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CIB2, defective in isolated deafness, is key for auditory hair cell mechanotransduction and survival
Journal article   Open access   Peer reviewed

CIB2, defective in isolated deafness, is key for auditory hair cell mechanotransduction and survival

Vincent Michel, Kevin T Booth, Pranav Patni, Matteo Cortese, Hela Azaiez, Amel Bahloul, Kimia Kahrizi, Ménélik Labbe, Alice Emptoz, Andrea Lelli, …
EMBO molecular medicine, Vol.9(12), pp.1711-1731
12/01/2017
DOI: 10.15252/emmm.201708087
PMCID: PMC5709726
PMID: 29084757
url
https://doi.org/10.15252/emmm.201708087View
Published (Version of record) Open Access

Abstract

Defects of CIB2, calcium-and integrin-binding protein 2, have been reported to cause isolated deafness, DFNB48 and Usher syndrome type-IJ, characterized by congenital profound deafness, balance defects and blindness. We report here two new nonsense mutations (pGln12* and pTyr110*) in CIB2 patients displaying nonsyn-dromic profound hearing loss, with no evidence of vestibular or retinal dysfunction. Also, the generated CIB2 À/À mice display an early onset profound deafness and have normal balance and reti-nal functions. In these mice, the mechanoelectrical transduction currents are totally abolished in the auditory hair cells, whilst they remain unchanged in the vestibular hair cells. The hair bundle morphological abnormalities of CIB2 À/À mice, unlike those of mice defective for the other five known USH1 proteins, begin only after birth and lead to regression of the stereocilia and rapid hair-cell death. This essential role of CIB2 in mechanotransduction and cell survival that, we show, is restricted to the cochlea, probably accounts for the presence in CIB2 À/À mice and CIB2 patients, unlike in Usher syndrome, of isolated hearing loss without balance and vision deficits.
Life Sciences Human health and pathology Sensory Organs

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