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. 2018 Dec 4;47(2):855–867. doi: 10.1093/nar/gky1213

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Published by Oxford University Press on behalf of Nucleic Acids Research 2018.

This work is written by (a) US Government employee(s) and is in the public domain in the US.

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Figure 4. — Overexpression of tRNA_i^Met suppresses the GCN4 induction, but not translation start codon stringency defect, caused by the eIF2γ-I318M mutation. A GCN4-lacZ reporter (A) or (B) his4(UUG)-lacZ and HIS4(AUG)-lacZ reporters were introduced into yeast strains expressing the indicated WT or mutant forms of eIF2γ with or without overexpression of tRNA_i^Met (IMT4). Means and standard deviations of β-galactosidase activities were calculated for three independent transformants. Statistically significant differences in β-galactosidase activities for strains expressing mutant versus WT eIF2γ with empty vector (*) or for strains overexpressing tRNA_i^Met versus empty vector (#) are indicated and were calculated using a Student’s t-test with a P-value threshold of P = 0.05.