PUBLICATION

The Stress-Response Gene redd1 Regulates Dorsoventral Patterning by Antagonizing Wnt/β-catenin Activity in Zebrafish

Authors
Feng, Q., Zou, X., Lu, L., Li, Y., Liu, Y., Zhou, J., and Duan, C.
ID
ZDB-PUB-130118-8
Date
2012
Source
PLoS One   7(12): e52674 (Journal)
Registered Authors
Duan, Cunming, Zhou, Jianfeng
Keywords
Embryos, Zebrafish, Wnt signaling cascade, Medical hypoxia, Reverse transcriptase-polymerase chain reaction, Gene expression, Signal inhibition, Stress signaling cascade
MeSH Terms
  • Animals
  • Body Patterning*
  • Embryo, Nonmammalian/metabolism
  • Gene Expression
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • HEK293 Cells
  • Humans
  • Intracellular Signaling Peptides and Proteins/genetics*
  • Intracellular Signaling Peptides and Proteins/metabolism
  • Intracellular Signaling Peptides and Proteins/physiology
  • Morpholinos/genetics
  • Organ Specificity
  • Stress, Physiological*
  • Wnt Signaling Pathway*
  • Wnt3A Protein/metabolism
  • Zebrafish
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/physiology
  • beta Catenin/metabolism
PubMed
23300740 Full text @ PLoS One
Abstract

REDD1/redd1 is a stress-response gene that is induced under various stressful conditions such as hypoxia, DNA damage, and energy stress. The increased REDD1 inhibits mTOR signaling and cell growth. Here we report an unexpected role of Redd1 in regulating dorsoventral patterning in zebrafish embryos and the underlying mechanisms. Zebrafish redd1 mRNA is maternally deposited. Although it is ubiquitously detected in many adult tissues, its expression is highly tissue-specific and dynamic during early development. Hypoxia and heat shock strongly induce redd1 expression in zebrafish embryos. Knockdown of Redd1 using two independent morpholinos results in dorsalized embryos and this effect can be rescued by injecting redd1 mRNA. Forced expression of Redd1 ventralizes embryos. Co-expression of Redd1 with Wnt3a or a constitutively active form of β-catenin suggests that Redd1 alters dorsoventral patterning by antagonizing the Wnt/β-catenin signaling pathway. These findings have unraveled a novel role of Redd1 in early development by antagonizing Wnt/β-catenin signaling.

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Human Disease / Model
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Mapping