About Wren

Multiple advances in molecular biology and the sequencing of large portions of the genomes of many species, including humans, have led to the creation of a field that meshes biology and information technology: bioinformatics.

Jonathan Wren, research assistant professor in the Advanced Center for Genome Technology and Department of Botany and Microbiology, is an expert in the new discipline.

“The biomedical sciences have become very data intensive, but there’s a difference between data and knowledge. Acquiring data is less of a challenge than understanding what it means,” Wren says. “A lot of my research is text mining – extracting and organizing information reported within the scientific literature into more computationally accessible forms. But it’s also integrating data and being able to draw inferences from it. A few decades ago, the biggest problem facing biomedical research was getting good data. This problem still persists, of course, but now we have another one on top of that – sorting through the enormous body of existing data.”

More than 570,000 biomedical articles are published in the online medical database Medline in a single year. As a consequence, no scientist can be aware of all that’s out there.

“Lots of scientists are making observations and hypotheses with the hope that other people will build on that work. But they can’t build on it if they don’t know about it,” Wren explains. We can use a computer to read and understand the literature and make associations and inferences based on a large set of seemingly unrelated observations.”

Wren’s own research includes a hypothesis on the connection between Type II diabetes, widely thought to be caused by mutations in DNA, and methylation, the chemical process that causes genes to shrink so they can’t be expressed. “The incidence of Type II diabetes is increasing. Four percent of Americans are actually documented to have it, and another seven percent are thought to have it but haven’t been diagnosed,” he explains. “My hypothesis is that it’s caused not by a mutation in any gene but by methylation. The loss of methylation as time goes by may cause normal, unmutated genes to be expressed later in life in tissues in which they are not normally expressed, which would explain why people can progress from pre-diabetic to full-blown diabetic but then can’t go back – the ‘brakes’ that shut off inappropriate gene expression gradually wear down and are ultimately lost.”

Wren hopes to test his hypothesis soon. “There’s so much evidence in the literature that suggests that I’m right. If I am, it will be a breakthrough in understanding Type II diabetes,” he says.

The technology Wren developed to find these undiscovered links has been patented.