L6E9 Myoblasts Are Deficient of Myostatin and Additional TGF- Members Are Candidates to Developmentally Control Their Fiber Formation
Figure 1
(a) Morphological visualization of C2C12 and L6E9 myoblasts undergoing differentiation. After Giemsa staining, phase contrast pictures were taken under the same magnification. Barβ=β. (b) The graph represents the quantification of myotube average size in differentiating C2C12 and L6E9 cells. . (c) Immunoblotting was performed to compare the time-course expression of myogenin, Cav-3 and MyHC between C2C12 and L6E9 cells. Tubulin was used as loading control. (d) Semiquantitative RT-PCR analysis was performed to detect the transcript levels of myostatin, follistatin, ActRIIa, and ActRIIb in C2C12 and L6E9 cells cultured in differentiating medium. Gapdh amplification was performed as loading control. (e) RT-PCR analysis was carried out to amplify a 377βbp long fragment of myostatin in both mouse and rat gastrocnemius muscles. The amplification was performed by using the total RNA processed in presence or absence of reverse transcriptase (RT+ or RTβ, resp.). Total RNAs are shown as loading control.
