XB-IMG-23489
Xenbase Image ID: 23489
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Figure 4. Relationships and Mechanisms of NC Induction by Msx1 and Pax3(A) Epistasis between Msx1 and Pax3 (stage 17 neurulae, dorsal views). When Msx1-MO, which downregulates Slug expression at the neural border (a), is coinjected with Pax3 mRNA (b), Slug expression is restored. The decreased Slug expression observed after injections of Pax3-MO (c) is not rescued by the coinjections of Pax3-MO and Msx1 mRNA (d).(B) RT-PCR analysis on animal caps injected with Msx1 + Noggin in the presence of control (lane 3), Pax3 (lane 4), or β-catenin (lane 5) MOs.(C) In animal cap dissociation assay, Sox2 is induced (lanes 4–6). NC induction observed in nondissociated sibling caps (lanes 5), but not obtained after dissociation (lanes 4 and 6). However, the dissociated cells induce Pax3 and ZicR1 expression (lane 6). Intact animal caps (+), dissociated AC (−).(D) Pax3 + ZicR1 coinjections induce Slug and FoxD3 when the animal caps are intact (lane 5), but not after dissociation (lane6). Intact animal caps (+), dissociated animal caps (–).(E) Pax3 + ZicR1 activation of Slug is blocked by NFz8, but not by cyp26 or a DNA binding mutant of Su(H) (SDBM).(F) Model part 1: Msx1 combined to BMP signaling attenuation activates Pax3 and ZicR1 in explants. Msx1 induction of Slug requires Pax3 activity in vivo and in explants. In turn, Pax3 + ZicR1 are sufficient to activate Slug in vivo and in explants in cooperation with a WNT signal.(G) Phenotype of the double knockdown, Msx1-MO + Pax3-MO. Twist expression is largely depleted in cephalic NC (a, frontal view) and trunk NC (b, white arrows, normal side; red arrows and dots, injected side; dorsal view of the spinal cord). Branchial arch cartilages do not differentiate or are strongly reduced (c and d, ventral views and dissected cartilage). Fin mesenchyme does not form when NC is fluorescently labeled on the injected side (e and f, see Supplemental Data). Image published in: Monsoro-Burq AH et al. (2005) Copyright © 2005. Image reproduced with permission of the Publisher, Elsevier B. V. Larger Image Printer Friendly View |