Maslennikova et al. identify the ER membrane protein CLCC1 as an interaction partner of the dystonia-linked AAA+ ATPase Torsin1A. Torsin1A sustains the function of CLCC1, which is proposed to facilitate fusion of the nuclear envelope during NPC biogenesis by forming an oligomer that promotes lipid bilayer approach and remodeling.

Fischer et al. uncover a fundamental mechanism of membrane fusion during nuclear pore complex (NPC) assembly. Brl1 and Brr6 form ring-shaped, membrane-remodeling complexes that interact and bridge the...

Maslennikova et al. identify the ER membrane protein CLCC1 as an interaction partner of the dystonia-linked AAA+ ATPase Torsin1A. Torsin1A sustains the function of CLCC1, which is proposed to facilitate fusion of the nuclear envelope during NPC biogenesis by forming an oligomer that promotes lipid bilayer approach and remodeling.

Fischer et al. uncover a fundamental mechanism of membrane fusion during nuclear pore complex (NPC) assembly. Brl1 and Brr6 form ring-shaped, membrane-remodeling complexes that interact and bridge the nuclear envelope at NPC-assembly sites to mediate fusion. This pathway is conserved in humans via the metazoan fusogen CLCC1.

Maslennikova et al. identify the ER membrane protein CLCC1 as an interaction partner of the dystonia-linked AAA+ ATPase Torsin1A. Torsin1A sustains the function of CLCC1, which is proposed to facilitate fusion of the nuclear envelope during NPC biogenesis by forming an oligomer that promotes lipid bilayer approach and remodeling.

Lewis et al. identify lamin B receptor (LBR) and lamina-associated polypeptide 2 (LAP2) as major factors that tether heterochromatin to the envelope. Deletion of these proteins causes changes in 3D ge...

Lewis et al. identify lamin B receptor (LBR) and lamina-associated polypeptide 2 (LAP2) as major factors that tether heterochromatin to the envelope. Deletion of these proteins causes changes in 3D ge...

Lewis et al. identify lamin B receptor (LBR) and lamina-associated polypeptide 2 (LAP2) as major factors that tether heterochromatin to the envelope. Deletion of these proteins causes changes in 3D ge...

DYT1 early-onset dystonia is a severe, incurable disorder of the central nervous system caused by mutations in the gene encoding Torsin1A (Tor1A, DYT1). Torsins are ER-resident AAA+-ATPases implicated...

DYT1 early-onset dystonia is a severe, incurable disorder of the central nervous system caused by mutations in the gene encoding Torsin1A (Tor1A, DYT1). Torsins are ER-resident AAA+-ATPases implicated...