|  Help  |  About  |  Contact Us

Publication : Characterization of dominant and recessive assembly-defective mutations in mouse neurofilament NF-M.

First Author  Wong PC Year  1990
Journal  J Cell Biol Volume  111
Issue  5 Pt 1 Pages  1987-2003
PubMed ID  2121743 Mgi Jnum  J:77598
Mgi Id  MGI:2182114 Doi  10.1083/jcb.111.5.1987
Citation  Wong PC, et al. (1990) Characterization of dominant and recessive assembly-defective mutations in mouse neurofilament NF-M. J Cell Biol 111(5 Pt 1):1987-2003
abstractText  We have generated a set of amino- and carboxy-terminal deletions of the neurofilament NF-M gene and determined the molecular consequences of forced expression of these mutant constructs in mouse fibroblasts. To follow the expression of mutant NF-M subunits in transfected cells, a 12 amino acid epitope (from the human c-myc protein) was expressed at the carboxy terminus of each mutant. We show that NF-M molecules missing up to 90 or 70% of the nonhelical carboxy-terminal tail or amino-terminal head domains, respectively, incorporate readily into an intermediate filament network comprised either of vimentin or NF-L, whereas deletions into either the amino- or carboxy-terminal alpha-helical rod region generate assembly-incompetent polypeptides. Carboxy-terminal deletions into the rod domain invariably yield dominant mutants which rapidly disrupt the array of filaments comprised of NF-L or vimentin. Accumulation of these mutant NF-M subunits disrupts vimentin filament arrays even when present at approximately 1% the level of the wild-type subunits. In contrast, the amino-terminal deletions into the rod produce pseudo-recessive mutants that perturb the wild-type NF-L or vimentin arrays only modestly. The inability of such amino-terminal mutants to disrupt wild-type subunits defines a region near the amino-terminal alpha-helical rod domain (residues 75-126) that is required for the earliest steps in filament assembly.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

2 Authors

1 Bio Entities

Trail: Publication

0 Expression