title: The WASp homologue Las17p functions with the WIP homologue End5p/verprolin and is essential for endocytosis in yeast.
abstract: Several end mutations that block the internalisation step of endocytosis in Saccharomyces cerevisiae also affect the cortical actin cytoskeleton [1]. END5 encodes a proline-rich protein (End5p or verprolin) required for a polarised cortical actin cytoskeleton and endocytosis [2,3]. End5p interacts with actin [4], but its exact function is not yet known. To help elucidate End5p function, we sought other End5p-interacting proteins and identified the LAS17/BEE1 gene (encoding the yeast homologue of the human Wiskott-Aldrich Syndrome protein, WASp) as a high-copy-number suppressor of the temperature-sensitive growth and endocytic defects of end5-1 cells (carrying a frameshift mutation affecting the last 213 residues of End5p). LAS17 is unable to suppress a full deletion of END5 (end5 delta), however, suggesting that the defective End5-1p in end5-1 mutants may be stabilised by Las17p. The amino terminus of Las17p interacts with the carboxyl terminus of End5p in the yeast two-hybrid system and similar interactions have been shown between WASp and a mammalian End5p homologue, WASp-interacting protein (WIP) [5]. As las17 delta deletion mutants are blocked in endocytosis, we conclude that Las17p and End5p interact and are essential for endocytosis.
authors.affiliation: Institute of Molecular Agrobiology, National University of Singapore, Republic of Singapore.
authors.forename: S N
authors.initials: SN
authors.lastname: Naqvi
authors.forename: R
authors.initials: R
authors.lastname: Zahn
authors.forename: D A
authors.initials: DA
authors.lastname: Mitchell
authors.forename: B J
authors.initials: BJ
authors.lastname: Stevenson
authors.forename: A L
authors.initials: AL
authors.lastname: Munn
mesh_terms: D002352:Carrier Proteins / Q000502:physiology; D003598:Cytoskeletal Proteins; D004705:Endocytosis / Q000502:physiology*; D016368:Frameshift Mutation; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism*; D018628:Gene Dosage; D005800:Genes, Fungal; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000502:physiology; D011993:Recombinant Fusion Proteins; D012441:Saccharomyces cerevisiae / Q000235:genetics / Q000502:physiology*; D029701:Saccharomyces cerevisiae Proteins; D017384:Sequence Deletion; D013489:Suppression, Genetic; D013696:Temperature; D014923:Wiskott-Aldrich Syndrome; D051316:Wiskott-Aldrich Syndrome Protein; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal
chemical_list: D002352:Carrier Proteins; D003598:Cytoskeletal Proteins; D005656:Fungal Proteins; D047908:Intracellular Signaling Peptides and Proteins; C480361:LAS17 protein, S cerevisiae; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins; D011993:Recombinant Fusion Proteins; D029701:Saccharomyces cerevisiae Proteins; C090350:VRP1 protein, S cerevisiae; C495771:WASL protein, human; C109903:WIPF1 protein, human; D051316:Wiskott-Aldrich Syndrome Protein; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal