ArticleScientific reports2016
Deletion of Brg1 causes abnormal hair cell planer polarity, hair cell anchorage, and scar formation in mouse cochlea.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 12 citations in OpenAlex.
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- Multiple PDZ domain protein maintains patterning of the apical cytoskeleton in sensory hair cells.Development (Cambridge, England) · 2021Article
- Espin distribution as revealed by super-resolution microscopy of stereocilia.American journal of translational research · 2020Article
- A cytoskeleton structure revealed by super-resolution fluorescence imaging in inner ear hair cells.Cell discovery · 2019Article
- The endocochlear potential as an indicator of reticular lamina integrity after noise exposure in mice.Hearing research · 2018Article
- Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice.Neural plasticity · 2016Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
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Abstract
Hair cells (HCs) are mechanosensors that play crucial roles in perceiving sound, acceleration, and fluid motion. The precise architecture of the auditory epithelium and its repair after HC loss is indispensable to the function of organ of Corti (OC). In this study, we showed that Brg1 was highly expressed in auditory HCs. Specific deletion of Brg1 in postnatal HCs resulted in rapid HC degeneration and profound deafness in mice. Further experiments showed that cell-intrinsic polarity of HCs was abolished, docking of outer hair cells (OHCs) by Deiter's cells (DCs) failed, and scar formation in the reticular lamina was deficient. We demonstrated that Brg1 ablation disrupted the Gαi/Insc/LGN and aPKC asymmetric distributions, without overt effects on the core planer cell polarity (PCP) pathway. We also demonstrated that Brg1-deficient HCs underwent apoptosis, and that leakage in the reticular lamina caused by deficient scar formation shifted the mode of OHC death from apoptosis to necrosis. Together, these data demonstrated a requirement for Brg1 activity in HC development and suggested a role for Brg1 in the proper cellular structure formation of HCs.
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