A zebrafish model for a particular form of human deafness (DFNB63) changes our view of this disease by revealing a defect in the localization of Transmembrane channel-like proteins that are essential for mechanotransduction in sensory cells.
Immunolabelling and morphological assessment, complemented by complete transcriptomic analysis, demonstrates that supporting cells can be induced to convert towards a hair cell-like phenotype in human vestibular sensory epithelia.
The remarkable lifelong stability of mechanotransducing stereocilia of the inner ear hair cells depends on the activity of the transduction ion channels located at the tips of these mechanosensory projections.
Computational modeling and molecular-biological analysis reveal the role of mechanical force and downstream Yap signaling in growth control during the development and regeneration of sensory epithelium of the inner ear.
Single-cell FRET measurements reveal large temporal activity fluctuations within this signaling pathway in Escherichia coli, caused by stochasticity of receptor methylation combined with allosteric interactions and slow rearrangements within receptor clusters.
Temporally delayed linear modelling provides a domain-general linear framework for sequence detection and statistical testing, and is able to detect replays in both human neuroimaging and animal electrophysiology.