The trouble with cloning
It has been known for some years now that fetuses and newborn animals produced after cloning and other embryo manipulations are not only at much greater risk of developmental defects, but are sometimes much larger than their uncloned counterparts. Lorraine Young, Ian Wilmut (of the Roslin Institute) and colleagues now provide a clue as to why this is so (Nature Genetics, Vol. 27, Issue 2, 01 Feb 2001). They compared the levels of the receptor of a protein that influences growth (an insulin growth factor receptor; IGF2R) between large, fetal sheep from 'test tube'-cultured embryos and those of 'normal' fetuses of the same age. The levels of IGF2R were indeed much lower in the large, cultured fetuses--30-60% lower--than the normal fetuses. Young and colleagues speculate that these fetuses are bigger because there is less IGF2R to inhibit other factors that keep growth in check in the fetus. They went on to analyse the IGF2R gene and found that it lacks a common type of chemical modification (known as methylation) which is known to be involved in determining the 'volume'at which some genes that influence growth are set. The findings support the hypothesis that the methylation of DNA of embryo-manipulated animals is prone to disruption--and the argument that cloned embryos should be screened for such disruptions before their implantation into surrogate mothers.
Dr. Lorraine E. Young
Roslin Institute (Edinburgh), Roslin
Telephone: +44 131 527 4200
Fax: +44 131 440 0434
Dr. Leif Andersson
Dept of Animal Breeding and Genetics
Swedish University of Agricultural Sciences
Uppsala Biomedical Center,
S-751 24 Uppsala, Sweden
Telephone: +46 011 46 18 47 14904
Fax: +46 18 50 4461
Dr. Mark Westhusin
Department. of Veterinary Physiology
Texas A&M University
College Station, Texas, USA
Telephone: +1 (409) 545-5885
Fax: +1 (409) 845-6544
(C) Nature Genetics press release.
Message posted by: Trevor M. D'Souza
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