Other than its function in mechanotransduction, TMC1 is indispensable for action potential firing of auditory hair cells by mediating a leak conductance that alters tonotopically along the cochlea coil.
ZCWPW1 has co-evolved with PRDM9, in particular the PRDM9-SET domain, and although not involved in PRDM9's role in positioning recombination events, it is required for PRDM9's role in pairing chromosomes.
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.
Biochemical and cell-based analyses reveal how a non-enveloped virus exploits the chaperone activity of an ER transmembrane protein to penetrate the ER membrane required for successful virus infection.
ZCWPW1 is a histone modification reader that localizes to DMC1-labelled double-strand break hotspots in a largely PRDM9-dependent manner, where it facilitates completion of synapsis by mediating DSB repair process.
A previously unrecognized transcriptional coactivator function of the dyskerin ribonucleoprotein complex and its associated small nucleolar RNA has been uncovered and mediates embryonic stem cell-specific transcription.
The meiotic recombination landscape in vertebrates was re-engineered via the co-evolution of a dual histone H3K4/H3K36 methylation 'writer' PRDM9 and its 'reader' ZCWPW1 that facilitates efficient double strand break repair.