By allowing AID to work on single-stranded viral DNA containing a mutational marker gene, the researchers (using specialized laboratory techniques) were able to identify which DNAs contained mutations and which did not.
"The action of AID yielded the same specific mutational hot and cold spots along DNA strands that are observed in human antibody proteins," explained Myron F. Goodman, a professor of molecular biology and chemistry in USC's College of Letters, Arts & Sciences and senior author of the Nature paper.
Those "hot" spots, identified by specific DNA sequences, allowed the researchers to clearly see where the mutations took place. In fact, the experiment yielded 14 out of 15 hot spots with perfect DNA sequences, demonstrating that the mutation process had gone off without a glitch.
"Remarkably, the results showed that AID acting alone on single-stranded DNA simulated the highly complex somatic hypermutation process that occurs in humans," Goodman said.
Furthermore, the team's data revealed that the AID enzyme works its way along individual DNA strands, as opposed to jumping from one strand to another.
Because many of the DNA strands remained untouched as part of this methodical process, the team found that 98 percent of its experimental DNA had no mutations.
Among the 2 percent that did, half exhibited between one and 20 mutations, while the other half showed up to 80.
"It confirms that AID is working on individual pieces of DNA, instead of jumping around," Goodman said.
Overall, the USC team of researchers was impressed by AID's role in the entire process.
"AID can't account for somatic hypermutation by itself because we know that other enzymes are involved," Goodman explained. "But it's pretty darn impressive to see that AID accounts fo
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Contact: Gia Scafidi
scafidi@usc.edu
213-740-9335
University of Southern California
30-Jun-2003