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The <jats:italic>Shh<\/jats:italic> descendants gradiently distributed from digit 5 to posterior half of digit 3 in wild\u2010type limbs, however, they abnormally increased in posterior digit 3 in <jats:italic>Wntless<\/jats:italic><jats:sup><jats:italic>Shh\u2010Cre<\/jats:italic><\/jats:sup>. <jats:italic>Wntless<\/jats:italic><jats:sup><jats:italic>Shh\u2010Cre<\/jats:italic><\/jats:sup> limbs displayed altered expression of hedgehog pathway genes and impaired noncanonical Wnt signaling activity. We further showed that the anterior limb mesenchymal cells in the <jats:italic>Wls<\/jats:italic><jats:sup><jats:italic>Shh\u2010Cre<\/jats:italic><\/jats:sup> served as a source of Wnt5a to reorientate the adjacent <jats:italic>Wls<\/jats:italic>\u2010lacking <jats:italic>Shh<\/jats:italic> lineage cells to move anteriorly and subsequently led to syndactyly, suggesting that aberrant mesenchymal cell movement\/condensation may underlie the pathogenesis of syndactyly.<\/jats:p>","DOI":"10.1002\/1873-3468.12963","type":"journal-article","created":{"date-parts":[[2018,1,2]],"date-time":"2018-01-02T04:12:42Z","timestamp":1514866362000},"page":"356-368","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Disruption of Wnt production in <i>Shh<\/i> lineage causes bone malformation in mice, mimicking human Malik\u2013Percin\u2010type 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