A Novel Mutation in the Myosin Binding Protein C Gene in a Prader-Willi Syndrome Pedigree.
Xiao-Qun LiuMan LuoQi LiuGuo-Can YangPublished in: Reproductive sciences (Thousand Oaks, Calif.) (2021)
Prader-Willi syndrome (PWS) is a neurogenetic disorder caused by deficiency expression of paternally imprinted genes of the chromosomal region 15. In this study, we report a novel mutation in the myosin binding protein C (MYBPC3) gene in a Prader-Willi syndrome pedigree. Next-generation sequencing (NGS) and Sanger sequencing were performed to define and confirm the MYBPC3 gene mutation. Bioinformatics analysis was also performed for the mutated MYBPC3 protein using available software tools. The proband was diagnosed as PWS with about 4.727Mb copy number missed in the long arm of chromosome 15 and treated with growth hormone on 0.3 IU/day. Sanger sequencing identified a novel heterozygous mutation in the MYBPC3 gene, c.2002C>G (p.R668G). Bioinformatics analysis suggested the variant disease-causing; the Pro residue at 668 in the MYBPC3 protein was highly conserved. Moreover, interactions among MYBPC3 and other proteins suggested the potential effects on the development of cardiomyopathies. This is the first report of PWS with MYBPC3 gene mutation. Besides general examinations, it is vital for physicians to amply molecular genetics to get an accurate diagnosis in the clinic especially for rare diseases.
Keyphrases
- copy number
- growth hormone
- binding protein
- hypertrophic cardiomyopathy
- bioinformatics analysis
- mitochondrial dna
- genome wide
- left ventricular
- dna methylation
- primary care
- case report
- genome wide identification
- poor prognosis
- transcription factor
- single cell
- heart failure
- high resolution
- gene expression
- protein protein
- amino acid
- atrial fibrillation
- smoking cessation