| Literature DB >> 32231217 |
Marzieh Mohseni1,2,3, Mojdeh Akbari1, Kevin T Booth4,5, Mojgan Babanejad1, Hela Azaiez4, Fariba Ardalani1, Sanaz Arzhangi1, Khadijeh Jalalvand1, Nooshin Nikzat1, Fatemeh Ghodratpour1, Payman Jamali6, Omid Ali Adeli7, Haleh Habibi8, Kimia Kahrizi1, Hossein Najmabadi9,10.
Abstract
Mutations in the CDC14A (Cell Division-Cycle 14A) gene, which encodes a conserved dual-specificity protein tyrosine phosphatase, have been identified as a cause of autosomal recessive non-syndromic hearing loss (DFNB32) and hearing impairment infertility male syndrome (HIIMS). We used next-generation sequencing to screen six deaf probands from six families segregating sensorineural moderate-to-profound hearing loss. Data analysis and variant prioritization were completed using a custom bioinformatics pipeline. We identified three homozygous loss of function variants (p.Arg345Ter, p.Arg376Ter, and p.Ala451Thrfs*43) in the CDC14A gene, segregating with deafness in each family. Of the six families, four segregated the p.Arg376Ter mutation, one family segregated the p.Arg345Ter mutation and one family segregated a novel frameshift (p.Ala451Thrfs*43) mutation. In-depth phenotyping of affected individuals ruled out secondary syndromic findings. This study implicates the p.Arg376Ter mutation might be as a founder mutation in the Iranian population. It also provides the first semen analysis for deaf males carrying mutations in exon 11 of CDC14A and reveals a genotype-phenotype correlation that delineates between DFNB32 and HIIMS. The clinical results from affected males suggest the NM_033313.2 transcript alone is sufficient for proper male fertility, but not for proper auditory function. We conclude that DFNB32 is a distinct phenotypic entity in males.Entities:
Year: 2020 PMID: 32231217 PMCID: PMC7651993 DOI: 10.1038/s10038-020-0740-z
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172