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. 2021 Nov 27;7:368. doi: 10.1038/s41420-021-00756-x

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© The Author(s) 2021

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. 4 — METTL3 was either overexpressed (METTL3) or knocked down (si-METTL3) in isolated KCs. A The protein level of METTL3 was examined by western blot in indicated cells. Control, parental KCs. B Wildtype and mutated (Mut; red letters) m6A methylation sequences in MALAT1 predicted using m6Avar database and constructs containing different mutations were illustrated. C m6A methylation on indicated MALAT1 constructs was examined by m6A mRNA immunoprecipitation assay followed by RT-qPCR. D, E m6A methylation status on indicated MALAT1 constructs in parental KCs, those overexpressing METTL3, or knocking down METTL3 (si-METTL3) was examined by m6A mRNA immunoprecipitation assay followed by RT-qPCR. F METTL3-expressing (left panel) or si-METTL3-expressing (right panel) KCs were transfected with MALAT1-WT or MALAT1-Mut1-2. The expressions of MALAT1 were analyzed by RT-qPCR. *P < 0.05 or **P < 0.01, ***P < 0.001.