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First published online August 24, 2007

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Sulfs set heparan sulfate code

Heparan sulfate (HS) regulates several extracellular signalling pathways during development, such as the FGF and Wnt pathways. The binding of HS to these ligands and their receptors is regulated by its precise 6-O-sulfated structure, but what controls this `HS code' and thus the signalling functions of HS? On p. 3327, Ai and colleagues provide the first evidence that the extracellular HS 6-O-endosulfatases SULF1 and SULF2 are essential in vivo regulators of HS-mediated developmental signalling. The researchers identify an oesophageal primary neuronal innervation defect in Sulf1^-/- Sulf2^-/- double-null mice and show that aberrant glial cell line-derived neurotrophic factor (GDNF) signalling causes this defect. Other experiments indicate that SULF1 and SULF2 are expressed in the developing oesophagus, that they function redundantly as the major regulators of HS 6-O-desulfation, and that Sulf activity decreases GDNF binding to HS (GDNF binds to HS through its 6-O-sulfate groups). The researchers conclude, therefore, that Sulf activity enhances GDNF signalling in normal mice, consequently promoting neurite sprouting in the embryonic oesophagus.

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SULF1 and SULF2 regulate heparan sulfate-mediated GDNF signaling for esophageal innervation

Xingbin Ai, Toshio Kitazawa, Anh-Tri Do, Marion Kusche-Gullberg, Patricia A. Labosky, and Charles P. Emerson, Jr
Development 2007 134: 3327-3338. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?