Xenopus Hindbrain Patterning Requires Retinoid Signaling

Xenopus Hindbrain Patterning Requires Retinoid Signaling We have asked how posterior neural tissue is patterned in Xenopus by assaying the involvement of endogenous retinoic acid (RA) in this process and by using the labial Hox gene, HoxD1, as a posterior marker. Although RA is able to inhibit anterior gene expression and activate expression of more posterior genes, the normal role of retinoids in anteroposterior (A/P) patterning is unclear. HoxD1 is an early posterior neurectodermal marker, expressed from midgastrula with a later anterior expression limit in the future hindbrain. We previously showed that HoxD1 was induced as an immediate early response to retinoic acid in naive ectoderm (animal caps). Here, we use a truncated RARα2.2 receptor (RARΔ) to dominantly interfere with retinoid signaling. In embryos injected with RARΔ expression of HoxD1 is eliminated. Conjugates of ectoderm and dorsolateral mesoderm show that retinoid receptors are required in the ectoderm for HoxD1 induction. Further, expression of Krox-20 in r3 and r5 of the presumptive hindbrain is compressed into a single stripe that suggests elimination of r5. RARα2.2 expression almost precisely overlaps that of HoxD1, suggesting that this receptor may normally activate HoxD1. Expression of neither more anterior genes including cement gland, forebrain, and midbrain markers nor a more posterior spinal cord marker is affected by RARΔ. These data suggest that the posterior hindbrain is the region of the nervous system most sensitive to retinoid loss. Finally, we compare the ability of RA and fibroblast growth factor (FGF) to posteriorize isolated anterior neurectoderm and show that both factors can act directly on this substrate. RA acts in a more anterior domain than does FGF; however, neither factor is equivalent to the natural posteriorizing capacity of the posterior mesoderm. We propose that endogenous retinoid and FGF signals pattern largely nonoverlapping regions along the A/P axis and that posterior neural patterning requires multiple inducers. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Developmental Biology Elsevier

Xenopus Hindbrain Patterning Requires Retinoid Signaling

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Publisher
Elsevier
Copyright
Copyright © 1997 Academic Press
ISSN
0012-1606
eISSN
1095-564X
D.O.I.
10.1006/dbio.1997.8754
Publisher site
See Article on Publisher Site

Abstract

We have asked how posterior neural tissue is patterned in Xenopus by assaying the involvement of endogenous retinoic acid (RA) in this process and by using the labial Hox gene, HoxD1, as a posterior marker. Although RA is able to inhibit anterior gene expression and activate expression of more posterior genes, the normal role of retinoids in anteroposterior (A/P) patterning is unclear. HoxD1 is an early posterior neurectodermal marker, expressed from midgastrula with a later anterior expression limit in the future hindbrain. We previously showed that HoxD1 was induced as an immediate early response to retinoic acid in naive ectoderm (animal caps). Here, we use a truncated RARα2.2 receptor (RARΔ) to dominantly interfere with retinoid signaling. In embryos injected with RARΔ expression of HoxD1 is eliminated. Conjugates of ectoderm and dorsolateral mesoderm show that retinoid receptors are required in the ectoderm for HoxD1 induction. Further, expression of Krox-20 in r3 and r5 of the presumptive hindbrain is compressed into a single stripe that suggests elimination of r5. RARα2.2 expression almost precisely overlaps that of HoxD1, suggesting that this receptor may normally activate HoxD1. Expression of neither more anterior genes including cement gland, forebrain, and midbrain markers nor a more posterior spinal cord marker is affected by RARΔ. These data suggest that the posterior hindbrain is the region of the nervous system most sensitive to retinoid loss. Finally, we compare the ability of RA and fibroblast growth factor (FGF) to posteriorize isolated anterior neurectoderm and show that both factors can act directly on this substrate. RA acts in a more anterior domain than does FGF; however, neither factor is equivalent to the natural posteriorizing capacity of the posterior mesoderm. We propose that endogenous retinoid and FGF signals pattern largely nonoverlapping regions along the A/P axis and that posterior neural patterning requires multiple inducers.

Journal

Developmental BiologyElsevier

Published: Dec 1, 1997

References

  • Xwnt-8 and lithium can act upon either dorsal mesodermal or neurectodermal cells to cause a loss of forebrain in Xenopus
    Fredieu, J.; Cui, Y.; Maier, D.; Danilchik, M.; Christian, J.
  • The cellular basis of the convergence and extension of the Xenopus
    Keller, R.; Shih, J.; Sater, A.
  • Regulation of the Xenopus
    Kolm, P.; Sive, H.
  • Transgenic Xenopus
    Kroll, K.; Amaya, E.
  • Vitamin A-deficient quail embryos have half a hindbrain and other neural defects
    Maden, M.; Gale, E.; Kostetskii, I.; Zile, M.
  • Specification of the anteroposterior neural axis through synergistic interaction of the Wnt signaling cascade with noggin follistatin
    McGrew, L.; Lai, C.; Moon, R.
  • XFGF-9: A new fibroblast growth factor from Xenopus
    Song, J.; Slack, J.
  • Anti-retinoic acid monoclonal antibody localizes all- trans
    Twal, W.; Roze, L.; Zile, M.

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