Figure 6.

CaMKII function during muscle regeneration and ERK-CaMKII pathway conservation

(A) WB of analysis of indicated proteins from CTX-induced injured muscle. Line indicates where a lane was purposely removed.

(B) Schematic illustration of the SC-specific double CaMKII KO mouse model.

(C) Schematic illustration depicting the timeline of the repeat-injury experimental design.

(D) WB validation of CaMKII depletion in WT or scDKO primary myoblasts isolated for 2 weeks following initial injury.

(E) IF staining of WT or scDKO primary myoblasts following ERKi-induced fusion at 24 h post treatment. Insets are enlarged to the right.

(F) Fusion index comparison between WT (n = 4) and scDKO (n = 4) primary myoblasts stratified by number of nuclei per fiber. Total number of nuclei assayed, n = 12,743.

(G) Representative field of WT and scDKO muscle 14 days after CTX-induced reinjury.

(H) Quantification of myofiber cross-sectional areas of WT (n = 4) and scDKO (n = 4) mice 14 days following reinjury.

(I) Average percentage of central nuclei in WT (n = 4) and scDKO (n = 4) mice 14 days following reinjury. At least 9,000 fibers per mouse were measured for (H) and (I).

(J) Representative IF staining of primary chicken myoblasts over 72 h of treatment either with ERKi in proliferation medium, or in conventional DM.

(K) Fusion index for the 48-h time point of (J).

(L) Representative WB analysis of CaMKII activation in chicken myoblasts, following treatment with ERKi or co-treatment with CaMKIIi. Error bars indicate SEM. All scale bars, 100 μm.