BioEd Online

Researchers have found reserve stocks of RNA strands in mouse cells, which allow the cells to quickly churn out proteins in response to stressful conditions.

The discovery of these back-up protein-coding strands has opened up new avenues for research in genetics and should help biologists to better understand how our bodies fight off infection.

The classic method by which molecules known as messenger RNAs produce proteins inside cells has long been established. Inside the cell nucleus, DNA gets transcribed into messenger RNA. The RNA strand is then modified so that it can leave the nucleus and be translated into a protein within the cell's cytoplasm.

But David Spector, a molecular biologist at the Cold Spring Harbor Laboratory in New York State, and his colleagues have found messenger RNAs with a difference.

Cat and mouse

The team had noticed some unmodified messenger RNAs lingering in the nucleus of mouse cells, inside tiny protein structures called paraspeckles.

Some of these RNA molecules were encoded by one particular gene, mCAT2. The mCAT2 gene helps cells to make nitric oxide, a compound thought to help the cells fight infection. Previous studies have also implicated poor function of the gene's protein product in Huntington's disease and Multiple Sclerosis.

The team suspected that this extra RNA could be called into action in stressful times, and to test the theory, they exposed mouse cells to an enzyme that inhibits the synthesis of fresh messenger RNA. The amount of reserve RNA dropped by about half, they report in Cell¹.

By using the back-up RNA, cells can quickly produce more proteins without having to go back to the DNA for new messenger RNA copies, Spector explains.

Protein pump

Cells are known to use other tricks to regulate gene expression and control protein levels; for example, DNA transcription can be varied and RNA molecules modified within the cell. But this is a new mechanism of gene regulation, says geneticist and Nobel laureate Phillip Sharp of the Massachusetts Institute of Technology in Cambridge, Massachusetts.

Spector's team suspects that human cells will have the same back-up system, and plan to investigate this next. "We are highly optimistic that this will prove to be a general mechanism," says Spector.

They also hope to understand how such reserve RNA strands in humans might help to protect cells against disease.