The dystonia-associated Torsin1A sustains CLCC1 function in membrane fusion of the nuclear envelope for NPC biogenesis.
The conserved membrane protein Chloride Channel CLIC-like protein 1 (CLCC1) is identified as a Torsin1A interaction partner whose absence phenocopies membrane fusion defects caused by Torsin deletion inform a model of nuclear envelope membrane fusion and imply that modulating CLCC1 expression is a promising therapeutic...