Noise Stress Abrogates Structure-Specific Endonucleases within the Mammalian Inner Ear
Nucleotide excision repair (NER) is a multistep biochemical process that maintains the integrity of the genome. Unlike other mechanisms that maintain genomic integrity, NER is distinguished by two irreversible nucleolytic events that are executed by the xeroderma pigmentosum group G (XPG) and xerode...
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/25/3/1749 |
| Summary: | Nucleotide excision repair (NER) is a multistep biochemical process that maintains the integrity of the genome. Unlike other mechanisms that maintain genomic integrity, NER is distinguished by two irreversible nucleolytic events that are executed by the xeroderma pigmentosum group G (XPG) and xeroderma pigmentosum group F (XPF) structure-specific endonucleases. Beyond nucleolysis, XPG and XPF regulate the overall efficiency of NER through various protein–protein interactions. The current experiments evaluated whether an environmental stressor could negatively affect the expression of <i>Xpg (Ercc5: excision repair cross-complementing 5)</i> or <i>Xpf (Ercc4: excision repair cross-complementing 4)</i> in the mammalian cochlea. Ubiquitous background noise was used as an environmental stressor. Gene expression levels for <i>Xpg</i> and <i>Xpf</i> were quantified from the cochlear neurosensory epithelium after noise exposure. Further, nonlinear cochlear signal processing was investigated as a functional consequence of changes in endonuclease expression levels. Exposure to stressful background noise abrogated the expression of both <i>Xpg</i> and <i>Xpf</i>, and these effects were associated with pathological nonlinear signal processing from receptor cells within the mammalian inner ear. Given that exposure to environmental sounds (noise, music, etc.) is ubiquitous in daily life, sound-induced limitations to structure-specific endonucleases might represent an overlooked genomic threat. |
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| ISSN: | 1661-6596 1422-0067 |