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Familial Twinning: A Case for Superfetation in Man*

Published online by Cambridge University Press:  01 August 2014

S.A. Rhine  and
Walter E. Nance
S.A. Rhine
Affiliation:
Department of Medical Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA
Walter E. Nance*
Affiliation:
Department of Medical Genetics, Indiana University School of Medicine, Indianapolis, Indiana, USA
*
Department of Human Genetics, Box 33, MCV Station, Richmond, Virginia 23298, USA

Abstract

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A family is described in which the tendency to bear twins is expressed in the offspring of males as well as females. All of the twins born in this family show marked discordance in birth weight and gestational age. In 5 of the 6 pairs, one twin was normal while the other was either a macerated fetal mass, stillborn, or died of prematurity in the neonatal period. The one pair in which both twins did survive is known to be DZ and showed a difference in maturity and a 21% discrepancy in birth weight. Thus, twinning in this family appears to be transmitted as an autosomal dominant trait which is expressed in the offspring of both female and male carriers. Of all possible genetic mechanisms which could explain this familial aggregation of markedly discordant twins, supcrfetation seems most consistent with the genetic transmission and expression of the trait in the offspring of both males and females. The most plausible explanation of the pedigree is that a dominant gene is segregating in the family which is expressed in the fetal placenta where it acts to reverse the normal hormonal inhibition of ovulation. Since both the father and the mother contribute to the genotype of the placenta, superfeiation could occur among offspring of both males and females who carry the gene.

Type
2. The Twinning Phenomenon
Information
Acta geneticae medicae et gemellologiae: twin research , Volume 25 , Issue 1 , January 1976 , pp. 66 - 69
Copyright
Copyright © The International Society for Twin Studies 1976

Footnotes

*

This is publication number 74-25 from the Department of Medical Genetics, and was supported in part by the Indiana University Human Genetics Center, POI HD 10291-01 and a grant from the John A. Hartford Foundation, Inc.

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