Complex asparagine (N)‐linked oligosaccharides appear late in phylogeny and are highly regulated in vertebrates. Variations in these structures are found on the majority of cell‐surface and secreted proteins. Complex N‐linked oligosaccharide biosynthesis is initiated in the Golgi apparatus by the action of Mgat‐1‐encoded UDP‐N‐acetylglucosamine:alpha‐3‐D‐ mannoside beta‐1,2‐N‐acetylglucosaminyltransferase I (GlcNAc‐TI). To determine if these structures govern ontogenic processes in mammals, mouse embryos were generated that lacked a functional Mgat‐1 gene. Inactivation of both Mgat‐1 alleles produced deficiencies in GlcNAc‐TI activity and complex N‐linked oligosaccharides. Embryonic lethality occurred by day 10.5, thus establishing that complex N‐linked oligosaccharides are required during post‐implantation development. Remarkably, embryonic development proceeded into day 9 with the differentiation of multiple cell types. Complex N‐linked oligosaccharides are important for morphogenic processes as neural tube formation, vascularization and the determination of left‐right body plan asymmetry were impaired in the absence of a functional Mgat‐1 gene.