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Main Topic: C) GENETIC ENGINEERING

Therapeutic Cloning Gets A Boost With New Research Findings

 

Germ cells which give rise to a mammal's sperm or eggs, exhibit a five to ten-fold lower rate of spontaneous point mutations than adult somatic cells which give rise to the body's remaining cell types, tissues and organs. Despite their comparatively higher mutation rates, however, adult somatic cells are used as the donor cells in a cloning process called somatic cell nuclear transfer (SCNT). This made researchers wonder if cloning by SCNT leads to progeny with more and faster mutations than their naturally conceived counterparts.

Researchers at The University of Texas Health Science Center at San Antonio in collaboration with and the University of Hawaii at Honolulu's John A. burns of Medicine spent more than five years analyzing mutation rates and types in cloned Big Blue mouse fetuses and demonstrated that cloning does not lead to an increase in the frequency of point mutations. The team also found that naturally conceived fetuses and cloned fetuses that are the same age have similar rates

of spontaneous mutation development. They attribute his finding to epigenetic reprogramming.

Germ cells contain an epigenome, a programmed state of the genome that keeps mutation rates low. They suggest this type of epigenome is found in germ cells because those cells are responsible for contributing genetic information to subsequent generations. Adult somatic cells (the donor cells in SCNT) have higher mutation rates and less stringent epigenetic programming to avoid mutations than germ cells, but offspring produced from somatic cells by cloning have mutation rates similar to those in offspring produced by natural reproduction, suggesting that the epigenome of an adult somatic cell is reprogrammed during cloning to maintain the genetic integrity of that cell's progeny.

To read more about this subject, please visit:
www.sciencedaily.com/releases/2009/03/
090325091805.htm

       
     
IOMS Newsletter - 12 August 2009  
Issue No. 002/09
 
 
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