IP3 receptor trafficking at the ER-mitochondria contacts impacts on mitochondrial Ca2+ homeostasis and metabolism

Abstract

The close contacts between endoplasmic reticulum and mitochondria (ERMCs) play a key role in metabolic regulation, Ca2+ homeostasis, reactive oxygen species production, and many other cell functions. Nevertheless, it is not fully clear how these contacts dynamically rearrange to support cell functions. In a recent Nature Communications article [1], Katona et al. elegantly showed that motile IP3Rs can be captured at ERMCs to promptly mediate Ca2+ transfer and stimulate mitochondrial oxidative metabolism.