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Fig. 2. The myogenic activity of HLH-1 in embryos lacking normal cell fate specification. All embryos shown are transgenic for the heat shock promoter-driven hlh-1 transgene that is inactive in controls (left) or activated by a heat pulse (right). Top: embryos were depleted of PAL-1 and SKN-1 activity by RNAi, allowed to develop overnight, and stained for MHC A. Control embryos (A) have only a small amount of muscle due to zygotic PAL-1 activity that is not completely eliminated by RNAi (Edgar et al., 2001). In the presence of ectopic HLH-1 activity (B), most cells in pal-1, skn-1 double RNAi-treated embryos strongly express MHC A as shown by this focal plane representative of the entire embryo. Bottom: embryos were treated with mex-1, pop-1 double RNAi to convert a majority of anterior blastomeres to ELT-2-positive intestinal cells (C); a small area of MHC A-positive muscle remains in these embryos (D). Heat shock-induced HLH-1 activity, in combination with mex-1, pop-1 double RNAi treatment, results in a complete loss of ELT-2 staining (E) and strong MHC A staining (F) in most blastomeres.





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