FEATURES

DESCRIPTION

Also known as ICSA_SHIFL, icsA, virG. Essential for bacterial spreading by eliciting polar deposition of filamentous actin (actin-based motility). Inside the host cell mediates nucleation and polymerization of actin molecules on the bacterial surface, which provides the propulsive force for intracellular movement and intercellular dissemination of the bacterium. During invasion of mammalian cells, triggers autophagy by binding to APG5L. Interaction with IcsB leads to escape from the autophagic host defense system. Also binds ATP and displays weak ATPase activity. Forms a ternary complex with host WASL (neural Wiskott-Aldrich syndrome protein) and ARP2/3. IcsA enhances the affinity of WASL for ARP2/3, thus assembling a tight complex which has maximal activity in actin assembly. Also binds directly to host vinculin, which may serve as an actin filament recruiter.

EXTERNAL LINKS

icsA

Mutations

Mutation(s) distribution

Mutations table