Additional file 1 of Transgenic mice expressing tunable levels of DUX4 develop characteristic facioscapulohumeral muscular dystrophy-like pathophysiology ranging in severity

Additional file 1: Figure S1.FLExDUX4 transgenic mice kept in different housing facilities acquire different mouth and gut microbiomes and have differing alopecia and GI health. Figure S2. Mosaic tamoxifen dose-dependent recombination in gastrocnemius muscle of ACTA1-MCM;R26NZG bi-transgenic mice. Figure S3. Increased TMX dosage leads to increased mosaic recombination in skeletal muscle of ACTA1-MCM;R26NZG bi-transgenic mice. Figure S4. There is no significant difference in the transgene recombination rate between male and female ACTA1-MCM/FLExD bi-transgenic FSHD-like mice. Figure S5. Quantification of DUX4-FL protein positive myonuclei. Figure S6. The moderate and severe FSHD-like mouse models show significant weight loss. Figure S7. Maximum isometric forces of the female FSHD-like mouse models. Figure S8. Maximum and specific isometric forces of the male mild and severe FSHD-like mouse models. Figure S9. Pax7 target genes are not significantly misexpressed in the FSHD-like mouse models. Figure S10. GO enrichment analysis of differentially expressed genes (>2-fold) in the different FSHD-like severity model mice. Figure S11. Fiber number per cross-section does not significantly change with severity. Figure S12. The heart is not affected by TMX treatment in control or bi-transgenic animals. Figure S13. Quantification of eMyHC positive muscle cells in different FSHD-like mouse models. Figure S14.Mstn gene mRNA expression decreases with increased DUX4-fl expression in the FSHD-like mouse models. Figure S15. Quantification of TUNEL positive nuclei in FSHD-like mouse models. Figure S16. Quantification of SR staining shows significant fibrosis in late stages of the moderate and severe FSHD-like mouse models. Figure S17. Cardiac muscle from FSHD-like mouse models shows no signs of increased fibrosis.