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. 2010 Jul 15;24(14):1491–1495. doi: 10.1101/gad.1930710

Figure 1.

Figure 1.

A mutation in the ALR1 gene counteracts the termination defect of NMD-deficient cells. (A) Nonsense suppression in NMD- and Alr1p-deficient cells. The indicated strains (MJY142, MJY67, MJY130, MJY447, MJY169, MJY193, MJY150, and MJY151) were grown overnight in liquid synthetic complete (SC) medium at 30°C. Cells were serially diluted; spotted onto SC, SC-leu, and SC-arg + can (200 μg/mL can) plates; and incubated for 3 d at 30°C. (B) Northern analysis of total RNA isolated from wild-type (MJY142), upf1Δ (MJY67), alr1Δ (MJY130), and upf1Δ alr1Δ (MJY447) cells grown in SC medium at 30°C. The blot was probed for leu2-2, can1-100, PGK1, and SCR1 transcripts using randomly labeled DNA fragments. The noncoding SCR1 transcript serves as a loading control. (C,D) Readthrough levels of UGA (C) and UAA (D) stop codons in the wild-type (MJY142), upf1Δ (MJY67), alr1Δ (MJY130), and upf1Δ alr1Δ (MJY447) strains. The values represent the average of five independent experiments. The standard deviation is indicated.