Vacuolar transporter Mnr2 safeguards organellar integrity in aged cells

Aging is associated with altered mitochondrial function, which 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. Here, we show the localization of Mnr2 as dynamic puncta at the vacuolar membrane, especially in the older Magnaporthe cells. Such vacuolar Mnr2 puncta are often localized in close proximity with the filamentous mitochondria in the older cells. Further, we show loss of integrity of mitochondria and vacuoles in older mnr2∆ null cells. Remarkably, exogenously added Mg+2 restores the mitochondrial structure as well as improves the lifespan of mnr2∆ null cells. Taken together, we propose an ion transporter Mnr2‐based Mg+2 homeostasis as a means in preserving mitochondrial and vacuolar integrity and function in older M. oryzae cells. This study, using a model filamentous blast fungus Magnaporthe oryzae, highlights a novel mechanism underlying sustained energy during aging or under starvation. We show that an ion transporter Mnr2, specifically in old cells, localizes to the membrane of vacuoles—a warehouse of the cell—and helps in providing previously stored magnesium ions essential for proper functioning of the mitochondria—the powerhouse of the cell–and thereby in sustenance during aging or starvation.