Open AccessAmplification of a novel gene, sanA, abolishes a vancomycin-sensitive defect in Escherichia coli
Author(s) -
S. M. Rida,
J. Caillet,
JeanHervé Alix
Publication year - 1996
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.178.1.94-102.1996
Subject(s) - escherichia coli , biology , gene , mutant , homologous recombination , genetics , chromosome , null allele , mutation , microbiology and biotechnology
We have isolated an Escherichia coli gene which, when overexpressed, is able to complement the permeability defects of a vancomycin-susceptible mutant. This gene, designated sanA, is located at min 47 of the E. coli chromosome and codes for a 20-kDa protein with a highly hydrophobic amino-terminal segment. A strain carrying a null mutation of the sanA gene, transferred to the E. coli chromosome by homologous recombination, is perfectly viable, but after two generations at high temperature (43 degrees C), the barrier function of its envelope towards vancomycin is defective.