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Trisomy 17 in a baboon ( Papio hamadryas ) with polydactyly, patent foramen ovale and pyelectasis
Author(s) -
Moore Charleen M.,
Hubbard Gene B.,
Dick Edward,
Dunn Betty G.,
Raveendran Muthuswamy,
Rogers Jeffrey,
Williams Vick,
Gomez Jeremiah J.,
Butler Stephanie D.,
Leland M. Michelle,
Schlabritzloutsevitch Natalia E.
Publication year - 2007
Publication title -
american journal of primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 81
eISSN - 1098-2345
pISSN - 0275-2565
DOI - 10.1002/ajp.20424
Subject(s) - polydactyly , trisomy , biology , genetics , aneuploidy , chromosome , anatomy , gene
Trisomy 13 in humans is the third most common autosomal abnormality at birth, after trisomy 21 and trisomy 18. It has a reported incidence of between 1:5,000 and 1:30,000 live births. It is associated with multiple abnormalities, many of which shorten lifespan. We describe here the first reported case of a baboon ( Papio hamadryas ) with trisomy of chromosome 17, which is homologous to human chromosome 13. The trisomic infant was born to a consanguineous pair of baboons and had morphological characteristics similar to those observed in human trisomy 13, including bilateral polydactyly in the upper limbs, a patent foramen ovale, and pyelectasis. Molecular DNA analysis using human chromosome 13 markers was consistent with the affected infant inheriting two copies of chromosome 17 derived from the same parental chromosome. This trisomy was, therefore, due to either an error in meiosis II or the result of postzygotic nondisjunction. The parental origin, however, could not be determined. Am. J. Primatol. 69:1105–1118, 2007. © 2007 Wiley‐Liss, Inc.