WORCESTER, Mass. Small, mobile sequences of DNA left over from viruses, called transposons or "jumping genes" because of their ability to move around the genome, pose a significant threat to the genetic integrity and stability of an organism. Considered genetic parasites, these transposable elements are believed to comprise as much as 50 percent of the human genome. Because of the damage transposons can do to an organism's DNA, an immune-like response has evolved to turn off, or silence, these mobile genetic elements.
New research published in the journal Cell by the labs of William E. Theurkauf and Zhiping Weng at the University of Massachusetts Medical School sheds light on how the genome defends itself from these invading DNA parasites.
While it's known that specific small RNAs called Piwi-interacting RNAs (piRNAs) are responsible for silencing transposons, how this biologically critical system reacts to the introduction of a new transposon isn't fully understood. "The genome is littered with these transposons," said William E. Theurkauf, PhD, professor of molecular medicine at UMass Medical School and lead author of the study. "In Drosophila there are over 120 different forms of transposons and these are the active pathogen that we are looking at in this host-pathogen response. Meanwhile, piRNAs are produced from regions of the genome that contain bits and pieces of these transposons, and are the foundation for how these elements get silenced."
To understand how a genome responds to the introduction of a new transposon, Theurkauf and colleagues turned to a wild Drosophila, or fruit flies. Unlike standard lab-bred fruit flies, wild Drosophila contain a transposon called the P element that first began appearing in the population after scientists started breeding fruit flies to study genetic heredity in the early part of the 20th century. As a result, lab-bred fruit flies lack the P element transposon and the maternally in
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University of Massachusetts Medical School