Research Article

You have full text access to this OnlineOpen article

Actin patch assembly proteins Las17p and Sla1p restrict cell wall growth to daughter cells and interact with cis-Golgi protein Kre6p

  1. Huijuan Li,
  2. Nicolas Pagé,
  3. Howard Bussey*

Article first published online: 29 AUG 2002

DOI: 10.1002/yea.904

Issue

Yeast

Yeast

Volume 19, Issue 13, pages 1097–1112, 30 September 2002

Additional Information

How to Cite

Li, H., Pagé, N. and Bussey, H. (2002), Actin patch assembly proteins Las17p and Sla1p restrict cell wall growth to daughter cells and interact with cis-Golgi protein Kre6p. Yeast, 19: 1097–1112. doi: 10.1002/yea.904

Author Information

  1. Department of Biology, McGill University, Montreal, Canada H3A 1B1

*Department of Biology, McGill University, Montreal, Quebec, Canada H3A 1B1.

Publication History

  1. Issue published online: 29 AUG 2002
  2. Article first published online: 29 AUG 2002
  3. Manuscript Accepted: 14 JUN 2002
  4. Manuscript Received: 21 FEB 2002

Funded by

  • NSERC, Canada

SEARCH

SEARCH BY CITATION

ARTICLE TOOLS

View Full Article (HTML) Get PDF (416K)

Keywords:

  • Golgi vesicle receptor;
  • cortical actin patch assembly;
  • cell wall synthesis;
  • β-1,6-glucan localization;
  • mother–daughter asymmetry

Abstract

The cytoplasmic tail of Kre6p, a Golgi membrane protein involved in cell wall synthesis, interacts with the actin patch assembly components Las17p and Sla1p in a two-hybrid assay, and Kre6p co-immunoprecipitates with Las17p. Kre6p showed extensive co-localization with Och1p-containing cis-Golgi vesicles. The correct localization of Kre6p requires its cytoplasmic tail, Las17p, Sla1p and Vrp1p, suggesting that the cytoplasmic tail of Kre6p acts as a receptor, linking this cis-Golgi protein to Las17p and Sla1p. The actin patch assembly mutants las17Δ, sla1Δ and vrp1Δ showed elevated levels of cell wall β-1,6-glucan, and mutant cells were capable of only a limited number of cell divisions compared to wild-type. EM image analysis and β-1,6-glucan localization indicated abnormal wall proliferation in the mother cells of these mutants. The pattern of cell wall hypertrophy indicates a failure to restrict cell wall growth to the bud. Copyright © 2002 John Wiley & Sons, Ltd.

View Full Article (HTML) Get PDF (416K)