{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,12]],"date-time":"2025-11-12T17:11:28Z","timestamp":1762967488610,"version":"3.45.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2025,8,20]],"date-time":"2025-08-20T00:00:00Z","timestamp":1755648000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","award":["R35 GM130351","R25 GM125597"],"award-info":[{"award-number":["R35 GM130351","R25 GM125597"]}],"id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]},{"name":"HHMI Gilliam"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,11,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Coffin-Siris syndrome (CSS) is a rare human genetic disorder that is characterized by developmental delay, fifth digit abnormalities, and craniofacial defects. Heterozygous mutations in 2 SoxC proteins, SOX4 and SOX11, are associated with this disorder. Caenorhabditis elegans has a single SoxC protein, SEM-2, which is essential for development. In this study, we use C. elegans as a model system to explore the molecular effects of one CSS-associated SOX11 mutation, Y116C, on SoxC protein function in vivo. The equivalent amino acid of SOX11 Y116 is SEM-2 Y160, a residue in the C-terminal tail of the highly conserved DNA-binding domain. Homozygous, but not heterozygous, sem-2[Y160C] animals exhibit a high rate of embryonic and larval lethality, egg-laying defects, reduced brood size, bivulval phenotype and a low penetrance of hermaphrodite tail abnormalities. Additionally, sem-2[Y160C] animals have reduced expression of hlh-8\/Twist, whose human counterparts, when mutated, are known to be associated with craniofacial disorders. All the phenotypes observed in sem-2[Y160C] animals resemble SEM-2 loss-of-function phenotypes, suggesting that SOX11[Y116C] is a loss-of-function, recessive mutation that likely causes defects due to haploinsufficiency. Our work suggests that using C. elegans as a model system to analyze the molecular effects of point mutations associated with craniofacial defects has the potential for unraveling the underlying mechanisms.<\/jats:p>","DOI":"10.1093\/g3journal\/jkaf194","type":"journal-article","created":{"date-parts":[[2025,8,20]],"date-time":"2025-08-20T09:01:54Z","timestamp":1755680514000},"source":"Crossref","is-referenced-by-count":0,"title":["A Coffin-Siris syndrome\u2013associated mutation modeled in\n                    <i>Caenorhabditis elegans<\/i>\n                    affects multiple developmental processes"],"prefix":"10.1093","volume":"15","author":[{"given":"Marissa","family":"Baccas","sequence":"first","affiliation":[{"name":"Department of Molecular Biology and Genetics, Cornell University , Ithaca, NY 14853 ,","place":["United 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