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Alleviating Chronic ER Stress by p38-Ire1-Xbp1 Pathway and Insulin-associated Autophagy in C. elegans Neurons
Liying Guan, Zhigao Zhan, Yongzhi Yang, Yue Miao, Xun Huang, Mei Ding
PLoS Genetics
Abstract
ER stress occurs in many physiological and pathological conditions. However, how chronic ER stress is alleviated in specific cells in an intact organism is an outstanding question. Here, overexpressing the gap junction protein UNC-9 (Uncoordinated) in C. elegans neurons triggers the Ire1-Xbp1-mediated stress response in an age-dependent and cell-autonomous manner. The p38 MAPK PMK-3 regulates the chronic stress through IRE-1 phosphorylation. Overexpressing gap junction protein also activates autophagy. The insulin pathway functions through autophagy, but not the transcription of genes encoding ER chaperones, to counteract the p38-Ire1-Xbp1-mediated stress response. Together, these results reveal an intricate cellular regulatory network in response to chronic stress in a subset of cells in multicellular organism.
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论文编号: |
DOI:10.1371/journal.pgen.1008704 |
论文题目: |
Alleviating Chronic ER Stress by p38-Ire1-Xbp1 Pathway and Insulin-associated Autophagy in C. elegans Neurons |
英文论文题目: |
Alleviating Chronic ER Stress by p38-Ire1-Xbp1 Pathway and Insulin-associated Autophagy in C. elegans Neurons |
第一作者: |
Liying Guan, Zhigao Zhan, Yongzhi Yang, Yue Miao, Xun Huang, Mei Ding |
英文第一作者: |
Liying Guan, Zhigao Zhan, Yongzhi Yang, Yue Miao, Xun Huang, Mei Ding |
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2020-09-29 |
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摘要: |
ER stress occurs in many physiological and pathological conditions. However, how chronic ER stress is alleviated in specific cells in an intact organism is an outstanding question. Here, overexpressing the gap junction protein UNC-9 (Uncoordinated) in C. elegans neurons triggers the Ire1-Xbp1-mediated stress response in an age-dependent and cell-autonomous manner. The p38 MAPK PMK-3 regulates the chronic stress through IRE-1 phosphorylation. Overexpressing gap junction protein also activates autophagy. The insulin pathway functions through autophagy, but not the transcription of genes encoding ER chaperones, to counteract the p38-Ire1-Xbp1-mediated stress response. Together, these results reveal an intricate cellular regulatory network in response to chronic stress in a subset of cells in multicellular organism. |
英文摘要: |
ER stress occurs in many physiological and pathological conditions. However, how chronic ER stress is alleviated in specific cells in an intact organism is an outstanding question. Here, overexpressing the gap junction protein UNC-9 (Uncoordinated) in C. elegans neurons triggers the Ire1-Xbp1-mediated stress response in an age-dependent and cell-autonomous manner. The p38 MAPK PMK-3 regulates the chronic stress through IRE-1 phosphorylation. Overexpressing gap junction protein also activates autophagy. The insulin pathway functions through autophagy, but not the transcription of genes encoding ER chaperones, to counteract the p38-Ire1-Xbp1-mediated stress response. Together, these results reveal an intricate cellular regulatory network in response to chronic stress in a subset of cells in multicellular organism. |
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PLoS Genetics |
英文刊物名称: |
PLoS Genetics |
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Liying Guan, Zhigao Zhan, Yongzhi Yang, Yue Miao, Xun Huang, Mei Ding. Alleviating Chronic ER Stress by p38-Ire1-Xbp1 Pathway and Insulin-associated Autophagy in C. elegans Neurons. PLoS Genetics. DOI:10.1371/journal.pgen.1008704 |
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