{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T13:21:05Z","timestamp":1788355265627,"version":"build-2803163510"},"reference-count":48,"publisher":"The Company of Biologists","issue":"8","license":[{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"vor","delay-in-days":31,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/100002889","name":"Foundation for Prader-Willi Research","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100002889","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100000266","name":"Engineering and Physical Sciences Research Council","doi-asserted-by":"crossref","award":["EP\/T02593X\/1"],"award-info":[{"award-number":["EP\/T02593X\/1"]}],"id":[{"id":"10.13039\/501100000266","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100007065","name":"Nvidia","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007065","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,8,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>The neurodevelopmental disorder Prader\u2013Willi syndrome (PWS) is caused by paternally derived loss of gene expression from the imprinted interval on chromosome 15q11-q13. Recently, it has been suggested that the abnormal feeding-related behaviours characteristic of PWS can, in part, be developmentally programmed in utero via abnormal placental function. Here, we report that several PWS-associated genes were expressed in mouse placenta with three PWS-associated RNA transcripts, i.e. genes Magel2 and Necdin, and the lncRNA Sngh14, colocalised to the Kdr-positive (Kdr+) foetal endothelial cells of the labyrinth zone central to nutrient transport. In a novel PWS mouse model (Large+\/\u2212) we found markedly reduced expression of PWS-associated genes in the placenta and an associated \u223c25% reduction in Kdr+ foetal endothelial cells. Although this did not directly translate into a significant reduction in foetal growth late in gestation, these data suggest that placental function and nutrient transfer from mother to foetus could be compromised in PWS contributing to later post-natal phenotypes.<\/jats:p>","DOI":"10.1242\/dmm.052833","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T06:12:41Z","timestamp":1783404761000},"source":"Crossref","is-referenced-by-count":1,"title":["Placental defects revealed by modelling Prader\u2013Willi syndrome in mice"],"prefix":"10.1242","volume":"19","author":[{"given":"Anna E.","family":"Webberley","sequence":"first","affiliation":[{"name":"Centre for Neuropsychiatric Genetics and Genomics 1 , Division of Psychological Medicine and Clinical Neurosciences , , Cardiff, CF24 4HQ ,","place":["UK"]},{"name":"School of Medicine, Cardiff University 1 , Division of Psychological Medicine and Clinical Neurosciences , , Cardiff, CF24 4HQ 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Cardiff, CF24 4HQ ,","place":["UK"]},{"name":"School of Medicine, Cardiff University 1 , Division of Psychological Medicine and Clinical Neurosciences , , Cardiff, CF24 4HQ ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3827-7617","authenticated-orcid":false,"given":"Rosalind M.","family":"John","sequence":"additional","affiliation":[{"name":"School of Biosciences, Cardiff University 2 Biomedicine Division , , Cardiff, CF10 3AX ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7587-5712","authenticated-orcid":false,"given":"Anthony R.","family":"Isles","sequence":"additional","affiliation":[{"name":"Centre for Neuropsychiatric Genetics and Genomics 1 , Division of Psychological Medicine and Clinical Neurosciences , , Cardiff, CF24 4HQ ,","place":["UK"]},{"name":"School of Medicine, Cardiff University 1 , Division of Psychological Medicine and Clinical 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