DOI: 10.53846/goediss-9683
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Molecular Mechanisms of Frequency Discrimination in the Drosophila Ear

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“…For example, amplification mechanisms involve both shared and unique features between flies and mammals, in that the force of transduction channel closing altering gating compliance can provide an energy source for amplification in both systems (Howard & Hudspeth, 1988;Nadrowski et al, 2008), whereas motility-based sources involve Prestin electromotility in mammals (Zheng et al, 2000) but (presumably) ciliary dynein motility in insects (Karak et al, 2015;Kavlie et al, 2010;Möckel et al, 2012;Warren et al, 2010). Physiological hearing disorders are also caused by dysfunction of other ion channels, such as the voltage-gated Na + and K + channel in insects (Ravenscroft et al, 2023;Zhang, 2023) and K + channels and Ca 2+ channels in mammals (Baig et al, 2011;Kharkovets et al, 2000Kharkovets et al, , 2006Kubisch et al, 1999;Neyroud et al, 1997;Schulze-Bahr et al, 1997). In addition, gap junctions play a key role, with the GJB2 gene, encoding Connexin 43, representing one the most prevalent hereditary deafness genes (Kelsell et al, 1997).…”
Section: Genetic Disordersmentioning
confidence: 99%
“…For example, amplification mechanisms involve both shared and unique features between flies and mammals, in that the force of transduction channel closing altering gating compliance can provide an energy source for amplification in both systems (Howard & Hudspeth, 1988;Nadrowski et al, 2008), whereas motility-based sources involve Prestin electromotility in mammals (Zheng et al, 2000) but (presumably) ciliary dynein motility in insects (Karak et al, 2015;Kavlie et al, 2010;Möckel et al, 2012;Warren et al, 2010). Physiological hearing disorders are also caused by dysfunction of other ion channels, such as the voltage-gated Na + and K + channel in insects (Ravenscroft et al, 2023;Zhang, 2023) and K + channels and Ca 2+ channels in mammals (Baig et al, 2011;Kharkovets et al, 2000Kharkovets et al, , 2006Kubisch et al, 1999;Neyroud et al, 1997;Schulze-Bahr et al, 1997). In addition, gap junctions play a key role, with the GJB2 gene, encoding Connexin 43, representing one the most prevalent hereditary deafness genes (Kelsell et al, 1997).…”
Section: Genetic Disordersmentioning
confidence: 99%