PUBLICATION
Cone photoreceptors transfer damaged mitochondria to Müller glia
- Authors
- Hutto, R.A., Rutter, K.M., Giarmarco, M.M., Parker, E.D., Chambers, Z.S., Brockerhoff, S.E.
- ID
- ZDB-PUB-230217-34
- Date
- 2023
- Source
- Cell Reports 42: 112115112115 (Journal)
- Registered Authors
- Brockerhoff, Susan
- Keywords
- CP: Neuroscience, Müller glia, mitochondria, mitophagy, photoreceptor, retina, zebrafish
- MeSH Terms
-
- Animals
- Mitochondria
- Neuroglia/metabolism
- Retina/metabolism
- Retinal Cone Photoreceptor Cells*/metabolism
- Zebrafish*
- PubMed
- 36795565 Full text @ Cell Rep.
Citation
Hutto, R.A., Rutter, K.M., Giarmarco, M.M., Parker, E.D., Chambers, Z.S., Brockerhoff, S.E. (2023) Cone photoreceptors transfer damaged mitochondria to Müller glia. Cell Reports. 42:112115112115.
Abstract
Mitochondria are vital organelles that require sophisticated homeostatic mechanisms for maintenance. Intercellular 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 mitochondrial stress that leads to loss of cristae, displacement of damaged mitochondria from their normal cellular location, initiation of degradation, and transfer to Müller glia cells, a key non-neuronal support cell in the retina. Our findings show transmitophagy from cones to Müller glia as a response to mitochondrial damage. Intercellular transfer of damaged mitochondria represents an outsourcing mechanism that photoreceptors use to support their specialized function.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping