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UVa-led team uncovers important secret in gene replication

s replicating early and the other is replicating, Dutta said. Even though we get two copies of the genes, not all of the genes are expressed from both copies. There are a significant number of gene pairs where the chromatin is packed differently between the copies.

What this means, unfortunately, is that one of the copies of a gene X might be inactive because of chromatin packaging, losing the redundancy that comes from both copies being active. If tumor suppressor genes, the ones that turn off cancer cells, reside in areas of the genome with asynchronous replication, the cancer cell can turn such genes off merely by mutating the one active copy instead of going through the trouble of separately mutating both copies.

Dutta and colleagues are now gearing up for their next project, looking at the remainder of the genome, grateful for significant findings they uncovered in just one percent of the genome, through the ENCODE project. This study could not have been done without NIH funding, Dutta stressed. This type of basic research is not funded by the pharmaceutical firms or the biotech firms. We are all anxious because later this summer we will find out if we will receive the money to study the remaining the 99 percent of the human genome.

If the next portion goes unfunded, it would be one the biggest missed opportunities in biology, Dutta says. We used the one percent of the genome as a trial area, and it would be a tragedy if we couldnt expand this to the remaining 99 percent of the genome and to different cell lines. The difference between cell lines is where biology lies.


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Contact: Mary Jane Gore
mjgore@virginia.edu
434-924-9241
University of Virginia Health System
13-Jun-2007


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