Effect of Tetracycline on Puromycin-Induced Polysome Degradation: Influence of Magnesium and Polyamines
Author(s) -
Peter Dionne,
Carmen L. Rosano,
Charles Hurwitz
Publication year - 1975
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.7.5.571
Subject(s) - puromycin , polysome , tetracycline , ribosome , guanosine , biochemistry , spermidine , protein biosynthesis , chemistry , guanosine triphosphate , spermine , fusidic acid , biology , gtp' , antibiotics , rna , enzyme , bacteria , genetics , staphylococcus aureus , gene
Puromycin-induced polysome degradation has been shown to require G factor, guanosine 5'-triphosphate, and the presence of a ribosome release factor (Hirashima and Kaji, 1972, 1973). Tetracycline, which does not inhibit formation of peptidyl-puromycin (Gottesman, 1967; Sarkar and Thach, 1968) nor the guanosine 5'-triphosphate hydrolysis mediated by elongation factor Tu (Ono et al., 1969), inhibits polysome degradation. The tetracycline inhibition requires Mg(2+) at concentrations above 8 mM, which are inhibitory to protein synthesis in vitro. At concentrations of Mg(2+) below 8 mM, polysome degradation is insensitive to tetracycline, but not to fusidic acid. Addition of spermidine, but not of other polyamines, enables the tetracycline inhibition to occur at concentrations of Mg(2+) as low as 2 mM. The inhibition by tetracycline and by fusidic acid suggests that ribosome movement may be essential for the function of ribosome release factor, or that these antibiotics may directly affect its action.
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