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[DOI] [PMC free article] [PubMed] [Google Scholar] [176].Wong K, Puthucheary S, Vadivelu J

1999), though this conclusion appears to be incorrect because a defect in the experimental design led to increased transcription of the entire leucine biosynthetic operon in cells that contained functional Atm1, because selective inactivation of Atm1 was achieved by using a plasmid that re-introduced functional Leu2 into a Leu2-null strain (reviewed in Rouault 2015a), and the comparison of leu 1 enzymatic activity that was performed on cells that contained inactivated Atm1 had markedly lower transcript levels of leu1, which would be expected to markedly decrease leu 1 protein levels and enzymatic activity in the cell line in which Atm1 function was knocked out using a construct that restored leu2 gene expression to the leu2 deficient strain