Drosophila melanogasterWIKIMEDIA, ANDRÉ KARWATHMost genomes harbor unruly, mobile DNA elements that can cause potentially harmful mutations. Transposons—thought to be related to viruses—can copy themselves and insert randomly around the genome. A paper published today (October 15) in Science provides a greater understanding of how cells shut down these rogue jumping genes. Greg Hannon of the Cancer Research UK Cambridge Institute and his colleagues have identified a protein in fruit flies that appears to halt transposons before they begin to leap.
“This is a mountain of impressive work, a huge amount of data, [the result of which] is that we now understand something about how piRNAs are transcriptionally silencing their targets,” said molecular geneticist Keith Slotkin of Ohio State University who was not involved in the work. “We knew that this was happening, but the mechanism was all question marks and hand-waving.”
Piwi-interacting RNAs, or piRNAs, are short noncoding RNAs that, as their name implies, interact with a protein called Piwi—a highly conserved transposon-suppressing factor. To protect the host against damaging tranposon-induced mutations, Piwi-piRNA complexes both destroy transposon transcripts in the cytoplasm (post-transcriptional silencing) and block transposon transcription in the nucleus (transcriptional silencing). Essentially, the piRNA pathway “mops up the water” and “turns off the spigot,” ...
