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Auteurs principaux: Pan, Yang, Iejima, Daisuke, Yoshitake, Kazutoshi, Tsunoda, Kazushige, Iwata, Takeshi
Format: Artículo científico
Langue:en
Publié: HGG advances 2025
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Accès en ligne:https://pubmed.ncbi.nlm.nih.gov/40450528/
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author Pan, Yang
Iejima, Daisuke
Yoshitake, Kazutoshi
Tsunoda, Kazushige
Iwata, Takeshi
author_facet Pan, Yang
Iejima, Daisuke
Yoshitake, Kazutoshi
Tsunoda, Kazushige
Iwata, Takeshi
Pan, Yang
Iejima, Daisuke
Yoshitake, Kazutoshi
Tsunoda, Kazushige
Iwata, Takeshi
collection PubMed - marine biology
contents Clinical features and molecular mechanisms of RP1L1 variants causing occult macular dystrophy. Pan, Yang Iejima, Daisuke Yoshitake, Kazutoshi Tsunoda, Kazushige Iwata, Takeshi Humans Macular Degeneration Male Female Eye Proteins Pedigree Mutation Middle Aged Adult Microtubule-Associated Proteins Exome Sequencing Phenotype Electroretinography Occult macular dystrophy (OMD) is an inherited retinopathy characterized by progressive bilateral vision loss despite normal findings on fundoscopic examination, fluorescein angiography, and full-field electroretinography. Its pathogenesis remains unknown, and no treatments are available. Here, we performed whole-exome sequencing on 133 samples from 78 OMD pedigrees to identify pathogenic variants, using filters for minor allele frequency, function prediction, and retinal expression. We identified the RP1L1 c.133C>T, p.Arg45Trp (R45W) mutation as the sole pathogenic variant in two families with dominantly inherited OMD. Additionally, we discovered five other potentially pathogenic RP1L1 variants. Together, these six variants accounted for 33.33% of pedigrees, with R45W being the most prevalent, at 16.6%. The R45W mutation correlated with earlier onset, more severe clinical phenotypes, and abnormal intracellular localization rather than altered expression levels. R45W disrupted the intracellular localization of RP1L1 and RP1, compromising cell viability. In induced photoreceptor-like cells derived from OMD patients carrying R45W, we observed downregulation of the long noncoding RNA MEG3 and the PI3K/Akt pathway, alongside upregulation of extracellular matrix organization. These findings validate the etiologic role of RP1L1 and offer insights into the pathogenesis of OMD, thereby facilitating future research and therapeutic development.
format Artículo científico
id pubmed_40450528
institution PubMed
language en
publishDate 2025
publisher HGG advances
record_format pubmed
spellingShingle Clinical features and molecular mechanisms of RP1L1 variants causing occult macular dystrophy.
Pan, Yang
Iejima, Daisuke
Yoshitake, Kazutoshi
Tsunoda, Kazushige
Iwata, Takeshi
Humans
Macular Degeneration
Male
Female
Eye Proteins
Pedigree
Mutation
Middle Aged
Adult
Microtubule-Associated Proteins
Exome Sequencing
Phenotype
Electroretinography
Clinical features and molecular mechanisms of RP1L1 variants causing occult macular dystrophy. Pan, Yang Iejima, Daisuke Yoshitake, Kazutoshi Tsunoda, Kazushige Iwata, Takeshi Humans Macular Degeneration Male Female Eye Proteins Pedigree Mutation Middle Aged Adult Microtubule-Associated Proteins Exome Sequencing Phenotype Electroretinography Occult macular dystrophy (OMD) is an inherited retinopathy characterized by progressive bilateral vision loss despite normal findings on fundoscopic examination, fluorescein angiography, and full-field electroretinography. Its pathogenesis remains unknown, and no treatments are available. Here, we performed whole-exome sequencing on 133 samples from 78 OMD pedigrees to identify pathogenic variants, using filters for minor allele frequency, function prediction, and retinal expression. We identified the RP1L1 c.133C>T, p.Arg45Trp (R45W) mutation as the sole pathogenic variant in two families with dominantly inherited OMD. Additionally, we discovered five other potentially pathogenic RP1L1 variants. Together, these six variants accounted for 33.33% of pedigrees, with R45W being the most prevalent, at 16.6%. The R45W mutation correlated with earlier onset, more severe clinical phenotypes, and abnormal intracellular localization rather than altered expression levels. R45W disrupted the intracellular localization of RP1L1 and RP1, compromising cell viability. In induced photoreceptor-like cells derived from OMD patients carrying R45W, we observed downregulation of the long noncoding RNA MEG3 and the PI3K/Akt pathway, alongside upregulation of extracellular matrix organization. These findings validate the etiologic role of RP1L1 and offer insights into the pathogenesis of OMD, thereby facilitating future research and therapeutic development.
title Clinical features and molecular mechanisms of RP1L1 variants causing occult macular dystrophy.
topic Humans
Macular Degeneration
Male
Female
Eye Proteins
Pedigree
Mutation
Middle Aged
Adult
Microtubule-Associated Proteins
Exome Sequencing
Phenotype
Electroretinography
url https://pubmed.ncbi.nlm.nih.gov/40450528/