Aug 2026· Frontiers in Medicine· Vol 13· 0 citations· 31 references
Medicine
TL;DR
This research contributed to the genetic assessment and guidance for two families affected by Charcot–Marie–Tooth disease, reinforcing the notion that MORC2 is a potential causative gene for CMT2Z.
Abstract
Background Charcot–Marie–Tooth disease type 2Z (CMT2Z) is an uncommon inherited condition characterized by autosomal dominant inheritance. It is marked by axonal neuropathy, leading to progressive muscle weakness, cramps, and sensory loss. MORC2 is one of the candidate pathogenic genes for CMT2Z. Methods Here, we enrolled two families affected by Charcot–Marie–Tooth (CMT) disease, with both families having probands who exhibit distal lower limb weakness. Whole-exome sequencing (WES) was used to explore the genetic lesion. Results Two heterozygous variants (NM_001303256, c.34G > C;p.A12P; NM_001303256, c.848G > A;p.R283H) of MORC2 gene were found. The c.848G > A;p.R283H variant is rare, and the c.34G > C;p.A12P variant has not been reported before. Functional studies revealed that the c.848G > A;p.R283H variant resulted in reduced transcription of the MORC2 gene. The c.34G > C;p.A12P variant did not impact MORC2 gene transcription, yet it influenced the protein’s half-life and stability. Based on genetic analysis, two probands were subsequently diagnosed with CMT2Z. Conclusion Our research contributed to the genetic assessment and guidance for these families, reinforcing the notion that MORC2 is a potential causative gene for CMT2Z.
The present study expands the mutation spectrum of the GDAP1 and SBF2 genes, with possible implications for improved understanding of disease pathophysiology and the importance of NGS, particularly WES, in achieving rapid and precise molecular genetic diagnosis for clinical purposes.
Zafar Ali, M. Jameel, J. Klar et al.· Frontiers in Neurology· 1 citation
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 expands the mutational spectrum of FBN1, establishes functional evidence for the pathogenicity of the LDLR variant, and represents the first report of a pediatric individual carrying three coexisting pathogenic variants for rare diseases.
Hang Shi, Xue-Jian Han, Shu-Kai Xing et al.· Genetics Research· 0 citations
The broad clinical spectrum associated with the SEPTIN9 R106W mutation in a Chinese pedigree spanning from childhood to adulthood is delineated, highlighting the critical role of active inter vention in childhood-onset HNA.
Jing Chen, Shuang Chen, Xin-Yi Zhu et al.· Frontiers in Genetics· 0 citations
Background and Objectives The aim of this study was to present a case report of the first familial case of multiple sclerosis (MS) in an X-linked Charcot-Marie-Tooth family with a novel variant in GJB1. Methods Clinical, neurophysiologic, neuroimaging, and genetic assessments were performed on 9 affected members of a l...
Marija Menih, Tanja Hojs Fabjan, A. Maver et al.· Neurology: Genetics· 0 citations
This case report emphasizes the phenotypic spectrum of this disorder and describes a variant that has not been previously reported in the literature, which is associated with heterozygous truncating pathogenic variants in the ASXL3 gene.
Şirin Sedef Baş, Burcu Yeter, N. Elçioğlu· Case Reports in Genetics· 0 citations
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