The role of dysregulated signalling by TORC1 in mitochondrial disease.

线粒体是微小的亚细胞区室，负责产生细胞90%以上的能量。线粒体缺陷在直接影响线粒体的遗传性疾病和大多数神经退行性疾病中都具有特征。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。使用一个简单的模式生物，网骨藻，以前的研究表明，失调的细胞内信号传导的细胞能量传感报警蛋白是负责不同的细胞病变的细胞病变的细胞。该项目将确定第二种细胞应激感应蛋白复合物TORC 1在这些途径中的作用。可能会出现新的治疗可能性。

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.