Shinichi Miyabara is a Fellow of Alexander von Humboldt-Stiftung.
Genetics and Cytogenetics
Trisomy 16 in the mouse fetus associated with generalized edema and cardiovascular and urinary tract anomalies
Article first published online: 31 MAY 2005
Copyright © 1982 Wiley-Liss, Inc., A Wiley Company
Volume 25, Issue 3, pages 369–380, June 1982
How to Cite
Miyabara, S., Gropp, A. and Winking, H. (1982), Trisomy 16 in the mouse fetus associated with generalized edema and cardiovascular and urinary tract anomalies. Teratology, 25: 369–380. doi: 10.1002/tera.1420250314
- Issue published online: 31 MAY 2005
- Article first published online: 31 MAY 2005
- Manuscript Accepted: 21 OCT 1981
- Manuscript Received: 4 APR 1981
Murine trisomy (Ts) 16 occurs in the fetal and neonatal progeny of males doubly heterozygous for the Robertsonian metacentric chromosomes Rb(16.17)7Bnr/Rb(9.16)9Rma and “all acrocentric” females. The developmental aspects of this trisomy were studied between day 12 of gestation and birth. So far, postnatal survival longer than a few hours after birth has not been observed. The frequency of Ts 16 among all implants decreased from more than 20% on day 14 to values between 4% and 7% shortly before term.
Main features of Ts 16 are moderate general hypoplasia, slight developmental retardation, and cardiovascular anomalies. These latter were found in 96% of the trisomies, the great majority belonging to the transposition type, i.e., riding aorta, double outlet right ventricle (DORV) and transposition of the great arteries (TGA). Association with common atrio ventricular (AV)-canal was frequent. Other anomalies as “open eyelid”, hydronephrosis, and hydroureter seem to be attributable to the effects of retardation. Generalized transient edema was frequent in the later gestational stages of Ts 16.
Severe cardiovascular malformation is possibly one of the factors responsible for late fetal or neonatal death in some cases. Another factor probably contributing to Ts 16 fetal mortality is insufficiency of placental function due to hypoplasia of the fetal vasculature of this organ. The teratological study of Ts 16 demands interest since evidence has been forwarded to consider this trisomy as an animal model of human trisomy 21.