We are excited to share that Dr. Stefan Taubert, an Investigator at the Edwin S.H. Leong Centre for Healthy Aging (ELCHA), has published a new study in Nature Communications on how cells survive when nutrients are scarce.
How Do Cells Survive Starvation?
When cells don’t get enough nutrients, they need to find ways to protect themselves. In cancer cells, a key protein —eEF2K— helps cells survive starvation by slowing down protein production to conserve energy. eEF2K is also found in the roundworm C. elegans, where it is called EFK-1, and helps them survive starvation as well. However, in a study lef by PhD student Junran Yan, Dr. Taubert’s team discovered that it functions quite differently in the worm compared to cancer cells.
In the worm, EFK-1 doesn’t function in the regular way to slow protein production. Instead, EFK-1 helps worms protect their DNA from damage and controls how much oxygen their mitochondria use. By doing this, cells can prevent harmful oxidative stress and survive for longer during times of nutrient scarcity.
Why Does This Matter?
As starvation resistance is linked to aging and disease, the way cells manage stress when nutrients are low can affect longevity and overall health. Previous research has focused on how eEF2K controls protein production, but this study shows that it could have other important functions in ensuring cellular health. Importantly, eEF2K is linked to age-related diseases, including cancer and neurodegenerative diseases such as Alzheimer’s, and eEF2K targeting drugs are being developed for cancer treatment. This study may help researchers better understand and evaluate how such drugs could be used in cancer and other aging-related diseases, where managing cell stress is critical.
How Was This Discovered?
Dr. Taubert’s team made this discovery by studying tiny roundworms called C. elegans, which are often used in aging research. They generated worms that didn’t have EFK-1 and compared them to normal worms when food was scarce. Worms without EFK-1 struggled to survive starvation, while normal worms with EFK-1 lived much longer.
When they looked deeper, they found something surprising—compared to normal worms, worms without EFK-1 don’t show overall changes in protein production. They deduced that something else must be at work.
To understand why, the researchers looked at what was happening inside the cells. They found that EFK-1 was working to improve other aspects of cell health—it was actually helping cells repair damage and control oxygen use.
- Cells with EFK-1 had better DNA repair, meaning they could fix harmful damage caused by stress.
- They also used oxygen more carefully, preventing toxic byproducts that can speed up aging-related processes in long starvation.
This discovery challenges what scientists previously thought about EFK-1, showing that it actively protects cells during starvation rather than just slowing things down.
📖 Read the full study here: Nature Communications