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. Author manuscript; available in PMC: 2017 Oct 11.
Published in final edited form as: Cell. 2016 Sep 15;167(1):122–132.e9. doi: 10.1016/j.cell.2016.08.053

Figure 2. Dhh1p selectively stimulates the decay of mRNAs with low codon optimality.

Figure 2

See also Figure S2. (A) Representation of the synthetic mRNAs (SYN) and the encoded polypeptide sequence. Optimal (OPT) or non-optimal (NON-OPT) codons encoding the same peptide were used. The artificial peptide has no similarity to any known proteins. (B) The half-lives of SYN OPT and NON-OPT mRNAs in WT and different mutant strains were obtained from GAL1 shutoff experiments. Quantitations were normalized to the amount of SCR1 RNA. *Denotes average of 3 experiments. (C) Half-lives of HIS3 reporters from Figure 1B (GAL1 UAS constructs) in WT or dhh1Δ cells. Right panel indicates fold stabilization in a dhh1Δ cells vs. WT. (D) Quantification of steady state levels of mRNAs transcripts by RNA-Seq in dhh1Δ cells (RPKM) relative to WT cells (RPKM). mRNA transcripts are binned by sTAI, a numerical proxy for overall optimality. Shown are two biological replicates. A two-tailed Mann-Whitney test shows that low optimality mRNAs (sTAI = 0.25, Med. = 1.52) are enriched relative to high optimality mRNAs (sTAI = 0.55, Med. = 0.72) upon Dhh1p depletion, U = 1668, p < 2.2×10−16.