Human Bin3 complements the F-actin localization defects caused by loss of Hob3p, the fission yeast homolog of Rvs161p

doi:10.1074/jbc.M101096200

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Papers In Press, published online ahead of print March 23, 2001
J. Biol. Chem, 10.1074/jbc.M101096200
Submitted on February 5, 2001
Revised on March 22, 2001
Accepted on March 23, 2001

Human Bin3 complements the F-actin localization defects caused by loss of Hob3p, the fission yeast homolog of Rvs161p

Eric L. Routhier, Timothy C. Burn, Ilgar Abbaszade, Matthew Summers, Charles F. Albright, and George C. Prendergast

Cancer Research Group, DuPont Pharmaceuticals Company, Glenolden, PA 19036

Corresponding Author: george.c.prendergast{at}dupontpharma.com

The BAR adaptor proteins Rvs167p and Rvs161p from Saccharomyces cerevisiae form a complex that regulates actin, endocytosis, and viability following starvation or osmotic stress. In this study, we identified a mammalian homolog of Rvs161p, termed Bin3 (Bridging INtegrator-3), and a Schizosaccharomyces pombe homolog of Rvs161p, termed Hob3p (Homolog Of Bin3). In mouse tissues, the Bin3 gene was expressed ubiquitously except for brain. S. pombe cells lacking Hob3p were often multinucleate and characterized by increased amounts of Calcofluor-stained material and mislocalized F-actin. For example, while wild-type cells localized F-actin to cell ends during interphase, hob3 mutants had F-actin patches distributed randomly around the cell. In addition, medial F-actin rings were rarely found in hob3 mutants. Notably, in contrast to S. cerevisiae rvs161 mutants, hob3 mutants showed no measurable defects in endocytosis or response to osmotic stress, yet hob3+ complemented the osmosensitivity of a rvs161 mutant. Bin3 failed to rescue the osmosensitivity of rvs161, but the actin localization defects of hob3 mutants were completely rescued by Bin3 and partially rescued by RVS161. These findings suggest that Hob3p and Bin3 regulate F-actin localization, like Rvs161p, but that other roles for this gene have diverged somewhat during evolution.

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