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Fig. 8
bHLH transcription factor activity provides mediolateral pattern to the entire mesodermal germ layer.
Homozygous myod;myf5 mutant embryos exhibit slightly expanded gata1a expression (D, red staining, arrow) and a complete loss of skeletal muscle marker actc1b (green staining). n = 49 controls (pooled +/+;+/+, +/+;+/-; +/-;+/+, and +/-;±genotyped embryos). 49/49 controls show normal actc1b, 0/49 controls have expanded gata1a. n = 9 mutants (-/-;-/- genotyped embryos). 9/9 show loss of actc1b, 7/9 show expanded gata1a (representative embryos shown). Loss of msgn1/myod/myf5 function results in an expansion of gata1a expression into somitic domains at the 22 s stage (E–F’). Cells from transgenic gata1a:dsRed x kdrl:GFP embryos injected with cascade blue dextran and msgn1/myod/myf5 MOs transplanted into unlabeled host embryos are excluded from somites and contribute extensively to endothelium (H, green arrow) and red blood cell lineages (H, red arrow). Control cascade blue injected gata1a:dsRed x kdrl:GFP transplanted cells contribute primarily to somitic muscle with minor contributions to endothelium (G, green arrow) and red blood cells (G, red arrow). Heat-shock induction of id3 at shield stage in mesodermally targeted transplanted cells that also contain the kdrl:GFP transgene causes a shift from predominantly somitic muscle fate to significant endothelial contribution in the trunk (J compared to I). Whole embryo induction of id3 expression at shield stage and analyzed at 24 hpf indicates a loss of medial mesoderm (notochord and muscle, (K–N), and an expansion of lateral mesoderm (pronephros, vasculature, and blood, (O–T’). Expression of gata1a in the trunk shows broad expansion into somite territories (S’ compared to T’). (U) A model for how FGF and BMP signaling control mediolateral patterning of the mesoderm through modulation of bHLH transcription factor activity.