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. 2016 Dec 23;7:14021. doi: 10.1038/ncomms14021

Figure 1. Accumulation of a 3′ RNA fragment from nonsense-containing mRNA in UPF1 ATP hydrolysis mutants.

Figure 1

(a) Schematic diagram of point mutations within the C-terminal helicase domain of UPF1 that impair ATP binding (K436E), ATP hydrolysis (DE572AA) or RNA binding (RR793AA). The cysteine/histidine-rich domain (CH) within the N-terminus of UPF1 is indicated. (b–d) Northern blot analysis of PGK1 reporter mRNA in upf1Δ cells (−) complemented with wild-type (WT) or mutant UPF1 using a probe complementary to the mRNA 3′ end. Reporter mRNA either harboured a PTC within its 416 codon open reading frame (b–d) or lacked a PTC (c; −). Full-length reporter mRNA (FL) and 3′ RNA fragments (arrow) are indicated. RNA levels were normalized to NMD-insensitive SCR1 RNA. Results are representative of three independent experiments. Nt, nucleotide.