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Keywords {🔍}

dfna, hearing, family, loss, variation, article, variations, splicesite, sequencing, members, impairment, affected, pubmed, identified, chinese, google, scholar, nature, related, wang, genes, case, gene, normal, exon, families, study, mechanism, pathogenic, patients, medical, genetics, journal, gainoffunction, frameshift, phenotype, exome, table, dna, showed, ear, cas, data, performed, sporadic, china, nonsyndromic, adnshl, individuals, human,

Topics {✒️}

mfi2/dfna5/nsun5/tecpr1/mllt3/cnot1/akap8 nature portfolio contributed reagents/materials/analysis tools privacy policy showed normal middle nature advertising open reading frame social media east asians reprints japan map-kinase-related activity noise-induced hearing loss disease-causing genes tjp2 age-related hearing loss heterozygous splice-site variation late-onset progressive splice-site variation affects original author specific variation-induced pathological sensorineural hearing loss pathogenic splice-site variations dfna5 splice-site variation materials ethics statement thermo scientific pure-tone average disease-causing gene variation outer hair cells permissions full size image cochlear hair cells similar content targeted genes capture nonsyndromic hearing impairment adnshl related genes syndromic hearing loss reverse transcriptase pcr moderated hearing loss hearing loss phenotype10 targeted exome sequencing splice-site variation splice site mutation hearing impairment affecting congenital hearing impairment significant hearing impairment splice-site variations 6 splice-site variations splice donor site article wang

Questions {❓}

• DFNA5: hearing impairment exon instead of hearing impairment gene?

Schema {🗺️}

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         headline:Further evidence for “gain-of-function” mechanism of DFNA5 related hearing loss
         description:To report two DFNA5 pathogenic splice-site variations and a novel benign frameshift variation to further support the gain-of-function mechanism of DFNA5 related hearing impairment, targeted genes capture and next generation sequencing were performed on selected members from Family 1007208, 1007081 and a sporadic case with sensorineural hearing loss. Reverse transcriptase polymerase chain reaction was conducted on the proband from Family 1007208 to test how the splice-site variation affects the transcription in RNA level. A novel heterozygous splice-site variation c.991-3 C > A in DFNA5 was found in Family 1007208; a known hotspot heterozygous splice-site variation c.991-15_991_13delTTC was identified in Family 1007081. Both the splice-site variations were segregated with the late onset hearing loss phenotype, leading to the skipping of exon 8 at RNA level. In addition, a novel DFNA5 frameshift variation c.116_119delAAAA was found in the sporadic case, but was not segregated with the hearing impairment phenotype. In conclusion, we identified one novel and one known pathogenic DFNA5 splice-site variation in two Chinese Families, as well as a novel DFNA5 frameshift variation c.116_119delAAAA in a sporadic case, which does not the cause for the hearing loss case. Both the two pathogenic splice-site variations and the nonpathogenic frameshift variation provide further support for the specific gain-of-function mechanism of DFNA5 related hearing loss.
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      headline:Further evidence for “gain-of-function” mechanism of DFNA5 related hearing loss
      description:To report two DFNA5 pathogenic splice-site variations and a novel benign frameshift variation to further support the gain-of-function mechanism of DFNA5 related hearing impairment, targeted genes capture and next generation sequencing were performed on selected members from Family 1007208, 1007081 and a sporadic case with sensorineural hearing loss. Reverse transcriptase polymerase chain reaction was conducted on the proband from Family 1007208 to test how the splice-site variation affects the transcription in RNA level. A novel heterozygous splice-site variation c.991-3 C > A in DFNA5 was found in Family 1007208; a known hotspot heterozygous splice-site variation c.991-15_991_13delTTC was identified in Family 1007081. Both the splice-site variations were segregated with the late onset hearing loss phenotype, leading to the skipping of exon 8 at RNA level. In addition, a novel DFNA5 frameshift variation c.116_119delAAAA was found in the sporadic case, but was not segregated with the hearing impairment phenotype. In conclusion, we identified one novel and one known pathogenic DFNA5 splice-site variation in two Chinese Families, as well as a novel DFNA5 frameshift variation c.116_119delAAAA in a sporadic case, which does not the cause for the hearing loss case. Both the two pathogenic splice-site variations and the nonpathogenic frameshift variation provide further support for the specific gain-of-function mechanism of DFNA5 related hearing loss.
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      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China
      name:Chinese PLA Institute of Otolaryngology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, China

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