{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T02:12:22Z","timestamp":1791079942619,"version":"4.1.0"},"reference-count":17,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2005,6,2]],"date-time":"2005-06-02T00:00:00Z","timestamp":1117670400000},"content-version":"vor","delay-in-days":4384,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Teratology"],"published-print":{"date-parts":[[1993,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Approximately 50% of <jats:italic>iv\/iv<\/jats:italic> mice have <jats:italic>situs inversus<\/jats:italic> (mirror image reversal of viscera) and 40% have heterotaxia (anomalous arrangement of viscera). The occurrence of heterotaxia is independent of <jats:italic>situs<\/jats:italic>. Using the cross\u2010intercross breeding system to put the iv gene on the SWV background, an occasional presumed <jats:italic>iv<\/jats:italic>\/ + mouse was found that had an IV (<jats:italic>situs inversus<\/jats:italic> and\/or heterotaxic) phenotype. Testcrosses of these reversed animals indicated an <jats:italic>iv<\/jats:italic>\/ + genotype. Since iv is linked tightly to <jats:italic>Igh\u2010C<\/jats:italic> on chromosome 12, we inferred the genotype with a polymorphism of <jats:italic>Igh\u2010C<\/jats:italic> demonstrated using the polymerase chain reaction (PCR). This confirmed them to be <jats:italic>iv<\/jats:italic>\/ +. The expression of the IV phenotype in animals heterozygous for the <jats:italic>iv<\/jats:italic> gene may be due to an interaction of <jats:italic>iv<\/jats:italic> with an autosomal recessive gene found in SWV. We have not found the IV phenotype in heterozygous <jats:italic>iv\/+<\/jats:italic> mice following placement of the <jats:italic>iv<\/jats:italic> gene on six other inbred strains. Rarely, we also found that presumed SWV +\/+ mice had the IV phenotype. Test matings of these phenodeviants, corroborated by PCR, have confirmed them to be +\/+. Although the phenotypes of the affected SWV +\/+ and <jats:italic>iv<\/jats:italic>\/ + mice resembled those found in <jats:italic>iv\/iv<\/jats:italic> mice, the occurrence of <jats:italic>situs inversus<\/jats:italic> and heterotaxia were not independent of each other, and most of the SWV mice with the IV phenotype had heterotaxia with <jats:italic>situs solitus<\/jats:italic>.<\/jats:p><jats:p>This infrequent dominant expression of the iv gene has so far only been seen when <jats:italic>iv<\/jats:italic> is on the SWV background. These findings are consistent with the idea that this phenomenon is due to the interaction of the <jats:italic>iv<\/jats:italic> gene with another gene found so far only in the SWV strain. \u00a9 1993 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/tera.1420470611","type":"journal-article","created":{"date-parts":[[2005,6,11]],"date-time":"2005-06-11T15:56:17Z","timestamp":1118505377000},"page":"595-602","source":"Crossref","is-referenced-by-count":20,"title":["Expression of the IV (reversed and\/or heterotaxic) phenotype in SWV mice"],"prefix":"10.1002","volume":"47","author":[{"given":"W. M.","family":"Layton","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. W.","family":"Layton","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Binder","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Kurnit","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrzej J.","family":"Hanzlik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret","family":"Van Keuren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fred G.","family":"Biddle","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,6,2]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/tera.1420440610"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.13.5035"},{"key":"e_1_2_1_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.jhered.a109486"},{"key":"e_1_2_1_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-349-04904-2"},{"key":"e_1_2_1_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0888-7543(90)90173-R"},{"key":"e_1_2_1_7_1","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.jhered.a110810"},{"key":"e_1_2_1_8_1","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.jhered.a106870"},{"key":"e_1_2_1_9_1","first-page":"317","article-title":"Abnormal facial development in the mouse mutant first arch","volume":"3","author":"Juriloff D. M.","year":"1983","journal-title":"J. Craniofac. Genet. Dev. Biol."},{"key":"e_1_2_1_10_1","first-page":"27","article-title":"Hemifacial deficiency induced by a shift in dominance of the mouse mutation far: A possible genetic model for hemifacial microsomia","volume":"7","author":"Juriloff D. M.","year":"1987","journal-title":"J. Craniofac. Gen. Dev. Biol."},{"key":"e_1_2_1_11_1","doi-asserted-by":"publisher","DOI":"10.1002\/tera.1420010208"},{"key":"e_1_2_1_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/tera.1420200206"},{"key":"e_1_2_1_13_1","first-page":"979","article-title":"Genetics, chance, and morphogenesis","volume":"41","author":"Kurnit D. M.","year":"1987","journal-title":"Am. J. Hum. Genet."},{"key":"e_1_2_1_14_1","doi-asserted-by":"publisher","DOI":"10.1093\/oxfordjournals.jhered.a108749"},{"key":"e_1_2_1_15_1","first-page":"277","article-title":"Heart malformations in mice homozygous for a gene causing situs inversus","volume":"14","author":"Layton W. 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