The developing retina undergoes mitochondrial remodeling via PINK1/PRKN-dependent mitophagy

2025 · doi:10.1101/2025.03.30.646079
preprint OA: gold CC-BY-NC-ND-4.0
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This study examined how mitophagy changes across mouse retinal development by using proteomics on isolated retinas at multiple developmental stages and the mito-QC mitophagy reporter mouse line. The authors found that mitolysosomes were more prevalent in the mature retina and that embryonic development features two distinct mitophagy peaks: an early peak independent of PINK1 activation associated with retinal ganglion cells, and a later peak that depended on PINK1 and was triggered after an increase in retinal oxidative stress. They reported that the PINK1-dependent, oxidative stress-induced mitophagy pathway is conserved in both mice and zebrafish, presenting evidence for programmed PINK1-dependent mitophagy during development. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Mitophagy, the selective degradation of mitochondria, is essential for retinal ganglion cell (RGC) differentiation and retinal homeostasis. However, the specific mitophagy pathways involved and their temporal dynamics during retinal development and maturation remain poorly understood. Using proteomics analysis of isolated mouse retinas across developmental stages and the mitophagy reporter mouse line, mito -QC, we characterized mitophagy throughout retinogenesis. While mitolysosomes were more prevalent in the mature retina, we observed two distinct mitophagy peaks during embryonic development. The first, independent of PTEN-induced kinase 1 (PINK1) activation, was associated with RGCs. The second, PINK1-dependent peak was triggered after an increase in retinal oxidative stress. This PINK1-dependent, oxidative stress-induced mitophagy pathway is conserved in mice and zebrafish, providing the first evidence of programmed, PINK1-dependent mitophagy during development.
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Abstract Mitophagy, the selective degradation of mitochondria, is essential for retinal ganglion cell (RGC) differentiation and retinal homeostasis. However, the specific mitophagy pathways involved and their temporal dynamics during retinal development and maturation remain poorly understood. Using proteomics analysis of isolated mouse retinas across developmental stages and the mitophagy reporter mouse line, mito-QC, we characterized mitophagy throughout retinogenesis. While mitolysosomes were more prevalent in the mature retina, we observed two distinct mitophagy peaks during embryonic development. The first, independent of PTEN-induced kinase 1 (PINK1) activation, was associated with RGCs. The second, PINK1-dependent peak was triggered after an increase in retinal oxidative stress. This PINK1-dependent, oxidative stress-induced mitophagy pathway is conserved in mice and zebrafish, providing the first evidence of programmed, PINK1-dependent mitophagy during development. Competing Interest Statement The authors have declared no competing interest.

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License: CC-BY-NC-ND-4.0