Regulation of nonmuscle myosin light chain 3 gene expression in response to exogenous MLC3nm mRNA.

We have evaluated the regulation of the nonmuscle alkali myosin light chain isoform, MLC3nm, in mouse C2 myoblasts, in vitro. We altered the normal MLC mRNA profile of these cells, using stable transfection to introduce an exogenous pool of human MLC3nm mRNA. We used an isoform-specific, species-specific mouse MLC3nm cDNA probe to examine the response of the endogenous gene to the exogenous expression. At high cell density, expression of the endogenous mouse MLC3nm mRNA in transfectants is reduced to 50-70% of that in vector-transfected controls. These results suggest that a feedback mechanism operates in vitro, to regulate the size of the total MLC3nm mRNA pool. The down regulation of the mRNA for endogenous isoform is not detected at low cell density, suggesting that the mechanism may be density dependent and related to myoblast differentiation.