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FGF signaling has also been implicated in cardiac specification in chick and zebrafish.
EmNCSCs expressed several transcription factors characteristic of early NC specification in chick, mouse, and Xenopus.
Similarly, endoderm is required for cardiac specification in chick embryos, and explants of early chick embryo hypoblast or anterior endoderm can promote cardiogenesis in non-cardiogenic mesoderm [3], [4].
It has not yet been established when NODAL signals contribute to the anterior midline specification in chick embryos.
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Previous work has implicated FGF signaling in cardiac specification in zebrafish and chick embryos, but little is known about the directness and cardiac specificity of this role [11] [15].
While the importance of FGF signalling in neuroectoderm specification has been clearly established in chick and amphibian embryos and in mESCs [21] [24], the function of Activin/Nodal in this cell fate choice in vertebrate embryogenesis has only recently been described.
In chick, the specification of both neural crest and placodal cells is ongoing at the late gastrula stage [4], [5], and around this stage, Bmp2 and Bmp4 are expressed in the ectoderm surrounding the entire neural plate [6], domains where phosphorylated Smad-1 is also detected, indicative of active BMP signaling [7].
In chick embryos, the specification of neural crest cells has been initiated at the late gastrula stage, stage 4 [4].
Both contribute to the specification of aPPs, and their loss leads to abnormal eye development in chick and zebrafish.
Wnt3a/Wnt5a signaling has been shown to affect the path of cardiac progenitor migration in chick embryos, but not to affect cardiac progenitor specification (Sweetman et al., 2008; Yue et al., 2008).
Finally, previous studies in chick demonstrated that BMP inhibition (e.g., with Noggin) can block NC specification during early, but not late stages of NC development [23].
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