ArticleClinical genetics2025
Expanding the genetic landscape of Usher syndrome type IV caused by pathogenic ARSG variants.
Article in Clinical genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Application of smooth OWA operators to classification of retinitis pigmentosa.Scientific reports · 2026Article
- Retinal Function Deficits in American Staffordshire Terriers with a Late-Onset Neurodegenerative Disease Associated with anVeterinary sciences · 2025Article
- Usher Syndrome: New Insights into Classification, Genotype-Phenotype Correlation, and Management.Genes · 2025Review
- Current approaches for Usher syndrome disease models and developing therapies.Frontiers in cell and developmental biology · 2025Review
- Expanding the genetic landscape of Usher syndrome type IV caused by pathogenic ARSG variants.Clinical genetics · 2025Article
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25 authors.
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Abstract
Usher syndrome (USH) is the most common cause of deafblindness. USH is autosomal recessively inherited and characterized by rod-cone dystrophy or retinitis pigmentosa (RP), often accompanied by sensorineural hearing loss. Variants in >15 genes have been identified as causative for clinically and genetically distinct subtypes. Among the ultra-rare and recently discovered genes is ARSG, coding for the lysosomal sulfatase Arylsulfatase G. This subtype was assigned as "USH IV" with a late onset of RP and usually late-onset progressive SNHL without vestibular involvement. Here, we describe nine new subjects and the clinical description of four cases with the USH IV phenotype bearing seven novel and two known pathogenic variants. Functional experiments indicated the complete loss of sulfatase enzymatic activity upon ectopic expression of mutated ARSG cDNA. Interestingly, we identified a homozygous missense variant, p.(Arg99His), previously described in dogs with neuronal ceroid lipofuscinosis. Our study expands the genetic landscape of ARSG-USH IV and the number of known subjects by more than 30%. These findings highlight that USH IV likely has been underdiagnosed and emphasize the need to test molecularly unresolved subjects with deafblindness syndrome. Finally, testing of ARSG should be considered for the genetic work-up of apparent isolated inherited retinal diseases.
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