When cells grow and reproduce, they must constantly produce new proteins from their building blocks, 20 different amino acids. These proteins are put together by ribosomes, which move along messenger RNA molecules to read and translate information to the sequences of amino acids that determine the function of all of the proteins in the cell.
It was previously known that short, tiny control RNA, called antisense RNA, can stop the activity of genes by placing themselves so that “reading” of the code is impeded. It has been shown that this occurs in bacteria in that antisense RNA sets up base pairs with a certain messenger RNA (m-RNA) precisely where the ribosomes would start their reading.
“This is inhibits the reading. Ribosomes need single-strand RNA in order to start,” says Gerhart Wagner, professor of procaryote microbiology at Uppsala University.
In the Uppsala researchers’ study, an unexpected and entirely new mechanism was uncovered for this regulation of protein synthesis, which cannot be explained by a model in which antisense RNA blocks the ribosomes’ starting site on messenger RNA. In this case, instead, antisense RNA sets up base pairs far away from where the reading should start-but still manages to stop the reading. It turns out that when a ribosome comes to a starting site that is “closed,” it attaches instead to an “open” site further along and waits for the proper site to become available.
“This is binding in stand-by, you might say. But we can show that antisense RNA competes with the ribosomes to be able to attach to this stand-by site as well. And if they get there first, then protein synthesis is prevented. This is something no one has seen before, and it provides a new picture of the innermost process of life,” says Gerhart Wagner.
Anneli Waara | alfa
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