Lps gene-associated functions.

Abstract

Listen

Translate article

As a result of a spontaneous mutation estimated to have occurred between 1960 and 1965, the C3H/HeJ mouse strain now exhibits a profound state of hyporesponsiveness to endotoxin, the ubiquitous lipopolysaccharide (LPS) cell wall component of Gram negative bacteria. The failure of C3H/HeJ mice to respond to LPS in vivo is reflected by the failure of a variety of cell types derived from these mice (i.e., B cells, T cells, macrophages, and fibroblasts) to respond to LPS in vitro (reviewed in Rosenstreich 1985). Based on genetic analyses using the C3H/HeJ mouse in crosses with other fully LPS-responsive strains, it is now recognized that the capacity to respond to LPS is controlled by a single, autosomal gene, Lps, for which a normal allele (Lps n) and a defective allele (Lps d) have been defined (reviewed in Rosenstreich 1985). The in vivo or in vitro responses to LPS exhibited by F1 progeny of Lps n/Lps n X Lps d/Lps d crosses have been found to be intermediate, indicating that the Lps gene is codominantly expressed (Sultzer 1972; Glode and Rosenstreich 1976; Watson et al. 1977b; Rosenstreich et al. 1978; McGhee et al. 1979).