ArticleBiophysical journal2008
Human deafness mutation E385D disrupts the mechanochemical coupling and subcellular targeting of myosin-1a.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Dominant effect of a single amino acid mutation in the motor domain of myosin VI on hearing in mice.Experimental animals · 2025Article
- The effect of novel mutations on the structure and enzymatic activity of unconventional myosins associated with autosomal dominant non-syndromic hearing loss.Open biology · 2014Article
- Molecular basis of dynamic relocalization of Dictyostelium myosin IB.The Journal of biological chemistry · 2012Article
- Myosin-1A targets to microvilli using multiple membrane binding motifs in the tail homology 1 (TH1) domain.The Journal of biological chemistry · 2012Article
- Proteomic analysis of the enterocyte brush border.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- A hearing loss-associated myo1c mutation (R156W) decreases the myosin duty ratio and force sensitivity.Biochemistry · 2011Article
- Myo1c mutations associated with hearing loss cause defects in the interaction with nucleotide and actin.Cellular and molecular life sciences : CMLS · 2011Article
- Targeting of the hair cell proteins cadherin 23, harmonin, myosin XVa, espin, and prestin in an epithelial cell model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Dynamic length regulation of sensory stereocilia.Seminars in cell & developmental biology · 2008Review
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Missense mutations in the membrane-binding actin-based motor protein, myosin-1a (Myo1a), have recently been linked to sensorineural deafness in humans. One of these mutations, E385D, impacts a residue in the switch II region of the motor domain that is present in virtually all members of the myosin superfamily. We sought to examine the impact of E385D on the function of Myo1a, both in terms of mechanochemical activity and ability to target to actin-rich microvilli in polarized epithelial cells. While E385D-Myo1a demonstrated actin-activated ATPase activity, the V(MAX) was reduced threefold relative to wild-type. Despite maintaining an active mechanochemical cycle, E385D-Myo1a was unable to move actin in the sliding filament assay. Intriguingly, when an enhanced-green-fluorescent-protein-tagged form of E385D-Myo1a was stably expressed in polarized epithelial cells, this mutation abolished the microvillar targeting normally demonstrated by wild-type Myo1a. Notably, these data are the first to suggest that mechanical activity is essential for proper localization of Myo1a in microvilli. These studies also provide a unique example of how even the most mild substitution of invariant switch II residues can effectively uncouple enzymatic and mechanical activity of the myosin motor domain.
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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.