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. 2020 Aug 18;8:138. doi: 10.1186/s40478-020-01021-5

Fig. 8.

Fig. 8

ALS-causing mutations in MATR3 cause aberrant RNA-binding of MATR3 and hnRNPM to transcriptomic transcripts. a Schematic of RNA-immunoprecipitation to probe for physical interaction between MATR3 WT, F115C and S85C and hnRNPM. b–d Fold change differences in RNA targets immunoprecipitated with FLAG-MATR3 and V5-HNRNPM from cells expressing MATR3 WT and ALS-causing mutations F115C and S85C (n = 3-4 per group; One-way ANOVA). (b, left) DYRK1A, (c, left) SMYD3, and (d, left) ZNF644 mRNA show significantly higher enrichment when immunoprecipitated with F115C and S85C mutants compared to MATR3 WT. (B, right) DYRK1A, (C, right) SMYD3, and (D, right) ZNF644 mRNA also show significantly higher enrichment when immunoprecipitated with hnRNPM in cells expressing F115C and S85C groups compared to MATR3 WT. e Top 20 unique GO:Biological Process terms that are enriched in gene ontology assessment of shared transcriptomic targets from K562 cells and f HepG2 cells. Green bars indicate biological processes unique to the cell type. Orange bars indicate biological processes commonly enriched in both cell types. Error bars indicate S.E.M. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001