ArticleMolecular biology of the cell2018
The V-ATPase V1 subunit A1 is required for rhodopsin anterograde trafficking in Drosophila.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Failure of lysosomal acidification and endomembrane network in neurodegeneration.Experimental & molecular medicine · 2025Review
- Nano-delivery platform with strong protection and efficient delivery: preparation of self-assembled RNA pesticide with dual RNAi targets against Apolygus lucorum.Journal of nanobiotechnology · 2025Article
- Article
- PERK prevents rhodopsin degradation during retinitis pigmentosa by inhibiting IRE1-induced autophagy.The Journal of cell biology · 2023Article
- Application of Fluorescent Proteins for Functional Dissection of theInternational journal of molecular sciences · 2021Review
- RACK1 modulates polyglutamine-induced neurodegeneration by promoting ERK degradation in Drosophila.PLoS genetics · 2021Article
- Article
- Suppression of retinal degeneration by two novel ERAD ubiquitin E3 ligases SORDD1/2 in Drosophila.PLoS genetics · 2020Article
- PE homeostasis rebalanced through mitochondria-ER lipid exchange prevents retinal degeneration in Drosophila.PLoS genetics · 2020Article
- ER complex proteins are required for rhodopsin biosynthesis and photoreceptor survival in Drosophila and mice.Cell death and differentiation · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Synthesis and maturation of the light sensor, rhodopsin, are critical for the maintenance of light sensitivity and for photoreceptor homeostasis. In Drosophila, the main rhodopsin, Rh1, is synthesized in the endoplasmic reticulum and transported to the rhabdomere through the secretory pathway. In an unbiased genetic screen for factors involved in rhodopsin homeostasis, we identified mutations in vha68-1, which encodes the vacuolar proton-translocating ATPase (V-ATPase) catalytic subunit A isoform 1 of the V1 component. Loss of vha68-1 in photoreceptor cells disrupted post-Golgi anterograde trafficking of Rh1, reduced light sensitivity, increased secretory vesicle pH, and resulted in incomplete Rh1 deglycosylation. In addition, vha68-1 was required for activity-independent photoreceptor cell survival. Importantly, vha68-1 mutants exhibited phenotypes similar to those exhibited by mutations in the V0 component of V-ATPase, vha100-1. These data demonstrate that the V1 and V0 components of V-ATPase play key roles in post-Golgi trafficking of Rh1 and that Drosophila may represent an important animal model system for studying diseases associated with V-ATPase dysfunction.
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