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Fig. 3 | Skeletal Muscle

Fig. 3

From: Prolonged FOS activity disrupts a global myogenic transcriptional program by altering 3D chromatin architecture in primary muscle progenitor cells

Fig. 3

Prolonged FOS activity perturbs a myogenic gene expression program in muscle progenitor cells. A Experimental design. Fresh SCs were isolated from skeletal muscle (see “Materials and methods” section), infected with either pSLIK-Fos or pSLIK-Gfp viral vectors 1 day after isolation, selected with hygromycin (100 μg/ml) for 6 days, and then re-seeded at 4000 cells per 96-well in GM supplemented with DOX (1 μg/ml) and RNA was isolated for RNA-seq after 48 h (n = cells from 3 mice). B Scatterplot showing the average log10 normalized gene RNA-seq counts for pSLIK-Fos or pSLIK-Gfp muscle progenitor cells. The significantly up- and downregulated genes are labeled as red and blue, respectively. C Heatmap showing the scaled transcripts per million (TPM) for a cohort of MAPK Signaling genes that were enriched in pSLIK-Fos versus pSLIK-Gfp muscle progenitor cells. D Plot showing the significantly enriched Gene Ontology (GO) terms associated with genes upregulated in pSLIK-Fos muscle progenitor cells. E Highlighting the Log2 fold change (FC) between myogenic determination (grey), myofiber structure (green), SC marker (yellow), and notch signaling (purple) genes that were depleted in pSLIK-Fos versus pSLIK-Gfp muscle progenitor cells. F Plot showing the significantly enriched Gene Ontology (GO) terms associated with genes downregulated in pSLIK-Fos muscle progenitor cells

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