Minina Elena A, Filonova Lada H, Fukada Kazutake, Savenkov Eugene I, Gogvadze Vladimir, Clapham David, Sanchez-Vera Victoria, Suarez Maria F, Zhivotovsky Boris, Daniel Geoffrey, Smertenko Andrei, Bozhkov Peter V
J Cell Biol. 2013 Dec 23;203(6):917-27. doi: 10.1083/jcb.201307082.
Although animals eliminate apoptotic cells using macrophages, plants use cell corpses throughout development and disassemble cells in a cell-autonomous manner by vacuolar cell death. During vacuolar cell death, lytic vacuoles gradually engulf and digest the cytoplasmic content. On the other hand, acute stress triggers an alternative cell death, necrosis, which is characterized by mitochondrial dysfunction, early rupture of the plasma membrane, and disordered cell disassembly. How both types of cell death are regulated remains obscure. In this paper, we show that vacuolar death in the embryo suspensor of Norway spruce requires autophagy. In turn, activation of autophagy lies downstream of metacaspase mcII-Pa, a key protease essential for suspensor cell death. Genetic suppression of the metacaspase–autophagy pathway induced a switch from vacuolar to necrotic death, resulting in failure of suspensor differentiation and embryonic arrest. Our results establish metacaspase-dependent autophagy as a bona fide mechanism that is responsible for cell disassembly during vacuolar cell death and for inhibition of necrosis.
虽然动物利用巨噬细胞清除凋亡细胞,但植物在整个发育过程中利用细胞尸体,并通过液泡细胞死亡以细胞自主的方式拆解细胞。在液泡细胞死亡过程中,裂解液泡逐渐吞噬并消化细胞质内容物。另一方面,急性应激会引发另一种细胞死亡——坏死,其特征是线粒体功能障碍、质膜早期破裂和细胞拆解紊乱。这两种细胞死亡是如何被调控的仍不清楚。在本文中,我们表明挪威云杉胚胎胚柄中的液泡死亡需要自噬。反过来,自噬的激活位于metacaspase mcII-Pa的下游,metacaspase mcII-Pa是胚柄细胞死亡所必需的一种关键蛋白酶。对metacaspase-自噬途径的基因抑制导致了从液泡死亡到坏死死亡的转变,从而导致胚柄分化失败和胚胎停滞。我们的结果确立了metacaspase依赖性自噬是一种真正的机制,它负责液泡细胞死亡期间的细胞拆解和坏死的抑制。