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. 2019 Dec 2;10:5492. doi: 10.1038/s41467-019-13420-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — ELP5 mediates wobble U₃₄ tRNA modification-dependent translation of hnRNPQ. a The content of U₃₄ cognate codons of the hnRNPQ ORF was the most enriched in P53 ITAFs. ITAF, IRES trans-acting factor. b, c ELP5 depletion downregulated the expression level of hnRNPQ protein (b), but not mRNA (c). d, e The hnRNPQ knockout significantly reduced P53 protein expression and activation under GEM treatment (d), but no effects were observed in the expression of Elongator subunits (d) and P53 mRNA (e). f The hnRNPQ knockout exhibited GEM resistance in NOZ^Cas9 cells. g Exogenous hnRNPQ with a WT ORF sequence was poorly expressed in ELP5-depleted cells. h WT and ELP5-depleted NOZ cells stably expressed Flag-RPL22 (left panel) to perform ribosome immunoprecipitation followed by RT-qPCR, and the results showed ribosome accumulation in hnRNPQ mRNAs in ELP5^−/− cells, but not in control mRNAs (β-Actin) (right panel). i Schematic drawing of the wobble U₃₄ cognate codon mutation (Um) in the hnRNPQ ORF sequence (hnRNPQ^Um). j Flag-hnRNPQ^Um was expressed normally in both WT and ELP5^−/− cells. k, l Successfully overexpressed hnRNPQ^Um could promote or rescue GEM sensitivity (k) and GEM-induced apoptosis (l) in WT and ELP5^−/− cells, respectively. m Overexpression of hnRNPQ^Um promoted P53 accumulation and activation in ELP5-depleted GBC cells. Data represent the mean ± S.D., n = 3 independent experiments in c, e, f, h, k, l, error bars represent S.D. Unpaired Student’s t tests were used in c, e, h, l (NS, non-significant, ^**P < 0.01 and ^***P < 0.001).