RUTGERS (US)—Scientists have found a chemical culprit responsible for the rapid, mysterious death of phytoplankton in the North Atlantic Ocean. This same chemical may hold unexpected promise in cancer research.
Phytoplankton are tiny, drifting plants, mostly invisible to the naked eye, but visible even from space when they bloom in great numbers at sea.
Rutgers marine biologists, Kay Bidle and Assaf Vardi, WHOI chemical ceanographer Benjamin Van Mooy, and members of their laboratories discovered a previously unknown lipid, or fatty compound, in a virus that has been attacking and killing Emiliania huxleyi, a phytoplankton that plays a major role in the global carbon cycle.
The lipids are the key ingredient in the virus that causes the phytoplankton to
die. The scientists believe the lipid they found is previously unknown to science.
E. huxleyi mediates the biological carbon pump through photosynthesis, calcifies like coral, and blooms widely in the Earth’s oceans. The phytoplankton die after about three days in what scientists call programmed cell death, or apoptosis.
Bidle, assistant professor of marine science at Rutgers’ Institute of Marine and Coastal Sciences, had been studying the interaction between the virus and the dying phytoplankton. He and Vardi had been using a particular virus to infect their E. Huxleyi in the lab, and they had previously found that the virus touched off the programmed cell death as part of its killing strategy. But they didn’t really know how, and they needed to test their results in nature.
After Vardi heard Van Mooy give a talk on marine microbes and lipids last year, he suggested the collaboration between WHOI and Rutgers.
Van Mooy collected samples of the phytoplankton at sea during a North Atlantic research cruise, analyzed them, and virus-infected samples that came from Bidle’s lab. He extracted and isolated the lipids from the virus and discovered that they were just like the ones in virally infected cells grown in the lab.
However, as Van Mooy discovered, they were of a different chemical structure. Van Mooy’s work enables scientists to tell the lipid in the virus from the one in the phytoplankton host. Combined with Vardi’s lab-based experiments, the research teams revealed the actual triggering mechanism for programmed cell death—a nearly complete lipid biosynethetic pathway encoded by the virus that was never described before in any other virus.
But there may be other, even farther-reaching implications. Both the virus and the newly found lipid deal their deadly blow by causing the upper-ocean plants to commit cellular suicide. As a major focus of their research at Rutgers, Bidle’s lab has found that programmed cell death is an important process in the fate of marine phytoplankton and in the demise of blooms in the oceans. Bidle’s group had previously found that successful infection of E. huxleyi induced, and actually required, the programmed cell death pathway.
These lipids can induce programmed cell death in many organisms, including animals and plants. They also enrich in plasma membrane, and they are the port of the cell, where pathogens get in and out of the cell. This is important in viral diseases.
The lipid may also help shed light on why cancer cells are unable to commit suicide. Cancer cells have found a way to turn off the programmed cell death pathway. Someday, the researchers say, it might suggest ways to correct that defect. Right now, the lipid is only known to be effective in algae, but in the future, the team is planning to test the effectiveness of their molecule on cancer cells.
Bidle and Vardi believe the discovery they’ve made with Van Mooy may help scientists find ways to turn that pathway on again.
Rutgers news: http://news.rutgers.edu/medrel