PMID:17504941

Citation	Allen, BL, Tenzen, T and McMahon, AP (2007) The Hedgehog-binding proteins Gas1 and Cdo cooperate to positively regulate Shh signaling during mouse development. Genes Dev. 21:1244-57
Abstract	Hedgehog (Hh) signaling is critical for patterning and growth during mammalian embryogenesis. Transcriptional profiling identified Growth-arrest-specific 1 (Gas1) as a general negative target of Shh signaling. Data presented here define Gas1 as a novel positive component of the Shh signaling cascade. Removal of Gas1 results in a Shh dose-dependent loss of cell identities in the ventral neural tube and facial and skeletal defects, also consistent with reduced Shh signaling. In contrast, ectopic Gas1 expression results in Shh-dependent cell-autonomous promotion of ventral cell identities. These properties mirror those of Cdo, an unrelated, cell surface Shh-binding protein. We show that Gas1 and Cdo cooperate to promote Shh signaling during neural tube patterning, craniofacial, and vertebral development. Overall, these data support a new paradigm in Shh signaling whereby positively acting ligand-binding components, which are initially expressed in responding tissues to promote signaling, are then down-regulated by active Hh signaling, thereby modulating responses to ligand input.
Links	PubMed PMC1865495 Online version:10.1101/gad.1543607
Keywords	Animals; Cell Adhesion Molecules/genetics; Cell Adhesion Molecules/metabolism; Cell Cycle Proteins/genetics; Cell Cycle Proteins/metabolism; DNA Primers; Electroporation; Embryonic Development/physiology; Fluorescent Antibody Technique; GPI-Linked Proteins; Gene Expression Profiling; Gene Expression Regulation, Developmental; Hedgehog Proteins/genetics; Hedgehog Proteins/metabolism; In Situ Hybridization; Membrane Proteins/genetics; Membrane Proteins/metabolism; Mice; Mice, Transgenic; Neural Tube/embryology; Neural Tube/metabolism; RNA, Small Interfering/genetics; Signal Transduction/physiology
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