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Time of initiation and site of action of the mouse chromosome 11 imprinting effects

Published online by Cambridge University Press:  14 April 2009

Bruce M. Cattanach ,
Colin V. Beechey ,
Carol Rasberry ,
Janet Jones  and
David Papworth
Bruce M. Cattanach*
Affiliation:
MRC Mammalian Genetics Unit Harwell, Didcot, Oxfordshire OX11 ORD, UK
Colin V. Beechey
Affiliation:
MRC Mammalian Genetics Unit Harwell, Didcot, Oxfordshire OX11 ORD, UK
Carol Rasberry
Affiliation:
MRC Mammalian Genetics Unit Harwell, Didcot, Oxfordshire OX11 ORD, UK
Janet Jones
Affiliation:
MRC Mammalian Genetics Unit Harwell, Didcot, Oxfordshire OX11 ORD, UK
David Papworth
Affiliation:
MRC Mammalian Genetics Unit Harwell, Didcot, Oxfordshire OX11 ORD, UK
*
* Corresponding author.
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Previous studies have shown that mice with paternal disomy for chromosome 11 are consistently larger at birth than their normal sibs, whereas mice with the maternal disomy are consistently smaller. An imprinting effect with monoallelic expression of some gene/s affecting growth was indicated. Here we show that the size differences become established prior to birth and are only maintained subsequently, indicating that the gene repression is limited to prenatal development. Fetal analysis was limited to 12·5–17·5 days post coitum. However by extrapolating the data backwards it could be calculated that both the maternal and paternal size effects might commence as early as 7 days post coitum, although possibly slightly later. It may be deduced that initiation of expression of the gene/s responsible may occur at about this time in development. The two disomy growth rates were mirror-images of each other, suggesting that expressed gene dosage is the underlying cause. Differential growth of the placentas of the two disomies was also found, and extrapolation of these data backwards suggested that the placental size differences were initiated later in development than those for the fetuses. The differential placental growth of the maternal and paternal disomies may therefore have developed independently or emerged as a consequence of the differential fetal growth. In either event it would seem that the expression of the responsible gene occurs in the fetus itself to cause the anomalies of growth. The data therefore provide information on the temporal and tissue specificity of the gene/s responsible for the chromosome 11 imprinting effects. Possible candidate genes are discussed.

Type
Research Article
Information
Genetics Research , Volume 68 , Issue 1 , August 1996 , pp. 35 - 43
Copyright
Copyright © Cambridge University Press 1996

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