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A Highlights from MBoC Selection: Lipid domain–dependent regulation of single-cell wound repair

机译:来自MBOC选择的亮点:单细胞伤口修复的脂质结构域依赖性调节

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After damage, cells reseal their plasma membrane and repair the underlying cortical cytoskeleton. Although many different proteins have been implicated in cell repair, the potential role of specific lipids has not been explored. Here we report that cell damage elicits rapid formation of spatially organized lipid domains around the damage site, with different lipids concentrated in different domains as a result of both de novo synthesis and transport. One of these lipids—diacylglycerol (DAG)—rapidly accumulates in a broad domain that overlaps the zones of active Rho and Cdc42, GTPases that regulate repair of the cortical cytoskeleton. Formation of the DAG domain is required for Cdc42 and Rho activation and healing. Two DAG targets, protein kinase C (PKC) β and η, are recruited to cell wounds and play mutually antagonistic roles in the healing process: PKCβ participates in Rho and Cdc42 activation, whereas PKCη inhibits Rho and Cdc42 activation. The results reveal an unexpected diversity in subcellular lipid domains and the importance of such domains for a basic cellular process.
机译:损伤后,细胞重新膜质膜并修复下面的皮质细胞骨架。虽然许多不同的蛋白质涉及细胞修复,但尚未探讨特异性脂质的潜在作用。在这里,我们认为细胞损伤引发了在损伤部位周围的空间组织的脂质结构域的快速形成,其不同的脂质由于DE Novo合成和运输而浓缩在不同的结构域中。这些脂质 - 二酰基甘油(DAG)中的一种 - 在宽域中积聚在具有调节皮质细胞骨架修复的GTP酶的宽域中。 CDC42和RHO活化和愈合需要形成DAG结构域。募集两个DAG靶标,蛋白激酶C(PKC)β和η被募集到细胞伤口并在愈合过程中起相互拮抗作用:PKCβ参与RHO和CDC42活化,而PKCH抑制RHO和CDC42活化。结果揭示了亚细胞脂质结构域的意外多样性以及这种域的基本细胞过程的重要性。

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