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Officials last week revealed that the U.S. contribution to ITER could cost $3.9 billion by 2034—roughly four times the...
An experimental hepatitis B drug that looked safe in animal trials tragically killed five of 15 patients in 1993. Now,...
Using the two high-quality genomes that exist for Neandertals and Denisovans, researchers find clues to gene activity...
A new report from the Intergovernmental Panel on Climate Change (IPCC) concludes that humanity has done little to slow...
Astronomers have discovered an Earth-sized planet in the habitable zone of a red dwarf—a star cooler than the sun—500...
Three years ago, Jennifer Francis of Rutgers University proposed that a warming Arctic was altering the behavior of the...
- 17 April 2014 12:48 pm , Vol. 344 , #6181
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Putting the Brakes on Cell Death
20 September 2007 (All day)
The sudden death of worms in room-temperature water has helped scientists identify a regulator of necrosis, a common form of cell death. Although preliminary, the discovery could help scientists better understand necrosis and perhaps figure out ways to stop it in human diseases.
There are several ways a cell can die. One, apoptosis, is a form of controlled cellular suicide, usually for the benefit of the organism. The gaps between our fingers and toes are one mark of this process. Necrosis is virtually the opposite: The cell isn't trying to die, but factors such as blood loss or oxygen deprivation make it swell and explode. Necrosis has gotten much less attention than apoptosis, and although some scientists have found ways to accelerate it, it's never been clear that it can be halted.
Neonatologist and molecular biologist Gary Silverman of the University of Pittsburgh in Pennsylvania and his colleagues came to necrosis in a roundabout fashion. The team was interested in proteins called serpins, some of which help control blood clotting and inflammation. So they knocked out the gene for a serpin called SRP-6 in worms. To their disappointment, the animals seemed unbothered.
But postdoc Cliff Luke noticed that the worms died rapidly when he washed them in room-temperature water. The death was necrotic, the team found, and appeared to be a stress response gone awry; the animals couldn't adjust the volume of fluid in their cells as normal worms do when exposed to water. Looking more closely, the scientists saw that lysosomes, sacs in cells that help break down cellular garbage, had burst. The worms without SRP-6 were also more likely to die than normal worms when subjected to other stressors, including heat and oxygen deprivation. Finally, the researchers found that, when they injured the worms' lysosomes, worms lacking SRP-6 could not repair their lysosomes, whereas normal worms could. Taken together, this suggests that SRP-6 protects worm cells against lysosome rupture and necrosis, the scientists conclude in the 21 September issue of Cell.
"I'm quite amazed," says Wei-Xing Zong, a molecular biologist who studies cell death at Stony Brook University in New York. "When people look at necrosis, ... they kind of never think that this can be controlled."
The distinction is important, says Guy Salvesen of the Burnham Institute for Medical Research in San Diego, California, because "if there's a pathway" governing the process, interfering with it may help fight the damage from those diseases. Still, it's not clear yet how well necrosis can be controlled, he cautions, and the jury's still out on whether Silverman's work will translate to humans.