Beta-arrestin 2 regulates zebrafish development through the hedgehog signaling pathway |
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Authors: | Wilbanks Alyson M Fralish Gregory B Kirby Margaret L Barak Larry S Li Yin-Xiong Caron Marc G |
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Institution: | Department of Cell Biology, Center for Models of Human Disease, Institute for Genome Science and Policy, Duke University Medical Center, Durham, NC 27710, USA. |
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Abstract: | 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. |
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