Premium
The AP‐2 complex is required for proper temporal and spatial dynamics of endocytic patches in fission yeast
Author(s) -
de León Nagore,
Hoya Marta,
Curto M.Angeles,
Moro Sandra,
Yanguas Francisco,
Doncel Cristina,
Valdivieso M.Henar
Publication year - 2016
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.13327
Subject(s) - endocytic cycle , biology , endocytosis , microbiology and biotechnology , yeast , mutant , clathrin , cell , genetics , gene
Summary In metazoans the AP‐2 complex has a well‐defined role in clathrin‐mediated endocytosis. By contrast, its direct role in endocytosis in unicellular eukaryotes has been questioned. Here, we report co‐ immunoprecipitation between the fission yeast AP‐2 component Apl3p and clathrin, as well as the genetic interactions between apl3 Δ and clc1 and sla2 Δ /end4 Δ mutants. Furthermore, a double clc1 apl3 Δ mutant was found to be defective in FM4‐64 uptake. In an otherwise wild‐type strain, apl3 Δ cells exhibit altered dynamics of the endocytic sites, with a heterogeneous and extended lifetime of early and late markers at the patches. Additionally, around 50% of the endocytic patches exhibit abnormal spatial dynamics, with immobile patches and patches that bounce backwards to the cell surface, showing a pervasive effect of the absence of AP‐2. These alterations in the endocytic machinery result in abnormal cell wall synthesis and morphogenesis. Our results complement those found in budding yeast and confirm that a direct role of AP‐2 in endocytosis has been conserved throughout evolution.