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首页 » Science报道 » Science:应激相关激活转录因子-1调节线粒体非折叠蛋白反应

Science:应激相关激活转录因子-1调节线粒体非折叠蛋白反应

来源:生物谷 2012-06-18 10:29


6月15日,Science在线报道应激相关激活转录因子-1进入线粒体的效率可调节线粒体非折叠蛋白反应的水平。

为了更好地理解线粒体功能障碍的反应,研究者研究了,应激相关激活转录因子-1(ATFS-1)感受线粒体应激过程,及其在线粒体非折叠蛋白反应(UPRmt)条件下与细胞核通信的机制。

研究发现,调控的关键点是ATFS-1进入线粒体的效率。除了一个核定位序列,ATFS-1还有一个氨基端的线粒体定位序列。这是UPRmt抑制反应所必不可少的。通常情况下,ATFS-1被导入到线粒体并降解。然而,在线粒体应激情况下,ATFS-1进入线粒体效率下降,使其相当一部分积聚在细胞质并转移到细胞核中。该研究结果表明,细胞通过ATFS-1监测线粒体蛋白输入效率,进而利用保护性转录反应协调线粒体功能障碍的水平。(生物谷bioon.com)

Mitochondrial Import Efficiency of ATFS-1 Regulates Mitochondrial UPR Activation

Amrita M. Nargund1,*, Mark W. Pellegrino1,*, Christopher J. Fiorese1,2, Brooke M. Baker1, Cole M. Haynes

To better understand the response to mitochondrial dysfunction, we examined the mechanism by which Activating Transcription Factor associated with Stress-1 (ATFS-1) senses mitochondrial stress and communicates with the nucleus during the mitochondrial unfolded protein response (UPRmt). We found that the key point of regulation was the mitochondrial import efficiency of ATFS-1. In addition to a nuclear localization sequence, ATFS-1 has an amino-terminal mitochondrial targeting sequence, which was essential for UPRmt repression. Normally, ATFS-1 is imported into mitochondria and degraded. However, during mitochondrial stress, import efficiency was reduced, allowing a percentage of ATFS-1 to accumulate in the cytosol and traffic to the nucleus. Our results show that cells monitor mitochondrial import efficiency via ATFS-1 to coordinate the level of mitochondrial dysfunction with the protective transcriptional response.

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