Journal
SCIENCE
Volume 306, Issue 5705, Pages 2264-2267Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1104193
Keywords
-
Categories
Funding
- NHLBI NIH HHS [HL61365, HL36059] Funding Source: Medline
- NIGMS NIH HHS [GM069086-01] Funding Source: Medline
- NINDS NIH HHS [NS19576] Funding Source: Medline
Ask authors/readers for more resources
beta-arrestins are multifunctional proteins that act as scaffolds and transducers of intracellular signals from heptahelical transmembrane-spanning receptors (7TMR). Hedgehog (Hh) signaling, which uses the putative 7TMR, Smoothened, is established as a fundamental pathway in development, and unregulated Hh signaling is associated with certain malignancies. Here, we show that the functional knockdown of beta-arrestin 2 in zebrafish embryos recapitulates the many phenotypes of Hh pathway mutants. Expression of wild-type beta-arrestin 2, or constitutive activation of the Hh pathway downstream of Smoothened, rescues the phenotypes caused by beta-arrestin 2 deficiency. These results suggest that a functional interaction between beta-arrestin 2 and Smoothened may be critical to regulate Hh signaling in zebrafish development.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available