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. 2019 Mar 13;15(3):e1008036. doi: 10.1371/journal.pgen.1008036

Fig 6. AGO2-associated L2-miRNAs and L2-carrying genes are altered in glioblastoma.

Fig 6

A) Bar graph showing the percentage of 20–24 nt long read mapping to mature miRNAs (miR), transposable elements (TE), piwi RNAs (piRNAs) and transfer RNAs (tRNA). Data are represented as mean ± SEM (RIP GBM n = 6). B) Bar graph showing the percentage of uniquely aligned reads of 20–24 nt mapping to transposons in AGO2 RIP samples of cortex (CTX) and glioblastoma (GBM) tissue (RIP CTX n = 3; RIP GBM n = 6). C) Number of uniquely aligned reads mapping to L2 elements giving rise to precursor miRNAs (mir) in AGO2 RIP-seq samples from cortex and glioblastoma tissue (RIP CTX n = 3; RIP GBM n = 6). D) Cumulative fraction plot of fold changes of all genes and genes with L2 in their 3’UTR in RIP versus INPUT samples. ***p<0.001 Kolmogorov–Smirnov test. E-G) Bar plots showing the percentage of genes with L2 / L2b / L2c in the 3’UTR of all genes, and of the top 100 highest-expressed genes that are more than 4-fold enriched in RIP compared to input samples from cortex and glioblastoma tissue. H) Overlap of UCSC genome browser tracks showing examples of L2-carrying transcripts with altered AGO2 binding in glioblastoma compared to cortex. I) Potential L2b-derived target sites in PCDH9 and AQP4. AGO2—Argonaute2, AGO2 RIP—AGO2 RNA immunoprecipitation, L1—LINE1, L2—LINE-2, LTR—long terminal repeat, SINE—short interspersed nuclear element.