{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T18:16:58Z","timestamp":1792174618919,"version":"4.4.0"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2001,3,26]],"date-time":"2001-03-26T00:00:00Z","timestamp":985564800000},"content-version":"vor","delay-in-days":25,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Teratology"],"published-print":{"date-parts":[[2001,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Genetic background of the fetus contributes to the pathogenesis of congenital malformation after teratogen exposure. Such contribution is illustrated in left\u2010right axis malformations observed in the F1 offspring of nonobese diabetic (NOD) mouse dams and sires from different strains. When sires of the NOD, ICR, or C57BL\/6J were mated with NOD dams, incidence varied depending on the fetal genotype, with 65% in NOD \u00d7 NOD, 24% in NOD \u00d7 ICR, and 7% in NOD \u00d7 C57BL\/6J.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>As a first step in elucidating the molecular basis of the interstrain differences in susceptibility to situs defects, we compared genomic sequences of six genes <jats:italic>HNF3beta<\/jats:italic>, <jats:italic>Acvr2b<\/jats:italic>, <jats:italic>Nodal<\/jats:italic>, <jats:italic>ZIC3<\/jats:italic>, <jats:italic>Lefty1<\/jats:italic>, and <jats:italic>Smad2<\/jats:italic>, which are involved in the normal development of left\u2010right axis among NOD, ICR, and C57BL\/6J strains.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The outbred strain ICR had 1) a 0.2\u2010kb insertion in the putative promoter region of the isoform E of <jats:italic>HNF3beta<\/jats:italic> together with a G to A change that could create a potential splice acceptor in the exon 3 of <jats:italic>HNF3beta<\/jats:italic> (gene frequency <jats:italic>P<\/jats:italic> = 0.36), 2) five single base substitutions within the 5\u2032 controlling element and a proline to serine substitution (P2S) of <jats:italic>Lefty1<\/jats:italic> (<jats:italic>P<\/jats:italic> = 0.77), and 3) a tyrosine to histidine substitution within the prodomain of <jats:italic>Nodal<\/jats:italic> (<jats:italic>P<\/jats:italic> = 0.48). The inbred strain NOD had the same G to A change as ICR and a three\u2010base deletion in the putative promoter of isoform E of <jats:italic>HNF3\u03b2<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We suggest that sequence variations in <jats:italic>HNF3\u03b2<\/jats:italic>, <jats:italic>Lefty1<\/jats:italic>, and <jats:italic>Nodal<\/jats:italic> might account, in part, for the interstrain differences in susceptibility to situs abnormalities among the offspring of diabetic dams. Teratology 63:119\u2013126, 2001. \u00a9 2001 Wiley\u2010Liss, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/tera.1022","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T21:27:27Z","timestamp":1030310847000},"page":"119-126","source":"Crossref","is-referenced-by-count":17,"title":["Mutation analysis of left\u2010right axis determining genes in NOD and ICR, strains susceptible to maternal 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