A View of Cellular Emergency Repair Mechanisms

Scientists at the Massachusetts Institute of Technology (MIT), in Cambridge, announce that they were recently able to gain more insight into the way cells respond to threatening situations, in which their very survival is at stake. A host of processes are triggered at that time, fulfilling multiple goals.

Among these defense mechanisms is a process that oversees the manufacturing of large amounts of critically important proteins, including some that are essential for repairing damaged DNA.

When it produces large amounts of these molecules, cells become very resilient to DNA damage. If the external threats are too great, the cell will indeed succumb to them, but not before putting up a good fight first.

In the new investigation, which MIT experts conducted in collaboration with colleagues from the University of Albany, scientists managed to discover a new mechanisms through which such proteins are produced inside cells.

Details of their discovery appear in the December 16 issue of PLoS Genetics, a open-access, peer-reviewed journal edited by the Public Library of Science.

During stressful situations, the investigators learned, cells gain the ability to reprogram a complicated system of chemical modifications of RNA molecules. This system usually enables the RNA to read the genetic code in the cell, and deliver protein building blocks according to demand.

According to MIT professor of biological engineering and senior paper author Peter Dedon, this mechanism is triggered in response to stressful stimuli (dangerous chemicals, radiation, etc.), growth factors, nutrients, and hormones.

This work also carried significant implications for the field of microbiology, Dedon says. He and colleagues are currently investigating how bacteria and other pathogens use similar mechanisms to repel the attacks of human white blood cells.

Our immune systems are heavily reliant on these cells, which it uses to fight a large number of invaders off. Knowing their targets' defense mechanisms could enable scientists to develop new antibiotics.

“Previously it was believed that transferRNA modification is static. This paper shows that under stress, the level of modification can continually change. The next thing is to understand how and why cells do it,” explains University of Chicago professor of biochemistry and molecular biophysics Tao Pan.