing edge migrating cells. Finally, we demonstrate required for RhoA guanosine triphosphatase mDia1 plasma Memo–RhoA–mDia1 signaling coordinates organization network, formation, outgrowth leading motility.