6月21日，Cell雜志報道,，科學(xué)家揭示一種PKC依賴的新機制可預(yù)防細胞損傷部位與極化細胞骨架之間的競爭，進而促進細胞愈合。
細胞損傷的愈合作用,，使細胞膜損傷得以修復(fù)，在真核生物中是普遍存在的,。損傷愈合反應(yīng)的一個重要方面是極化的細胞骨架和細胞內(nèi)分泌機器朝向損傷位點的重新定向,。
雖然關(guān)于參與損傷愈合過程的保守蛋白的研究屢有進展，科學(xué)家一直沒能將這些參與成員聯(lián)系為一個連貫的反應(yīng)機制,。通過在芽殖酵母中使用激光損傷的方法,，研究者證明，局部細胞壁/膜的損傷觸發(fā)蛋白質(zhì)從極性生長部位擴散,，從而使這些蛋白在傷口部位積累,。
研究者發(fā)現(xiàn)了一個蛋白激酶-C依賴的機制，可介導(dǎo)成形素蛋白Bni1（一組參與肌動蛋白聚合并與快速增長的肌動蛋白微絲末端相關(guān)的蛋白）和胞吐囊組件Sec3蛋白的降解,。
這種蛋白降解對防止極化生長部位和細胞損傷部位之間的相互競爭構(gòu)建的原材料是必不可少的,。避免與預(yù)先存在的極化細胞骨架發(fā)生競爭，可能是高效的極化細胞損傷愈合的一般特征,。
該研究,，為眾多細胞損傷相關(guān)疾病，如,，心肌細胞,、神經(jīng)細胞損傷，肌肉萎縮等的研究提供了新的啟示,。（生物谷bioon.com）
doi:10.1016/j.cell.2011.10.017
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Proteasomal Degradation Resolves Competition between Cell Polarization and Cellular Wound Healing
Keiko Kono, Yasushi Saeki, Satoshi Yoshida, Keiji Tanaka, David Pellman
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.
