Back

Regulation of membrane homeostasis by TMC1 mechanoelectrical transduction channelsis essential for hearing

Ballesteros, A.; Swartz, K. J.

2021-09-25 neuroscience
10.1101/2021.09.24.461722 bioRxiv
Show abstract

The mechanoelectrical transduction (MET) channel complex of auditory hair cells converts sound into electrical signals, allowing us to hear. After decades of research, the transmembrane-like channel 1 and 2 (TMC1 and TMC2) have been recently identified as pore-forming subunits of the MET channels, but the molecular peculiarity that differentiates these two proteins and makes TMC1 essential for hearing remains elusive. Here, we show that TMC1, but not TMC2, is essential for membrane remodeling triggered by a decrease in intracellular calcium concentration. We demonstrate that inhibition of MET channels or buffering of intracellular calcium lead to pronounced phosphatidylserine externalization, membrane blebbing and ectosome release at the hair cell sensory organelle, culminating in the loss of TMC1 protein. Moreover, three TMC1 deafness-causing mutations cause constitutive phosphatidylserine externalization that correlates with the deafness phenotype, suggesting that the mechanisms of hearing loss involve alterations in membrane homeostasis.

Matching journals

The top 3 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.