WASP suppresses the growth defect of Saccharomyces cerevisiae las17Δ strain in the presence of WIP

Abstract

Wiskott–Aldrich syndrome is caused by alterations in the Wiskott–Aldrich syndrome protein (WASP) and several of these mutations affect WASP’s interaction with WIP (WASP-interacting protein), suggesting that loss of interaction between WASP and WIP is causal to the disease. Las17p is the yeast homologue of WASP and las17Δ strain is unable to grow at 37 °C. We show that Human WASP suppresses the growth defect of Saccharomyces cerevisiae las17Δ strain, only in the presence of WIP. WIP mediates cortical localisation of WASP as well as stabilise WASP in yeast cells. Mutations which affected WASP–WIP interaction abolished WASP’s ability to suppress the growth defect of las17Δ strain. We have demonstrated that WASP–WIP is an active complex and WASP’s ability to suppress the growth defect of las17Δ strain is dependent on the presence of a functional Arp2/3 activating domain of WASP and also the Verprolin domain (V) of WIP.