Arabidopsis mitochondrial protein TIM50 affects hypocotyl cell elongation through intracellular ATP level
Arabidopsis mitochondrial protein TIM50 affects hypocotyl cell elongation through intracellular ATP level
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DOI：
10.1016/j.plantsci.2011.08.014
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发表时间：
2012-02-01
期刊：
影响因子：
5.2
通讯作者：
Matsui, Minami
中科院分区：
文献类型：
--
作者：
Kumar, Shailesh;Yoshizumi, Takeshi;Matsui, Minami
植物下胚轴是分析细胞伸长的一个很好的模型。我们描述了拟南芥TIM50基因的敲除突变体，该突变体显示黄化幼苗的下胚轴长度减少。我们还发现，敲除TIM50会导致线粒体结构的扩大和变形以及细胞内ATP水平的降低。TIM50是线粒体TIM23内膜蛋白复合物的一个组成部分，参与线粒体蛋白的进口。通过添加化合物C（一种AMPK抑制剂）恢复了短的下胚轴表型。因此，线粒体ATP水平可能通过AMPK信号传导控制拟南芥下胚轴的细胞伸长。2011爱思唯尔爱尔兰有限公司版权所有。
The plant hypocotyl is an excellent model for the analysis of cell elongation. We have characterized a knockout mutant of the Arabidopsis TIM50 gene that showed a reduction in the hypocotyls length of etiolated seedlings. We also found that a knockout of TIM50 caused enlargement and deformation of the mitochondrial structure and a reduction in intracellular ATP levels. TIM50 is a component of the mitochondrial TIM23 inner membrane protein complex and is involved in the import of mitochondrial proteins. The short hypocotyl phenotype was recovered by the addition of Compound C, an inhibitor of AMPK. Thus, the mitochondrial ATP level controls cell elongation in Arabidopsis hypocotyls through possible signaling via AMPK. (C) 2011 Elsevier Ireland Ltd. All rights reserved.