ArticleBiochemistry2011
A hearing loss-associated myo1c mutation (R156W) decreases the myosin duty ratio and force sensitivity.
Article in Biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 41 citations in OpenAlex.
- Danicamtiv reduces myosin's working stroke but activates the thin filament by accelerating actomyosin attachment.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- High-resolution structures of Myosin-IC reveal a unique actin-binding orientation, ADP release pathway, and power stroke trajectory.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- High resolution structures of Myosin-IC reveal a unique actin-binding orientation, ADP release pathway, and power stroke trajectory.bioRxiv : the preprint server for biology · 2025Article
- Danicamtiv reduces myosin's working stroke but enhances contraction by activating the thin filament.bioRxiv : the preprint server for biology · 2024Article
- Myosin-1C differentially displaces tropomyosin isoforms altering their inhibition of motility.The Journal of biological chemistry · 2024Article
- Myosin-5 varies its step length to carry cargo straight along the irregular F-actin track.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Pathophysiology of human hearing loss associated with variants in myosins.Frontiers in physiology · 2024Review
- Switch-2 determines MgFrontiers in physiology · 2024Article
- Motility Assay to Probe the Calcium Sensitivity of Myosin and Regulated Thin Filaments.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Review
- Loss of Motor Protein MYO1C Causes Rhodopsin Mislocalization and Results in Impaired Visual Function.Cells · 2021Article
- Functional Role of Class III Myosins in Hair Cells.Frontiers in cell and developmental biology · 2021Review
- Opposing Pressures of Speed and Efficiency Guide the Evolution of Molecular Machines.Molecular biology and evolution · 2019Article
- N-terminal splicing extensions of the humanThe Journal of biological chemistry · 2017Article
- ROS induced distribution of mitochondria to filopodia by Myo19 depends on a class specific tryptophan in the motor domain.Scientific reports · 2017Article
- Kinetic adaptation of human Myo19 for active mitochondrial transport to growing filopodia tips.Scientific reports · 2017Article
- Chemomechanical regulation of myosin Ic cross-bridges: Deducing the elastic properties of an ensemble from single-molecule mechanisms.PLoS computational biology · 2017Article
- Kinetic Adaptations of Myosins for Their Diverse Cellular Functions.Traffic (Copenhagen, Denmark) · 2016Review
- Myosin-I molecular motors at a glance.Journal of cell science · 2016Review
- A Perspective on the Role of Myosins as Mechanosensors.Biophysical journal · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
myo1c is a member of the myosin superfamily that has been proposed to function as the adaptation motor in vestibular and auditory hair cells. A recent study identified a myo1c point mutation (R156W) in a person with bilateral sensorineural hearing loss. This mutated residue is located at the start of the highly conserved switch 1 region, which is a crucial element for the binding of nucleotide. We characterized the key steps on the ATPase pathway at 37 °C using recombinant wild-type (myo1c(3IQ)) and mutant myo1c (R156W-myo1c(3IQ)) constructs that consist of the motor domain and three IQ motifs. The R156W mutation only moderately affects the rates of ATP binding, ATP-induced actomyosin dissociation, and ADP release. The actin-activated ATPase rate of the mutant is inhibited >4-fold, which is likely due to a decrease in the rate of phosphate release. The rate of actin gliding, as measured by the in vitro motility assay, is unaffected by the mutation at high myosin surface densities, but the rate of actin gliding is substantially reduced at low surface densities of R156W-myo1c(3IQ). We used a frictional loading assay to measure the affect of resisting forces on the rate of actin gliding and found that R156W-myo1c(3IQ) is less force-sensitive than myo1c(3IQ). Taken together, these results indicate that myo1c with the R156W mutation has a lower duty ratio than the wild-type protein and motile properties that are less sensitive to resisting forces.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.