| Literature DB >> 33035451 |
Cassidy C Daw1, Karthik Ramachandran1, Benjamin T Enslow1, Soumya Maity1, Brian Bursic2, Matthew J Novello2, Cherubina S Rubannelsonkumar1, Ayah H Mashal1, Joel Ravichandran1, Terry M Bakewell3, Weiwei Wang1, Kang Li1, Travis R Madaris1, Christopher E Shannon3, Luke Norton3, Soundarya Kandala1, Jeffrey Caplan4, Subramanya Srikantan1, Peter B Stathopulos2, W Brian Reeves1, Muniswamy Madesh5.
Abstract
Mg2+ is the most abundant divalent cation in metazoans and an essential cofactor for ATP, nucleic acids, and countless metabolic enzymes. To understand how the spatio-temporal dynamics of intracellular Mg2+ (iMg2+) are integrated into cellular signaling, we implemented a comprehensive screen to discover regulators of iMg2+ dynamics. Lactate emerged as an activator of rapid release of Mg2+ from endoplasmic reticulum (ER) stores, which facilitates mitochondrial Mg2+ (mMg2+) uptake in multiple cell types. We demonstrate that this process is remarkably temperature sensitive and mediated through intracellular but not extracellular signals. The ER-mitochondrial Mg2+ dynamics is selectively stimulated by L-lactate. Further, we show that lactate-mediated mMg2+ entry is facilitated by Mrs2, and point mutations in the intermembrane space loop limits mMg2+ uptake. Intriguingly, suppression of mMg2+ surge alleviates inflammation-induced multi-organ failure. Together, these findings reveal that lactate mobilizes iMg2+ and links the mMg2+ transport machinery with major metabolic feedback circuits and mitochondrial bioenergetics.Entities:
Keywords: Mrs2; calcium; cancer; channel; endoplasmic reticulum; inflammation; lactate; magnesium; metabolism; mitochondria
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Year: 2020 PMID: 33035451 PMCID: PMC7572828 DOI: 10.1016/j.cell.2020.08.049
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582