ECB-ART-40580Dev Cell 2008 Jan 01;141:97-107. doi: 10.1016/j.devcel.2007.10.012.
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The primary (animal-vegetal) (AV) and secondary (oral-aboral) (OA) axes of sea urchin embryos are established by distinct regulatory pathways. However, because experimental perturbations of AV patterning also invariably disrupt OA patterning and radialize the embryo, these two axes must be mechanistically linked. Here we show that FoxQ2, which is progressively restricted to the animal plate during cleavage stages, provides this linkage. When AV patterning is prevented by blocking the nuclear function of beta-catenin, the animal plate where FoxQ2 is expressed expands throughout the future ectoderm, and expression of nodal, which initiates OA polarity, is blocked. Surprisingly, nodal transcription and OA differentiation are rescued simply by inhibiting FoxQ2 translation. Therefore, restriction of FoxQ2 to the animal plate is a crucial element of canonical Wnt signaling that coordinates patterning along the AV axis with the initiation of OA specification.
PubMed ID: 18194656
Article link: Dev Cell
Genes referenced: foxe3l LOC100887844 LOC594353 nodall
Antibodies: foxe3l Ab1 gscl Ab1
Morpholinos: foxe3l MO1