Scientists Solve 50-Year Mystery of How Cells Stay ‘in Balance’
When it comes to survival on the cellular level, mysteries have abounded for decades. In a paper published recently in Nature Cell Biology, Cheryl Walker, Ph.D., and her team at Texas A&M Health Science Center’s Institute of Biosciences and Technology in the Texas Medical Center reveal the answers behind one such mystery.
|Cheryl Walker, Ph.D.|
The researchers discovered that a gene known as TSC2 monitors the tiny organisms within cells that break down the fat inside the cells.
The organisms, known as peroxisomes, were discovered in the mid-1960s, and scientists knew that peroxisomes and TSC2 somehow worked together for the good of the human body – but they were unsure of how the two “teamed up.”
Now, Walker and her team know that TSC2 keeps peroxisomes at the right levels to maintain healthy cells.
“Without TSC2 to balance peroxisomes, healthy cells could proliferate in an uncontrolled way – just like cancer,” said Walker, director of the Institute of Biosciences and Technology. “Knowing how TSC2 behaves to keep cells balanced could help us learn how to balance or counteract diseases like cancer and heart disease, as well as inflammation and maladies associated with aging. In short, it is a concept that could lead to cures.”
The journal article explains the biology behind the team’s work. Human cells use peroxisomes to break down the fat necessary for survival. When peroxisomes do their job, the conversion of fat creates reactive oxygen species, or ROS. These ROS are similar to the harmful oxidants found in the environment. At low levels ROS play important and normal roles in our cells. Too much ROS, and they damage anything they touch, including proteins, lipids and DNA.
“In a way, the TSC2 is Mother Nature’s do-it-yourself antioxidant,” Walker said. “It recognizes when there is too much ROS so that our cells can protect themselves.”
In addition to creating ROS, peroxisomes boast a tricky talent. Unlike other organisms in cells, peroxisomes can replicate themselves autonomously. As the number of peroxisomes increases, so does the level of ROS, and cells must keep it all in check.
To do this, Walker’s team discovered that TSC2 acts as a censor on every peroxisome to monitor how much ROS is being made. If TSC2 detects too much ROS, it notifies the cell to dispose of the peroxisome. Just as fire triggers a smoke alarm, too much ROS prompts a signal from TSC2, ensuring balance within the cell.
“We have known for decades that some of the worst childhood diseases are caused by a lack of healthy peroxisomes,” said Walker. “The possibility that other diseases, such as cancers, may also be due to defective peroxisomes is totally unexpected, and this information enables the exciting possibility of new cancer therapies targeting the peroxisome.”