It is presently accepted that streptomycin (Sm) and the related aminoglycoside antibiotics (these include neomycin (Nm), Kanamycin (Km), paromomycin, and gentamycin) can suppress mutant phenotypes by virtue of their interaction with the ribosome (Gorini and Kataja, 1964; Davies, Gilbert, and Gorini, 1964; Anderson, Gorini, and Breckenridge, 1965; Gorini and Beckwith, 1966); it also seems likely that this interaction is the primary event in the lethal action of these drugs, although this point has not been completely resolved. Sensitivity to both Sm-misreading and inhibition of polypeptide synthesis has been shown to be a property of the 30 S subunit of the ribosome (Davies, 1964a; Cox, White, and Flaks, 1964; Davies, unpublished results), and has been shown to affect specifically the recognition process (Pestka, Marshall, and Nirenberg, 1965; Pestka, 1966b; Kaji and Kaji, 1965) presumably by disturbing the normal messenger RNA-ribosome-transfer RNA interaction in such a way that incorrect base pairing can...
No takes yet. Share an insight, caveat, or question.
Jane C. Davies (1966) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: