San Antonio Germ cells, the 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 mutations than their naturally conceived counterparts. Also, would cloned fetuses receive DNA programming predisposing them to develop mutations faster than natural fetuses of the same age?
Those scenarios are simply not likely, say researchers at The University of Texas at San Antonio, The University of Texas Health Science Center at San Antonio and The University of Hawaii at Honolulu's John A. Burns School of Medicine. The team, which spent more than five years analyzing mutation rates and types in cloned Big Blue mouse fetuses recently published its findings in the online Early Edition of the Proceedings of the National Academy of Sciences in a paper titled "Epigenetic regulation of genetic integrity is reprogrammed during cloning."
The paper offers the first direct demonstration that cloning does not lead to an increase in the frequency of point mutations.
John McCarrey, professor of cellular and molecular biology at UTSA and the study's principal investigator, suggests a "bottleneck effect" is partially responsible for the observations his team recorded. "To create a cloned fetus by somatic cell nuclear transfer, only one adult somatic cell -- one donor cell -- is needed," he explains. "Because a random cell population exhibits a low mutation rate overall and only one cell from that population is used for cloning, the likelihood is remote that the cell chosen to be cloned will transfer a genetic mutation to its cloned offspring.
|Contact: Christi Fish|
University of Texas at San Antonio