Open AccessThe Saccharomyces cerevisiae Arf3 protein is involved in actin cable and cortical patch formation
Author(s) -
Lambert Alexandra A.,
Perron Marjorie P.,
Lavoie Elyse,
Pallotta Dominick
Publication year - 2007
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2007.00239.x
Subject(s) - biology , microbiology and biotechnology , actin remodeling , actin cytoskeleton , profilin , mdia1 , actin remodeling of neurons , actin , cytoskeleton , genetics , cell
We show that Arf3p, a member of the ADP ribosylation family, is involved in the organization of actin cables and cortical patches in Saccharomyces cerevisiae . Profilin‐deficient cells ( pfy1 Δ) have severe growth defects and lack actin cables. Overexpression of ARF3 restores actin cables and corrects growth defects in these cells. Cells deficient for the cortical patch proteins Las17p and Vrp1p have growth defects and a random cortical patch distribution. Overexpression of ARF3 in las17 Δ and in vrp1 Δ cells partially corrects growth defects and restores the polarized distribution of cortical patches. The N‐terminal glycine, a myristoylation site in Arf3p, is necessary for its suppressor activity. arf3 Δ cells show a random budding pattern. Overexpression of BNI1 , GEA2 or SYP1 , three genes involved in actin cytoskeleton formation, restores the normal axial budding pattern of arf3 Δ cells. BUD6 is a polarity gene and GEA2 is involved in retrograde transport and the organization of the actin cytoskeleton. We have identified genetic interactions between ARF3 and BUD6 , and between ARF3 and GEA2 . Both double mutant strains have actin cytoskeleton defects. Our results support a role for ARF3 in cell polarity and the organization of the actin cytoskeleton.