Shiori Sekine Lab

Lab Focus

Mitochondria are considered to have evolved from bacteria that invaded our ancestral cells about 300 million years ago (endosymbiotic theory). However, mitochondria are now intricately involved in various function within the cells, and their existence has become indispensable for our vital activities.

During the process of performing their variety of functions, mitochondria are constantly exposed to various stresses. For example, ROS, inevitable byproducts of the ATP production, damage mitochondria by oxidizing mitochondrial membrane lipids and proteins. Recent research has revealed that mitochondria are equipped with several strategies to cope with these stresses and maintain the quality of mitochondria. These mechanisms are called the “mitochondrial stress response” or “mitochondrial quality control”. For example, mitophagy is a mechanism that eliminates dysfunctional mitochondria from the cells by autophagy. It has been found that mitochondria are actively communicating with other intracellular organelles to evoke the proper stress response. For example, the accumulation of abnormal mitochondrial proteins has been shown to be signaled to the nucleus and promote a specific transcriptional program to relieve mitochondrial proteotoxic stress (mtUPR). In order to drive these mitochondrial stress responses, proteins that can monitor the abnormalities in mitochondria and transmit that information to other proteins are necessary. In our laboratory, we are interested in identifying critical molecular players in mitochondrial stress responses and elucidating their roles. Our mission is therefore to enhance human health through basic mitochondrial biology research.

What question I’d like to answer

Can you improve human health by modulating the mitochondrial stress response? 

For more information: https://www.shiorilab.net