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Fathering Problems
A 21-year-old SIUC student explained her research to the country's lawmakers last April on Capitol Hill.
Microbiology major Sara Reardon took second place at the inaugural St. Louis Area Undergraduate Research Symposium in 2006. This year, she was one of 60 students chosen by the Council on Undergraduate Research from a national pool of hundreds of applicants to participate in the group's annual "Posters on the Hill" exhibit in Washington, D.C.
Her work focuses on a gene, called DEAF-1, that when mutated may drive cancer development and impair fertility in mammals, including humans.
Reardon joined the research team of physiologists Michael Collard and Jodi Huggenvik in her freshman year. She started out by maintaining their mouse colony. Some of these mice lack a working copy of DEAF-1.
"We knew there was this defect in male fertility," Collard said of the mice. "It was Sara who established to what degree this loss occurs and the genetic background that produces it."
Male offspring of these so-called "DEAF-1 knockout" mice often have a normal DEAF-1 gene—yet they still have impaired fertility. Collard, Huggenvik, and Reardon believe the explanation lies with DNA methylation. As part of reproduction and development, methyl groups attach to DNA, affecting gene expression. The team thinks that the absence of the DEAF-1 gene changes the methylation of other genes in a mouse's sperm or eggs.
These methylation abnormalities get passed along to the mouse's offspring. That's why the offspring—even if they have a normal copy of the DEAF-1 gene—can still suffer inherited fertility problems, obesity, and prostate cancer.
Reardon, now working as a graduate student in Collard's lab, is testing that hypothesis, which may have applications to human health. She has invented techniques to look at changes in DNA in 7,000 mouse genes to determine which genes may be affected by methylation abnormalities. After graduate school, she plans on a career in biomedical research.
—by Tom Woolf and Marilyn Davis
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