Perinatal loss of Ts65Dn Down syndrome mice

Randall J. Roper, Heidi K. St. John, Jessica Philip, Ann Lawler, Roger H. Reeves

Research output: Contribution to journalArticlepeer-review

Abstract

Ts65Dn mice inherit a marker chromosome, T(1716)65Dn, producing segmental trisomy for orthologs of about half of the genes on human chromosome 21. These mice display a number of phenotypes that are directly comparable to those in humans with trisomy 21 and are the most widely used animal model of Down syndrome (DS). However, the husbandry of Ts65Dn mice is complicated. Males are sterile, and only 20-40% of the offspring of Ts65Dn mothers are trisomic at weaning. The lower-than-expected frequency of trisomic offspring has been attributed to losses at meiosis, during gestation and at postnatal stages, but no systematic studies support any of these suppositions. We show that the T(1716)65Dn marker chromosome is inherited at expected frequency and is fully compatible with development to midgestation. Disproportional loss of trisomic offspring occurs in late gestation and continues through birth to weaning. Different maternal H2 haplotypes are significantly associated with the frequency of trisomy at weaning in patterns different from those reported previously. The proportion of trisomic mice per litter decreases with age of the Ts65Dn mother. These results provide the first statistical and numerical evidence supporting the prenatal and perinatal pattern of loss in the Ts65Dn mouse model of DS.

Original languageEnglish (US)
Pages (from-to)437-443
Number of pages7
JournalGenetics
Volume172
Issue number1
DOIs
StatePublished - Jan 2006

ASJC Scopus subject areas

  • Genetics

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