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ZFIN ID: ZDB-PUB-061108-8
Cdx-Hox code controls competence for responding to Fgfs and retinoic acid in zebrafish neural tissue
Shimizu, T., Bae, Y.K., and Hibi, M.
Date: 2006
Source: Development (Cambridge, England) 133(23): 4709-4719 (Journal)
Registered Authors: Bae, Young Ki, Hibi, Masahiko, Shimizu, Takashi
Keywords: caudal-related genes, hox, Hindbrain, Fibroblast growth factor, Retinoic acid, Zebrafish
MeSH Terms:
  • Animals
  • Fibroblast Growth Factors/pharmacology
  • Gene Expression Regulation, Developmental
  • Gene Targeting
  • Genes, Homeobox
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism
  • Rhombencephalon/drug effects
  • Rhombencephalon/embryology*
  • Rhombencephalon/metabolism
  • Signal Transduction
  • Spinal Cord/drug effects
  • Spinal Cord/embryology
  • Spinal Cord/metabolism
  • Transcription Factors/deficiency
  • Transcription Factors/genetics
  • Transcription Factors/metabolism
  • Tretinoin/pharmacology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 17079270 Full text @ Development
FIGURES
ABSTRACT
Fibroblast growth factor (Fgf) and retinoic acid (RA) signals control the formation and anteroposterior patterning of posterior hindbrain. They are also involved in development processes in other regions of the embryo. Therefore, responsiveness to Fgf and RA signals must be controlled in a context-dependent manner. Inhibiting the caudal-related genes cdx1a and cdx4 in zebrafish embryos caused ectopic expression of genes that are normally expressed in the posterior hindbrain and anterior spinal cord, and ectopic formation of the hindbrain motor and commissure neurons in the posteriormost neural tissue. Combinational marker analyses suggest mirror-image duplication in the Cdx1a/4-defective embryos, and cell transplantation analysis further revealed that Cdx1a and Cdx4 repress a posterior hindbrain-specific gene expression cell-autonomously in the posterior neural tissue. Expression of fgfs and retinaldehyde dehydrogenase 2 suggested that in the Cdx1a/4-defective embryos, the Fgf and RA signaling activities overlap in the posterior body and display opposing gradients, compared with those in the hindbrain region. We found that Fgf and RA signals were required for ectopic expression. Expression of the posterior hox genes hoxb7a, hoxa9a or hoxb9a, which function downstream of Cdx1a/4, or activator fusion genes of hoxa9a or hoxb9a (VP16-hoxa9a, VP16-hoxb9a) suppressed this loss-of-function phenotype. These data suggest that Cdx suppresses the posterior hindbrain fate through regulation of the posterior hox genes; the posterior Hox proteins function as transcriptional activators and indirectly repress the ectopic expression of the posterior hindbrain genes in the posterior neural tissue. Our results indicate that the Cdx-Hox code modifies tissue competence to respond to Fgfs and RA in neural tissue.
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