Evidence against involvement of Bmp receptor 1b signaling in fate specification of the chick mesencephalic alar plate at HH16.
Studies in the developing spinal cord have established that morphogenes secreted from the roof- and floor plate influence pattern formation along the dorsal-ventral axis of the neural tube. Bone morphogenetic proteins (Bmps), secreted from the roof plate, act on the more laterally located alar plates to induce position dependent gene expression and cell fate changes. The dorsalizing activity of Bmps is counteracted by Sonic hedgehog (Shh), which is secreted from the floor plate and underlying notochord. Bmps are also expressed in the roof plate of the mesencephalic vesicle, yet it is unclear at present if they also provide patterning information to the mesencephalic alar plates. We have experimentally tested the hypothesis that Bmp signaling is required for fate specification of the mesencephalic alar plate by manipulating Bmp receptor signaling in the early chick embryo through ectopic expression of mutated forms of Bmp receptor 1b (BmpR1b), which render the receptor constitutively active or dominant negative, respectively. In contrast to published data on the embryonic spinal cord, neither activation nor blockage of BmpR1b signaling in stage 16 embryos altered expression of markers of the mesencephalic alar plates including Pax3, Pax7, Meis2 and efnb1. Moreover, simultaneous activation of BmpR1b signaling and blockage of Shh signaling was not sufficient to induce Meis2 expression in the ventral mesencephalon. Therefore, whereas the importance of Bmp signaling for dorsal differentiation in the spinal cord is well established, it appears to play a less prominent role in the dorsal specification of the developing mesencephalon during the same developmental stages.
Bobak
Nicole
N
Max Planck Institute for Brain Research, Deutschordenstr. 46, 60528 Frankfurt, Germany.
Agoston
Zsuzsa
Z
Schulte
Dorothea
D
D000818:Animals; D052005:Bone Morphogenetic Protein Receptors, Type I / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D002642:Chick Embryo; D053823:Hedgehog Proteins / Q000502:physiology; D006801:Humans; D017403:In Situ Hybridization; D008636:Mesencephalon / Q000033:anatomy & histology / Q000196:embryology / Q000378:metabolism*; D009154:Mutation; D020033:Protein Isoforms / Q000096:biosynthesis / Q000235:genetics; D015398:Signal Transduction
D053823:Hedgehog Proteins; D020033:Protein Isoforms; D052005:Bone Morphogenetic Protein Receptors, Type I