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• W2078233149 abstract "The class I myosin Myo1c is a mediator of adaptation of mechanoelectrical transduction in the stereocilia of the inner ear. Adaptation, which is strongly affected by Ca 2+ , permits hair cells under prolonged stimuli to remain sensitive to new stimuli. Using a Myo1c fragment (motor domain and one IQ domain with associated calmodulin), with biochemical and kinetic properties similar to those of the native molecule, we have performed a thorough analysis of the biochemical cross-bridge cycle. We show that, although the steady-state ATPase activity shows little calcium sensitivity, individual molecular events of the cross-bridge cycle are calcium-sensitive. Of significance is a 7-fold inhibition of the ATP hydrolysis step and a 10-fold acceleration of ADP release in calcium. These changes result in an acceleration of detachment of the cross-bridge and a lengthening of the lifetime of the detached M–ATP state. These data support a model in which slipping adaptation, which reduces tip-link tension and allows the transduction channels to close after an excitatory stimulus, is mediated by Myo1c and modulated by the calcium transient." @default.
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• W2078233149 date "2008-04-15" @default.
• W2078233149 modified "2023-09-26" @default.
• W2078233149 title "Calcium sensitivity of the cross-bridge cycle of Myo1c, the adaptation motor in the inner ear" @default.
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• W2078233149 doi "https://doi.org/10.1073/pnas.0710520105" @default.
• W2078233149 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2299219" @default.
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