Rapid cell-cycle reentry and cell death after acute inactivation of the retinoblastoma gene product in postnatal cochlear hair cells
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Unlike lower vertebrates, mammals are unable to replace damaged mechanosensory hair cells (HCs) in the cochlea. Recently, ablation of the retinoblastoma protein (Rb) in undifferentiated mouse HC precursors was shown to cause cochlear HC proliferation and the generation of new HCs, raising the hope that inactivation of Rb in postmitotic HCs could trigger cell division and regenerate functional HCs postnatally. Here, we acutely inactivated Rb in nearly all cochlear HCs of newborn mice, using a newly developed HC-specific inducible Cre mouse line. Beginning 48 h after Rb deletion, ≈40% of HCs were in the S and M phases of the cell cycle, demonstrating an overriding role for Rb in maintaining the quiescent state of postnatal HCs. Unlike Rb -null HC precursors, such HCs failed to undergo cell division and died rapidly. HC clusters were restricted to the less differentiated cochlear regions, consistent with differentiation-dependent roles of Rb. Moreover, outer HCs expressed the maturation marker prestin, suggesting an embryonic time window for Rb-dependent HC specification. We conclude that Rb plays essential and age-dependent roles during HC proliferation and differentiation, and, in contrast to previous hypotheses, cell death after forced cell-cycle reentry presents a major challenge for mammalian HC regeneration from residual postnatal HCs.
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In the cochlea, Rb deletion increases proliferation of precursor cells; mature mechanosensory hair cells can re-enter the cell cycle but fail to complete division.
“In the cochlea, Rb deletion allows increased proliferation of precursor cells, and although mature mechanosensory hair cells are capable of re-entering the cell cycle, they fail to complete cellular division48.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [48]
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- Authors
- Weber, T., Corbett, M. K., Chow, L. M. L., Valentine, M. B., Baker, S. J., & Zuo, J.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Departments of *Developmental Neurobiology and
- Corresponding author
- Zuo, Jian
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2008-01-15
- Volume
- 105
- Issue
- 2
- Pages
- 781-785
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2206613
- OpenAlex
- W2044168912
- Cited by
- 89
- References
- 38
- Citations by year
- 2024: 1 · 2023: 1 · 2021: 1 · 2020: 3 · 2019: 6 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 4 · 2014: 10 · 2013: 6 · 2012: 14
- FWCI
- 5.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- St. Jude Children's Research Hospital (CA21765)
- American Lebanese Syrian Associated Charities (CA023944, CA 21765)
- National Institutes of Health (CA21765), DC008800)
- U.S. Public Health Service (A096832)
- Canadian Institutes of Health Research
- National Cancer Institute (CA023944, CA21765, R25CA023944, P30CA021765)
- National Institute on Deafness and Other Communication Disorders (DC06471, R01DC006471, R21DC008800, DC05168, R21DC005168, DC008800)
- National Institute of Neurological Disorders and Stroke (R01NS044172, NS044172)
- Topics
- Life Sciences › Neuroscience › Sensory Systems › Hearing, Cochlea, Tinnitus, Genetics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Keywords
- retinoblastoma protein, cochlear hair cells, hair cell regeneration, cell cycle re-entry, hair cell death, hair cell differentiation, prestin, mechanosensory hair cells, mouse model
- MeSH terms
- Animals, Animals, Newborn, Cell Cycle, Chromatin, Hair Cells, Auditory, Humans, Mice, Transgenic, Microscopy, Fluorescence, Mitosis, Recombination, Genetic, Regeneration, Retinoblastoma Protein, Genes, Retinoblastoma, Molecular Motor Proteins, Cell Proliferation, Mice
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