| Abstract: |
Selection of mutant Mv1Lu mink lung epithelial cells resistant to growth inhibition by transforming growth factor-β (TGF-β) has led to the isolation of cell clones with distinct alterations in type I and II TGF-β receptors. Certain mutant clones present a decreased number or complete loss of detectable type I receptor. Other clones show a loss and/or altered electrophoretic mobility of the type II receptor, with concomitant loss of the type I receptor. Using somatic cell hybridization analysis we demonstrate the recessive nature of these mutants with respect to the wild-type phenotype and define various mutant complementation groups. Among these, hybrids between cells that express only type II receptor (R mutants) and cells that express neither receptor type (DRa mutants) rescue wild-type expression of type I receptors. Moreover, these hybrids regain full responsiveness to TGF-β1, as measured by inhibition of DNA synthesis as well as stimulation of fibronectin and plasminogen activator inhibitor-1 production. These results provide evidence for an interaction between TGF-β receptor components I and II and show that, in Mv1Lu cells, expression of both receptor types is required for mediation of biological responses to TGF-β1. |
| Keywords: |
signal transduction; mutation; nonhuman; animal cell; animal; cell division; gene expression; transforming growth factor beta; cell line; animalia; lung; receptors, transforming growth factor beta; epithelium cell; in vitro; mink; receptors, cell surface; genetic complementation test; growth factor receptor; hybrid cells; fibronectins; genes, recessive; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; mustela vison; plasminogen inactivators
|
