Proteasomal Degradation Resolves Competition between Cell Polarization and Cellular Wound Healing
Proteasomal Degradation Resolves Competition between Cell Polarization and Cellular Wound Healing
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DOI：
10.1016/j.cell.2012.05.030
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发表时间：
2012-07-06
期刊：
影响因子：
64.5
通讯作者：
Pellman, David
中科院分区：
文献类型：
--
作者：
Kono, Keiko;Saeki, Yasushi;Pellman, David
细胞创伤愈合，使膜损伤的修复，是普遍存在于真核生物。伤口愈合反应的一个方面是将极化的细胞骨架和分泌机制重定向到损伤部位。虽然最近在鉴定参与伤口愈合的保守蛋白质方面取得了进展，但将这些组分连接成一致反应的机制尚未确定。使用激光损伤芽殖酵母，我们表明，局部细胞壁/膜损伤触发的蛋白质的分散从极化生长的网站，使其在伤口处的积累。我们定义了一个蛋白激酶C依赖的机制，介导的破坏的p53 Bni 1和外囊组分Sec 3。这种降解对于防止极化生长位点与伤口之间的竞争至关重要。克服来自预先存在的极化细胞骨架的竞争的机制可能是极化细胞中有效伤口愈合的一般特征。
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 preexisting polarized cytoskeleton may be a general feature of effective wound healing in polarized cells.