International journal of molecular sciences · 2024
PRPH2-Related Retinal Dystrophies: Mutational Spectrum in 103 Families from a Spanish Cohort.
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Fernández-Caballero Lidia, Martín-Merida Inmaculada, Blanco-Kelly Fiona, Avila-Fernandez Almudena, Carreño Ester, Fernandez-San Jose Patricia, Irigoyen Cristina, Jimenez-Rolando Belen, Lopez-Grondona Fermina, Mahillo Ignacio, Martin-Gutierrez María Pilar, Minguez Pablo, Perea-Romero Irene, Del Pozo-Valero Marta, Riveiro-Alvarez Rosa, Rodilla Cristina, Rodriguez-Peña Lidya, Sánchez-Barbero Ana Isabel, Swafiri Saoud T, Trujillo-Tiebas María José, Zurita Olga, García-Sandoval Blanca, Corton Marta, Ayuso Carmen
Аннотация
PRPH2, one of the most frequently inherited retinal dystrophy (IRD)-causing genes, implies a high phenotypic variability. This study aims to analyze the PRPH2 mutational spectrum in one of the largest cohorts worldwide, and to describe novel pathogenic variants and genotype-phenotype correlations. A study of 220 patients from 103 families recruited from a database of 5000 families. A molecular diagnosis was performed using classical molecular approaches and next-generation sequencing. Common haplotypes were ascertained by analyzing single-nucleotide polymorphisms. We identified 56 variants, including 11 novel variants. Most of them were missense variants (64%) and were located in the D2-loop protein domain (77%). The most frequently occurring variants were p.Gly167Ser, p.Gly208Asp and p.Pro221_Cys222del. Haplotype analysis revealed a shared region in families carrying p.Leu41Pro or p.Pro221_Cys222del. Patients with retinitis pigmentosa presented an earlier disease onset. We describe the largest cohort of IRD families associated with PRPH2 from a single center. Most variants were located in the D2-loop domain, highlighting its importance in interacting with other proteins. Our work suggests a likely founder effect for the variants p.Leu41Pro and p.Pro221_Cys222del in our Spanish cohort. Phenotypes with a primary rod alteration presented more severe affectation. Finally, the high phenotypic variability in PRPH2 hinders the possibility of drawing genotype-phenotype correlations.