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A follow-up analysis of RNA-Seq data showed that a significant portion of non-coding RNAs is also regulated by metTL3-mediated m6A modification (Figure S7A, B and Table S3). Unlike protein coding genes, most regulated LincNAs were heavily regulated in metTL3 (Figure S7B) MGG8-GCs. Other studies have shown that RNAs have been compared to genes encoding proteins (Figure S7C). Comparison of the black line with the red line) were less frequent [28]. However, modified M6A protein coding and LincRNAs transcriptions were more frequent and were lost during metTL3 silencing (Figure S7D, E; red line comparison with black line). The loss of peaks m6A and sorting transcript for XIST, MALAT1 and H19 lincRNA is illustrated by figure S7F. XIST and MALAT1 are well-studied m6atargets in different cell types, indicating a functional maintenance of this modification [29,30]. Together, these results establish that a metTL3-mediated m6A modification is essential for RNA stabilization, whether coding or not. However, the reason for the increase in the majority of RNAs in the mute condition of METTL3 has yet to be investigated. It is interesting to note that only a small fraction of the AEN (0.25%) m6A compared to protein coding scripts (6.04%). In addition to protein coding genes, we studied METTL3-controlled regulation by m6A modification on LincRNAs and GSCs NNNs. We found that a significant portion of LincRNAs was modified by METTL3 silencing.

Unlike protein coding genes, most LincNAs were heavily regulated in shMETTL3-GSCs. We believe that METTL3 could regulate the RNA-specific extraction machine. However, only a few of the LincNAs were re-regulated after metTL3 silencing and made metTL3-dependent m6A modifications. The results indicate that m6A modification is involved in an overall RNA stabilization phenomenon. Although a previous report showed that m6A modification is involved in primary mRNA treatment [65], the number of mRNA detected was low and no iRNA was identified as a direct target.

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