Merrifield P A, Kiely R, Konigsberg I R
Department of Biology, University of Virginia, Charlottesville 22901.
Exp Neurol. 1990 Sep;109(3):342-8. doi: 10.1016/s0014-4886(05)80025-1.
We have used a monoclonal antibody (Mab) raised against the fast alkali light chains of quail pectoral muscle myosin to study the expression of MLC1f and MLC3f in the hindlimb muscle of a staged series of control chick embryos and 16-day embryos that had been paralyzed with curare. The Mab (QBM-2) is highly specific for the fast myosin alkali light chains of chick, hamster, and human muscle myosin. On Western blots, MLC1f is detected in hindlimb actomyosin at all of the stages examined, whereas MLC3f cannot be detected until Embryonic Day 14 (E14). Most of the E16 embryos that had been paralyzed with curare since E4 express detectable levels of both MLC1f and MLC3f in their hindlimb muscles, even though embryos incubated under these conditions do not exhibit spontaneous limb movements. Contrary to other reports, our results demonstrate that muscle contraction is not required for the accumulation of MLC3f. In light of our previous finding that innervation is essential for MLC3f accumulation in limb buds grafted onto the chorioallantoic membrane of chick hosts, these results suggest that some neural influence other than contraction, possibly a trophic factor, may play a role in the developmentally regulated expression of MLC3f in avian limb muscle.
