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Updated: May 19, 2026

Dissection of the Auditory Bulla in Postnatal Mice: Isolation of the Middle Ear Bones and Histological Analysis
Published on: January 4, 2017
Anti-apoptotic gene Bcl2 is required for stapes development and hearing
M R Carpinelli1, A K Wise, B D Arhatari
1Molecular Hearing Laboratory, The Murdoch Children's Research Institute, Royal Children's Hospital, 50 Flemington Road, Parkville, Victoria 3052, Australia. marina.carpinelli@mcri.edu.au
The anti-apoptotic regulator Bcl2 is crucial for stapes development and normal hearing. Its absence causes severe hearing loss and stapes malformation in mice, a defect rescued by genetic modification.
Area of Science:
- Developmental Biology
- Otolaryngology
- Genetics
Background:
- The apoptotic regulators Bcl2 (anti-apoptotic) and Bim (pro-apoptotic) play critical roles in cell survival and death.
- Understanding their specific functions in auditory development is essential for identifying causes of hearing impairment.
Purpose of the Study:
- To investigate the roles of Bcl2 and Bim in the development of the auditory system, particularly the stapes.
- To elucidate the cellular and developmental origins of hearing defects associated with these apoptotic regulators.
Main Methods:
- Analysis of auditory systems in mice genetically deficient for Bcl2 and Bim.
- Histological examination of the stapes, malleus, and incus.
- Assessment of hearing function and inner ear sensory cell integrity.
Main Results:
- Bcl2-deficient mice exhibited severe conductive hearing loss and malformed stapes, with normal inner ear sensory cells.
- Stapes defects originated in utero during the cartilage development stage.
- Complete rescue of stapes defects and hearing loss was observed in Bcl2⁻/⁻Bim⁻/⁻ mice, with partial rescue in Bcl2⁻/⁻Bim⁺/⁻ mice.
Conclusions:
- Bcl2 is indispensable for normal stapes formation and hearing.
- Bcl2 and Bim are key regulators of cell survival during embryonic development of the stapes, likely acting on second pharyngeal arch or neural crest-derived cells.
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