Jul 2026· Movement Disorders· 0 citations· 12 references
Medicine
TL;DR
This study supplemented the evidence on the role of PCDHGB1 in dystonia and expanded the genotypic and phenotypic spectrum of PCDHGB1.
Abstract
Background
Recently, PCDHGB1 has been identified as a novel causative gene of dystonia predominantly affecting the cervical muscles. However, no large cohort study has been conducted to confirm the association.
Objectives
The objective of the study was to systematically evaluate the genetic associations of PCDHGB1 with dystonia in a large Chinese dystonia cohort.
Methods
We analyzed rare variants of PCDHGB1 in a discovery cohort, including 878 dystonia patients, and a validation cohort, including 509 dystonia patients, using whole-exome sequencing. The overrepresentation of rare variants in patients was examined using Fisher's exact test at allele and gene levels.
Results
Twenty-seven rare variants of PCDHGB1 were identified in 55 individuals in the discovery cohort, including 3 frameshift variants (p.Leu177Valfs*7, p.Arg635Profs*24, p.Asp797Glufs*51) and 24 missense variants. Another 10 rare variants were detected in 12 patients in the validation cohort, including 1 frameshift variant (p.Leu709Argfs*13) and 9 missense variants. Fourteen patients carried the frameshift variant p.Leu177Valfs*7. Thirteen patients carried the p.Met111Val variant, including 3 patients from one family. At variant level, p.Pro773Ser and p.Arg408Gln were significantly associated with a higher risk of dystonia, whereas 15 variants (including p.Arg635Profs*24, p.Asp797Glufs*51, p.Leu709Argfs*13, and 12 missense variants) were nominally associated with a higher risk of dystonia. Gene-based burden analysis detected the enrichment of ultra-rare variants of PCDHGB1 in dystonia. Western blot experiments revealed that these four frameshift variants (p.Leu177Valfs*7, p.Arg635Profs*24, p.Asp797Glufs*51, p.Leu709Argfs*13) induced a truncated PCDHGB1 protein.
This study identifies novel loss-of-function RSPH4A variants causing PCD through distinct molecular mechanisms, expanding the mutational spectrum of radial spoke head protein-related ciliopathies.
Yuting Lu, Hui-Yan Tang, Kai Chen et al.· Frontiers in Genetics· 0 citations
It is demonstrated that early-onset MORC2-associated disorders segregate into two principal neurological phenotypes: a predominantly neuromuscular form and a central nervous system-predominant form.
A. Murtazina, Eugenii Tatarsky, I. Viakhireva et al.· Journal of Medical Genetics· 0 citations
This study identified compound heterozygous GBA1 variants, including two novel candidate pathogenic splice site variants, in Gaucher disease type 3 patients, expanding the known mutational spectrum.
Yang-Mei Ou, Ming-Feng He, Fu-Jiang Yan et al.· Brain & development (Tokyo....· 0 citations
An upregulated interferon signature was revealed, and monocytes were identified as a major cellular source of inflammation in patients with SPENCDI, expanding the genetic and clinical spectrum of ACP5 deficiency.
Shiling Zhong, Shuang-Yue Ma, Y. El Chazli et al.· Arthritis & Rheumatology· 0 citations
A novel missense variant is characterized that causes aberrant splicing of PKHD1 in CD and underscores the necessity of functional analysis for evaluating the pathogenicity of missense variants, especially those at the last nucleotide of an exon.
In this study, pathogenic FBN1 variants were identified in three patients, thereby confirming the clinical diagnosis of MFS and contributing two novel variants to the FBN1 variant repository, and provide a comparative assessment of genotype-phenotype correlations.
Xing Zhao, La-Mei Yuan, Yan Sun et al.· Clinica chimica acta; intern...· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.