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961.
Xiangqian Zhang Xu Zheng Shanwen Ke Haitao Zhu Fang Liu Zemin Zhang Xinxiang Peng Lin Guo Ruizhen Zeng Pei Hou Ziqiang Liu Suowei Wu Meifang Song Jianping Yang Guiquan Zhang 《Plant molecular biology》2016,92(6):701-715
Most environmental perturbations have a direct or indirect deleterious impact on photosynthesis, and, in consequence, the overall energy status of the cell. Despite our increased understanding of convergent energy and stress signals, the connections between photosynthesis, energy and stress signals through putative common nodes are still unclear. Here we identified an endoplasmic reticulum (ER)-localized adenine nucleotide transporter1 (ER-ANT1), whose deficiency causes seedling lethality in air but viable under high CO2, exhibiting the typical photorespiratory phenotype. Metabolic analysis suggested that depletion of ER-ANT1 resulted in circadian rhythm disorders in sucrose synthesis and induced sucrose signaling pathways, indicating that the ER is involved in the regulation of vital energy metabolism in plants. In addition, the defect of ER-ANT1 triggers ER stress and activates the unfolded protein response in plant cells, suggesting ER stress and photorespiration are closely linked. These findings provide an important evidence for a key role of ER-localized ER-ANT1 in convergent energy and stress signals in rice. Our findings support the idea that ATP is a central signal involved in the plant response to a variety of stresses. 相似文献
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FUNDC1 regulates mitochondrial dynamics at the ER–mitochondrial contact site under hypoxic conditions 下载免费PDF全文
Wen Li Haixia Zhuang Xingliang Zhang Hao Chen Shupeng Li Yue Yang Yue Lu Jingjing Wang Runzhi Zhu Liangqing Zhang Senfang Sui Ning Tan Bin Zhao Jingjing Zhang Longxuan Li Du Feng 《The EMBO journal》2016,35(13):1368-1384
In hypoxic cells, dysfunctional mitochondria are selectively removed by a specialized autophagic process called mitophagy. The ER–mitochondrial contact site (MAM) is essential for fission of mitochondria prior to engulfment, and the outer mitochondrial membrane protein FUNDC1 interacts with LC3 to recruit autophagosomes, but the mechanisms integrating these processes are poorly understood. Here, we describe a new pathway mediating mitochondrial fission and subsequent mitophagy under hypoxic conditions. FUNDC1 accumulates at the MAM by associating with the ER membrane protein calnexin. As mitophagy proceeds, FUNDC1/calnexin association attenuates and the exposed cytosolic loop of FUNDC1 interacts with DRP1 instead. DRP1 is thereby recruited to the MAM, and mitochondrial fission then occurs. Knockdown of FUNDC1, DRP1, or calnexin prevents fission and mitophagy under hypoxic conditions. Thus, FUNDC1 integrates mitochondrial fission and mitophagy at the interface of the MAM by working in concert with DRP1 and calnexin under hypoxic conditions in mammalian cells. 相似文献
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