Cone photoreceptors transfer damaged mitochondria to Mu euro ller glia

Mitochondria are vital organelles that require sophisticated homeostatic mechanisms for maintenance. Inter-cellular transfer of damaged mitochondria is a recently identified strategy broadly used to improve cellular health and viability. Here, we investigate mitochondrial homeostasis in the vertebrate cone photoreceptor, the specialized neuron that initiates our daytime and color vision. We find a generalizable response to mito-chondrial stress that leads to loss of cristae, displacement of damaged mitochondria from their normal cellular location, initiation of degradation, and transfer to Mueuroller glia cells, a key non-neuronal support cell in the retina. Our findings show transmitophagy from cones to Mueuroller glia as a response to mitochondrial damage. Intercellular transfer of damaged mitochondria represents an outsourcing mechanism that photo-receptors use to support their specialized function.