ArticleInvestigative ophthalmology & visual science2015
Varying the GARP2-to-RDS Ratio Leads to Defects in Rim Formation and Rod and Cone Function.
Article in Investigative ophthalmology & visual science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Selective knockout of murine glutamic acid-rich protein 2 significantly alters dark continuous noise in rod photoreceptors.The Journal of physiology · 2026Article
- A new mouse model for PRPH2 pattern dystrophy exhibits functional compensation prior and subsequent to retinal degeneration.Human molecular genetics · 2024Article
- CNG channel-related retinitis pigmentosa.Vision research · 2023Article
- Biology, Pathobiology and Gene Therapy of CNG Channel-Related Retinopathies.Biomedicines · 2023Review
- Residual rod function in CNGB1 mutant dogs.Documenta ophthalmologica. Advances in ophthalmology · 2022Article
- Oligomerization of Prph2 and Rom1 is essential for photoreceptor outer segment formation.Human molecular genetics · 2018Article
- The K153Del PRPH2 mutation differentially impacts photoreceptor structure and function.Human molecular genetics · 2016Article
- Role of RDS and Rhodopsin in Cngb1-Related Retinal Degeneration.Investigative ophthalmology & visual science · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
purposeThe beta subunit of the rod cyclic nucleotide gated channel B1 (CNGB1) contains a proline/glutamic acid-rich N-terminal domain (GARP), which is also present in rods as a non-membrane-bound protein (GARP1/2). GARP2 and CNGB1 bind to retinal degeneration slow (RDS), which is present in the rims of rod and cone outer segment (OS) layers. Here we focus on the importance of RDS/GARP complexes in OS morphogenesis and stability.
methodsRetinal structure, function, and biochemistry were assessed in GARP2-Tg transgenic mice crossed onto rds+/+, rds+/-, and rds-/- genetic backgrounds.
resultsGARP2 expression decreased in animals with reduced RDS levels. Overexpression of GARP2 led to abnormalities in disc stacking in GARP2-Tg/rds+/+ and the accumulation of abnormal vesicular structures in GARP2-Tg/rds+/- OS, as well as alterations in RDS-ROM-1 complex formation. These abnormalities were associated with diminished scotopic a- and b-wave amplitudes in GARP2-Tg mice on both the rds+/+ and rds+/- backgrounds. In addition, severe defects in cone function were observed in GARP2-Tg mice on all RDS backgrounds.
conclusionsOur results indicate that overexpression of GARP2 significantly exacerbates the defects in rod function associated with RDS haploinsufficiency and leads to further abnormalities in OS ultrastructure. These data also suggest that GARP2 expression in cones can be detrimental to cones. RDS/GARP interactions remain under investigation but are critical for both OS structure and function.
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