Defective gamma subunit of ATP synthase (F1F0) from Escherichia coli leads to resistance to aminoglycoside antibiotics.

摘要: A strain of Escherichia coli which was derived from a gentamicin-resistant clinical isolate found to be cross-resistant neomycin and streptomycin. The molecular nature the genetic defect an insertion two GC base pairs in uncG gene mutant. led production truncated gamma subunit 247 amino acids length instead 286 that are present normal subunit. plasmid carried ATP synthase genes mutant produced resistance aminoglycoside antibiotics when it introduced into with chromosomal deletion genes. Removal coding for beta epsilon subunits abolished antibiotic coded by plasmid. relationship between investigated testing plasmids carrying various combinations unc presence F0 portion or absence not sufficient cause resistance. alpha, beta, were detected on washed membranes immunoblotting. first acid residues may allow its association other F1 such way proton gate is held open F1.