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 increment null cells. Remarkably, exogenously added Mg+2 restores the mitochondrial structure as well as improves the lifespan of mnr2 increment 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.

Automated summary

The research reveals that the ion transporter protein Mnr2 in Magnaporthe cells is dynamically distributed as puncta on the vacuolar membrane, closely associated with filamentous mitochondria in older cells. Loss of Mnr2 can lead to loss of integrity of mitochondria and vacuoles in older cells, while exogenously added Mg+2 can restore mitochondrial structure and prolong cell lifespan.