{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,24]],"date-time":"2025-12-24T12:41:19Z","timestamp":1766580079139,"version":"build-2065373602"},"reference-count":93,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,12,10]],"date-time":"2013-12-10T00:00:00Z","timestamp":1386633600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:p>Synpolydactyly (SPD, OMIM 186000) is a rare congenital limb disorder characterized by syndactyly between the third and fourth fingers and between the fourth and fifth toes, with partial or complete digit duplication in the syndactylous web. The majority of these anomalies co\u2010segregate with mutations in the <jats:italic>HOXD13<\/jats:italic> gene, a homeobox transcription factor crucial for distal limb development. Different classes of <jats:italic>HOXD13<\/jats:italic> mutations are involved in the pathogenesis of synpolydactyly, but an unequivocal genotype\u2013phenotype correlation cannot always be achieved due to the clinical heterogeneity and reduced penetrance of SPD. All mutations identified so far mapped to the N\u2010terminal polyalanine tract or to the C\u2010terminal homeodomain of <jats:italic>HOXD13<\/jats:italic>, causing typical or atypical features of SPD, respectively. However, mutations outside of these domains cause a broad variety of clinical features that complicate the differential diagnosis. The existing animal models that are currently used to study <jats:italic>HOXD13<\/jats:italic> (mal)function are therefore instrumental in unraveling potential genotype\u2010phenotype correlations. Both mouse\u2010 and chick\u2010based approaches allow the in vivo study of the pathogenic mechanism by which <jats:italic>HOXD13<\/jats:italic> mutations cause SPD phenotypes as well as help in identifying the transcriptional targets. <jats:italic>Developmental Dynamics 243:37\u201348, 2014<\/jats:italic>. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/dvdy.24037","type":"journal-article","created":{"date-parts":[[2013,8,29]],"date-time":"2013-08-29T08:11:29Z","timestamp":1377763889000},"page":"37-48","source":"Crossref","is-referenced-by-count":23,"title":["Joining the fingers: A <i>HOXD13<\/i> story"],"prefix":"10.1002","volume":"243","author":[{"given":"Nathalie","family":"Brison","sequence":"first","affiliation":[{"name":"Center for Human Genetics University Hospitals Leuven, University of Leuven  Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philippe","family":"Debeer","sequence":"additional","affiliation":[{"name":"Department of 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