Vacuolar transporter Mnr2 safeguards mitochondrial integrity in aged cells

Abstract

Aging is associated with altered mitochondrial function. Mitochondrial function is dependent on the magnesium (Mg+2) ion flux. The molecular mechanism underlying Mg+2 homeostasis, especially during aging has not been well understood. We previously demonstrated that the absence of a vacuolar ion transporter Mnr2 accelerates cell death in the older part of the colony in Magnaporthe oryzae presumably due to an altered Mg+2 homeostasis. Localization of Mnr2 as dynamic puncta at the vacuolar membrane especially in the older Magnaporthe cells further suggests its association with aged cells. Interestingly, such vacuolar Mnr2 puncta colocalized with the filamentous mitochondria in the aged cells. Further, we show that aged mnr2Δ null cells displayed loss of integrity of mitochondria and vacuoles. Remarkably, exogenously added Mg+2 restored the mitochondrial structure as well as improved the lifespan of mnr2Δ null cells. Thus, we uncover a mechanism of maintenance of mitochondrial integrity and function by the ion transporter Mnr2-based Mg+2 homeostasis during aging.