JNK protects Drosophila from oxidative stress by trancriptionally activating autophagy.
JNK protects Drosophila from oxidative stress by trancriptionally activating autophagy.
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DOI：
10.1016/j.mod.2009.06.1082
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发表时间：
2009-08
影响因子：
2.6
通讯作者：
Bohmann, Dirk
中科院分区：
文献类型：
--
作者：
Wu, Hai;Wang, Meng C.;Bohmann, Dirk
JNK signaling functions to induce defense mechanisms that protect organisms against acute oxidative and xenobiotic insults. Using Drosophila as a model system, we investigated the role of autophagy as such a JNK-regulated protective mechanism. We show that oxidative stress can induce autophagy in the intestinal epithelium by a mechanism that requires JNK signaling. Consistently, artificial activation of JNK in the gut gives rise to an autophagy phenotype. JNK signaling can induce the expression of several autophagy-related (ATG) genes, and the integrity of these genes is required for the stress protective function of the JNK pathway. In contrast to autophagy induced by oxidative stress, non-stress related autophagy, as it occurs for example in starving adipose or intestinal tissue, or during metamorphosis, proceeds independently of JNK signaling. Autophagy thus emerges as a multifunctional process that organisms employ in a variety of different situations using separate regulatory mechanisms.
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