Degradation of the Endoplasmic Reticulum by Autophagy during Endoplasmic Reticulum Stress in Arabidopsis
Degradation of the Endoplasmic Reticulum by Autophagy during Endoplasmic Reticulum Stress in Arabidopsis
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DOI：
10.1105/tpc.112.101535
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发表时间：
2012-11-01
期刊：
影响因子：
11.6
通讯作者：
Bassham, Diane C.
中科院分区：
文献类型：
--
作者：
Liu, Yimo;Burgos, Junmarie Soto;Bassham, Diane C.
在本文中，我们表明拟南芥的内质网（ER）在 ER 应激过程中会发生结构形态变化，这可归因于自噬。自噬体产生的增加证明了内质网应激剂会触发自噬。响应 ER 应激，可溶性 ER 标记物定位于自噬体，并在液泡蛋白酶受到抑制后在液泡中积累。在自噬体内部观察到用核糖体装饰的膜片，表明内质网应激期间内质网的部分通过自噬传递到液泡。此外，还发现内质网应激诱导的自噬需要内质网应激传感器肌醇需要酶-1b (IRE1b)。然而，IRE1b 剪接靶标 bZIP60 似乎并未参与其中，这表明植物中存在一条未被发现的信号通路来调节内质网应激诱导的自噬。总之，这些结果表明自噬是植物响应内质网应激而内质网膜及其内容物更新的途径。
In this article, we show that the endoplasmic reticulum (ER) in Arabidopsis thaliana undergoes morphological changes in structure during ER stress that can be attributed to autophagy. ER stress agents trigger autophagy as demonstrated by increased production of autophagosomes. In response to ER stress, a soluble ER marker localizes to autophagosomes and accumulates in the vacuole upon inhibition of vacuolar proteases. Membrane lamellae decorated with ribosomes were observed inside autophagic bodies, demonstrating that portions of the ER are delivered to the vacuole by autophagy during ER stress. In addition, an ER stress sensor, INOSITOL-REQUIRING ENZYME-1b (IRE1b), was found to be required for ER stress-induced autophagy. However, the IRE1b splicing target, bZIP60, did not seem to be involved, suggesting the existence of an undiscovered signaling pathway to regulate ER stress-induced autophagy in plants. Together, these results suggest that autophagy serves as a pathway for the turnover of ER membrane and its contents in response to ER stress in plants.