Suppression of a nonsense mutation in mammalian cells in vivo by the aminoglycoside anthiotics G–418 and paromomycin
JF Burke, AE Mogg - Nucleic acids research, 1985 - academic.oup.com
JF Burke, AE Mogg
Nucleic acids research, 1985•academic.oup.comAminoglycoside antibiotics in Escherichia coli and yeast can cause ribosomes to read
through stop codons during translation. This can result in the phenotypic suppression of
nonsense nutations. We show here for the first time that the aminoglycosides G–418 and
paronomycin have similar effects in monkey (COS–7) cells in vivo. Suppression of an amber
mutation (TAG) by aninoglycosides can restore the activity of a mutant gene transfected into
COS–7 cells to almost 20% of wild type levels.
through stop codons during translation. This can result in the phenotypic suppression of
nonsense nutations. We show here for the first time that the aminoglycosides G–418 and
paronomycin have similar effects in monkey (COS–7) cells in vivo. Suppression of an amber
mutation (TAG) by aninoglycosides can restore the activity of a mutant gene transfected into
COS–7 cells to almost 20% of wild type levels.
Abstract
Aminoglycoside antibiotics in Escherichia coli and yeast can cause ribosomes to read through stop codons during translation. This can result in the phenotypic suppression of nonsense nutations. We show here for the first time that the aminoglycosides G–418 and paronomycin have similar effects in monkey (COS–7) cells in vivo. Suppression of an amber mutation (TAG) by aninoglycosides can restore the activity of a mutant gene transfected into COS–7 cells to almost 20% of wild type levels.
Oxford University Press