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No vertebrate model for SEDT has been generated thus far. To address this gap, we generated a Sedlin knockout animal by mutating the orthologous\n                    <jats:italic>TRAPPC2<\/jats:italic>\n                    gene (\n                    <jats:italic>olSedl<\/jats:italic>\n                    ) of\n                    <jats:italic>Oryzias latipes<\/jats:italic>\n                    (medaka) fish.\n                    <jats:italic>OlSedl<\/jats:italic>\n                    deficiency leads to embryonic defects, short size, diminished skeletal ossification and altered Col2 production and secretion, resembling human defects observed in SEDT patients. Moreover, SEDT knock\u2010out animals display photoreceptor degeneration and gut morphogenesis defects, suggesting a key role for Sedlin in the development of these organs. Thus, by studying Sedlin function in vivo, we provide evidence for a mechanistic link between TRAPPC2\u2010mediated membrane trafficking, Col2 export, and developmental disorders.\n                  <\/jats:p>","DOI":"10.1111\/tra.12924","type":"journal-article","created":{"date-parts":[[2023,11,14]],"date-time":"2023-11-14T21:00:36Z","timestamp":1699995636000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Role of trafficking protein particle complex 2 in medaka development"],"prefix":"10.1111","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1263-3828","authenticated-orcid":false,"given":"Francesca","family":"Zappa","sequence":"first","affiliation":[{"name":"Telethon Institute of Genetics and Medicine, TIGEM  Pozzuoli (Naples) Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniela","family":"Intartaglia","sequence":"additional","affiliation":[{"name":"Telethon Institute of 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