Lincosamide antibiotics stimulate dissociation of peptidyl-tRNA from ribosomes.
At nonpermissive temperatures the peptidyl-tRNA hydrolase of pth(Ts) bacterial mutants is inactivated, and cells accumulate peptidyl-tRNA and die. Doses of erythromycin, lincomycin, or clindamycin that inhibited the growth of antibiotic-hypersensitive DB-11 pth+ cells accelerated the killing of DB-11 pth(Ts) cells at nonpermissive temperatures. Erythromycin and lincomycin also stimulated the accumulation of peptidyl-tRNA. Lincomycin and clindamycin stimulated peptidyl-tRNA dissociation from ribosomes.
Menninger
J R
JR
Department of Biological Sciences, University of Iowa, Iowa City 52242-1324.
Coleman
R A
RA
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002265:Carboxylic Ester Hydrolases / Q000235:genetics / Q000378:metabolism; D002981:Clindamycin / Q000494:pharmacology; D004917:Erythromycin / Q000494:pharmacology; D004926:Escherichia coli / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics; D008034:Lincomycin / Q000494:pharmacology; D055231:Lincosamides; D018942:Macrolides; D009154:Mutation; D012346:RNA, Transfer, Amino Acyl / Q000235:genetics / Q000378:metabolism*; D012270:Ribosomes / Q000187:drug effects / Q000378:metabolism*; D013696:Temperature
D000900:Anti-Bacterial Agents; D055231:Lincosamides; D018942:Macrolides; D012346:RNA, Transfer, Amino Acyl; C019037:tRNA, peptidyl-; D002981:Clindamycin; D004917:Erythromycin; D008034:Lincomycin; D002265:Carboxylic Ester Hydrolases; C019674:aminoacyl-tRNA hydrolase