Open AccessModulation of microfilament protein composition by transfected cytoskeletal actin genes.
Author(s) -
S Y Ng,
Harry P. Erba,
G Latter,
Larry Kedes,
John Leavitt
Publication year - 1988
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.8.4.1790
Subject(s) - biology , actin , transfection , microfilament , microbiology and biotechnology , actin binding protein , actin remodeling , gene isoform , cytoskeleton , tropomyosin , actin remodeling of neurons , beta (programming language) , gene , actin cytoskeleton , cell , biochemistry , computer science , programming language
HuT-14T is a highly tumorigenic fibroblast cell line which exhibits a reduced steady-state level of beta-actin due to coding mutations in one of two beta-actin alleles. The normal rate of total actin synthesis could be restored in some clones of cells following transfection of the functional beta-actin gene but not following transfection of the functional gamma-actin gene. In gamma-actin gene-transfected substrains that have increased rates of gamma-actin synthesis, beta-actin synthesis is further reduced in a manner consistent with an autoregulatory mechanism, resulting in abnormal ratios of actin isoforms. Thus, both beta- and gamma-actin proteins can apparently regulate the synthesis of their coexpressed isoforms. In addition, decreased synthesis of normal beta-actin seems to correlate with a concomitant down-regulation of tropomyosin isoforms.