PUBLICATION

Expression and retinoic acid regulation of the zebrafish nr2f orphan nuclear receptor genes

Authors
Love, C.E., and Prince, V.E.
ID
ZDB-PUB-120802-2
Date
2012
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   241(10): 1603-1615 (Journal)
Registered Authors
Love, Crystal, Prince, Victoria E.
Keywords
zebrafish, nr2f, retinoic acid, Fgf, hindbrain, neural patterning, transcription factors, orphan nuclear receptors
MeSH Terms
  • Animals
  • COUP Transcription Factors/genetics
  • COUP Transcription Factors/metabolism*
  • Central Nervous System/metabolism*
  • DNA Primers/genetics
  • Fibroblast Growth Factors/metabolism*
  • Gene Expression Profiling
  • Gene Expression Regulation, Developmental/physiology*
  • In Situ Hybridization
  • Signal Transduction/physiology*
  • Tretinoin/metabolism*
  • Zebrafish/embryology*
PubMed
22836912 Full text @ Dev. Dyn.
Abstract

Background:

The vertebrate nuclear receptor subfamily 2, group f (nr2f) genes encode orphan receptors that have the capacity to act as negative regulators of retinoic acid (RA) signaling.

Results:

We describe embryonic and larval expression of four of the six zebrafish nr2f genes, nr2f1a, nr2f1b, nr2f2 and nr2f5. These genes show highly regulated patterns of expression within the CNS, including in the developing hindbrain, as well as in the mesoderm and endoderm. We also investigated the role of RA and Fgf signaling in regulating early nr2f gene expression. RA is not required for nr2f expression in the hindbrain; however, exogenous RA can repress this expression. Conversely, we find that RA positively regulates nr2f1a expression in trunk endoderm and mesoderm. Fgf signaling is not required for nr2f expression onset in the hindbrain; however, it may play a role in maintaining rhombomere-specific expression.

Conclusions:

We report detailed expression analysis of four nr2f genes in all three germ layers. The onset of nr2f expression in the hindbrain does not require RA or Fgf signals. Our finding that RA positively regulates nr2f1a expression in the trunk supports the possibility that Nr2fs function in a negative feedback loop to modulate RA signaling in this region.

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