MOESM1 of Phosphorylation of TET2 by AMPK is indispensable in myogenic differentiation

Additional file 1. Fig. S1. SDS-PAGE analysis of the recombinant N-terminus of murine TET2 (aa 1-181) and its mutant. Fig. S2. AMPK knockout impaired the differentiation of C2C12 cells. Fig. S3. Gene ontology analysis of upregulated genes between AMPK-KO and wild-type C2C12 cells at myoblast- (differentiation d0, A) or myotube- stage (differentiation d8, B). Fig. S4. Increased DNA methylation at a potential intragenic enhancer of Pax7. Fig. S5. CRISPR/Cas9-mediated deletion of the Pax7 intragenic enhancer in C2C12 cells. Fig. S6. Knocking in (KI) the pS97E mutation of Tet2 in AMPK-/- C2C12 cells. Fig. S7. S97E mutation of TET2 partly rescues the differentiation defect of the AMPK-/- C2C12 cells. Fig. S8. Increased myosin heavy chain (MHC) expression in AMPK-/- C1C12 cells rescued with TET2 harboring S97E. Table S1. ELISA analysis of pTET2 [Ser99 (h); Ser97(m)] antibodies*. Table S3. Antibodies. Table S4: Primers and Oligos.