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In one mutant allele, <jats:italic>sl23<\/jats:italic>, axons arising from the epibranchial sensory ganglia do not form their stereotypical terminal fields in the hindbrain. These embryos also had small eyes and deformed jaws, suggesting a pleiotropic effect. Using positional cloning, a 20\u2010nucleotide deletion in the carbamoyl\u2010phosphate\u2010synthetase2\u2010aspartate\u2010transcarbamylase\u2010dihydroorotase (<jats:italic>cad<\/jats:italic>) gene was found. Injection of a CAD morpholino phenocopied the mutant and mutants were rescued by injection of <jats:italic>cad<\/jats:italic> RNA. Cad activity is required for pyrimidine biosynthesis, and thus is a prerequisite for nucleic acid production and UDP\u2010dependent protein glycosylation. Perturbation of nucleic acid biosynthesis can result in cell death. <jats:italic>sl23<\/jats:italic> mutants did not exhibit elevated cell death, or gross morphological changes, in their hindbrains. To determine if defective protein glycosylation was involved in the aberrant targeting of sensory axons, we treated wild type embryos with tunicamycin, which blocks N\u2010linked protein glycosylation. Interference with glycosylation via tunicamycin treatment mimicked the <jats:italic>sl23<\/jats:italic> phenotype. Loss of <jats:italic>cad<\/jats:italic> reveals a critical role for protein glycosylation in cranial sensory circuit formation.<\/jats:p>","DOI":"10.1016\/j.ijdevneu.2013.11.003","type":"journal-article","created":{"date-parts":[[2013,11,24]],"date-time":"2013-11-24T15:15:11Z","timestamp":1385306111000},"page":"41-48","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Novel role for carbamoyl phosphate synthetase 2 in cranial sensory circuit formation"],"prefix":"10.1002","volume":"33","author":[{"given":"Jane A.","family":"Cox","sequence":"first","affiliation":[{"name":"Department of Pharmacological and Physiological Science Saint Louis University School of Medicine 1402 S. 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