The role of dysregulated signalling by TORC1 in mitochondrial disease.

线粒体是微小的亚细胞隔间，负责产生超过90%的细胞能量。线粒体缺陷既存在于直接影响线粒体的遗传病中，也存在于大多数神经退行性疾病中。预计到2040年，这些不治之症将超过癌症，成为全球第二大死亡原因。利用一个简单的模式生物，Dictyostelius，以前的研究表明，由细胞能量感应警报蛋白调节的细胞内信号失调导致了线粒体疾病细胞中的各种细胞病理。该项目将确定第二个细胞应激敏感蛋白复合体TORC1在这些途径中的作用。可能会出现新的治疗方法。

The mitochondria are tiny subcellular compartments responsible for producing over 90 per cent of the cell's energy. Mitochondrial defects feature both in genetic diseases that directly affect the mitochondria and in most neurodegenerative diseases. These incurable diseases are expected to eclipse cancer as the second major cause of death worldwide by 2040. Using a simple model organism, Dictyostelium, previous research showed that dysregulated intracellular signalling by a cellular energy-sensing alarm protein is responsible for diverse cellular pathologies in mitochondrially diseased cells. This project will determine the role in these pathways of a second cellular stress-sensing protein complex, TORC1. New treatment possibilities may emerge.