Proteasomal degradation resolves competition between cell polarization and cellular wound healing

Keiko Kono, Yasushi Saeki, Satoshi Yoshida, Keiji Tanaka, David Pellman

研究成果: Article査読

60 被引用数 (Scopus)

抄録

Cellular wound healing, enabling the repair of membrane damage, is ubiquitous in eukaryotes. One aspect of the wound healing response is the redirection of a polarized cytoskeleton and the secretory machinery to the damage site. Although there has been recent progress in identifying conserved proteins involved in wound healing, the mechanisms linking these components into a coherent response are not defined. Using laser damage in budding yeast, we demonstrate that local cell wall/membrane damage triggers the dispersal of proteins from the site of polarized growth, enabling their accumulation at the wound. We define a protein-kinase-C-dependent mechanism that mediates the destruction of the formin Bni1 and the exocyst component Sec3. This degradation is essential to prevent competition between the site of polarized growth and the wound. Mechanisms to overcome competition from a pre-existing polarized cytoskeleton may be a general feature of effective wound healing in polarized cells.

本文言語English
ページ(範囲)151-164
ページ数14
ジャーナルCell
150
1
DOI
出版ステータスPublished - 2012 7 6
外部発表はい

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学(全般)

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