Phytoplankton – single-cell micro algae – play a hugely important role in photosynthesis, the process by which plant life absorbs carbon dioxide to live. In fact, half of all photosynthetic activity takes place at sea. “Carbon is stored in blooms of algae, which can spread for thousands of kilometres,” explains Virocellsphere project coordinator Assaf Vardi. “A drop of this seawater would contain thousands of these single cells.” These blooms are typically infected by giant viruses and die within a matter of a week, releasing massive amounts of organic carbon, sulphur and other molecules. This process is a major component of the marine food chain, and thus critical to sustaining life. “Current scientific approaches to understand this process tend to focus simply on quantifying viral abundance and diversity,” says Vardi. “They don’t fully capture viral infection in action.”
Vardi, a professor in the Department of Plant and Environmental Sciences at the Weizmann Institute of Science in Israel, wanted to take a closer look at the actual host-virus interactions. His goal was to track not only what happens at the single-cell level – when a virus invades a single cell – but what happens in terms of host-virus interactions at the scale of phytoplankton blooms. “The members of my lab and I are marine ecologists at heart,” he adds. “But in practice, what we do is study cell biology. I wanted to marry these two disciplines.” To achieve this, Vardi developed ways to quantify and target specific infected cells. This enabled his lab to then examine what was actually going on at the intracellular level. Vardi next wanted to scale up his study, to see whether infected cells were releasing signalling molecules to defend or propagate the viral attack. For this, he applied single-cell techniques developed in the lab coupled with chemical analyses, to map the metabolites – small molecules – that are released during infection.
Message in a bottle
“We looked for the specific giant virus that was killing the bloom of our model alga species,” he says. “What Flora Vincent, a postdoc researcher in the Vardi lab, and I found was that only about a third of the algae population was infected. So why does the entire phytoplankton bloom collapse in a synchronised manner?” Vardi and another colleague, Daniella Schatz, discovered that algal cells infected by these viruses were releasing vesicles, or ‘messages in a bottle’, containing small RNA molecules that can prime uninfected cells for a viral invasion. This could help to explain why phytoplankton bloom crashes appear to be synchronised. “At first we thought this was a defence mechanism,” he notes. “Only by looking inside the cells could we see what was actually going on.” This finding underlines the success of the Virocellsphere project in advancing the study of viral infection. At the most fundamental level, Vardi and his team have shown that it is possible to track specific viruses in the field, through their single-cell and chemical approaches. Importantly, these tools could help scientists to explore in greater depth the impact of viruses on the marine environment, shaping its ecology, evolution and the cycling of major nutrients such as carbon and sulfur.
Virocellsphere, algae, bloom, virus, antiviral, infection, evolution, phytoplankton