植物 Bax 抑制剂-1 与 ATG6 相互作用，调节自噬和程序性细胞死亡。
Plant Bax Inhibitor-1 interacts with ATG6 to regulate autophagy and programmed cell death.
机构信息
a MOE Key Laboratory of Bioinformatics, Center for Plant Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences , Tsinghua University , Beijing , China.
b Department of Biology , Duke University , Durham , NC , USA.
出版信息
Autophagy. 2017 Jul 3;13(7):1161-1175. doi: 10.1080/15548627.2017.1320633.
Abstract
Autophagy is an evolutionarily conserved catabolic process and is involved in the regulation of programmed cell death during the plant immune response. However, mechanisms regulating autophagy and cell death are incompletely understood. Here, we demonstrate that plant Bax inhibitor-1 (BI-1), a highly conserved cell death regulator, interacts with ATG6, a core autophagy-related protein. Silencing of BI-1 reduced the autophagic activity induced by both N gene-mediated resistance to Tobacco mosaic virus (TMV) and methyl viologen (MV), and enhanced N gene-mediated cell death. In contrast, overexpression of plant BI-1 increased autophagic activity and surprisingly caused autophagy-dependent cell death. These results suggest that plant BI-1 has both prosurvival and prodeath effects in different physiological contexts and both depend on autophagic activity.
摘要
自噬是一种进化上保守的分解代谢过程，参与植物免疫反应中程序性细胞死亡的调节。然而，调节自噬和细胞死亡的机制尚不完全清楚。在这里，我们证明植物 Bax 抑制剂-1（BI-1），一种高度保守的细胞死亡调节剂，与 ATG6，一种核心自噬相关蛋白相互作用。BI-1 的沉默降低了由 N 基因介导的对烟草花叶病毒（TMV）和甲紫精（MV）的抗性诱导的自噬活性，并增强了 N 基因介导的细胞死亡。相比之下，植物 BI-1 的过表达增加了自噬活性，令人惊讶的是还导致了自噬依赖性细胞死亡。这些结果表明，植物 BI-1 在不同的生理环境中具有生存和死亡促进作用，并且都依赖于自噬活性。
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