“In science, we often focus on a single ‘wild type’ organism, but even a single species of bacteria has as much variation as the instruments in a symphony. The French Horn produces a lovely sound, but if all you do is focus on French Horn, you’ll never know the joys of a symphony.” This is how Prof Darrell Desveaux of Cell & Systems Biology explains his approach to studying virulent bacteria.

Desveaux and his colleague Prof David Guttman study plant infection by the Pseudomonas syringae bacteria. Their “systems-level” approach takes into account the natural diversity of this species. In a new study published in Nature Microbiology, they find that distinct bacteria living in a community are collectively able to provoke disease without any single bacterium being the cause.

Graduate student Tatiana Ruiz-Bedoya conducted these experiments in the Desveaux and Guttman labs. “I find it fascinating that P syringae is found wherever there is water, including in clouds and snow. The versatility of P syringae to survive in each of these ecological niches makes it a species complex with different evolutionary pressures in each niche.”

The most consequential niche to humans is within plant leaves, which can be infected by P. syringae to extract extra resources that help the bacteria grow. “The community of P syringae researchers is a huge benefit for us,” asserts Guttman, “The genomics, ecology, and pathology are well-established, and the resources and tools we have developed make the system easy to manipulate. The insights we gained in this study would not be currently possible with any other plant or animal pathogen..”

Infection carries risk for the bacteria since they must evade the immune system of the plant host. P. syringae employs a diverse array of “effector” proteins to support bacterial growth (virulence) by suppressing the plant immune system. This new research assesses the ability of effectors from separate individuals to work in concert in causing virulence in the plant Arabidopsis.

The commonly used Pst strain DC3000 has 36 effectors. Ruiz-Bedoya started with a strain that is non-virulent due to its lack of effectors. She created a ‘metaclone’ with one effector per bacteria in a culture that contained all 36 effectors. Each individual strain of bacteria in the metaclone is non-virulent, but she hypothesized that effector functions within the community of bacteria would drive the emergence of virulence in the invading population.

When Ruiz-Bedoya sprayed her metaclone on Arabidopsis leaves, the effector metaclone was indeed virulent, demonstrating the cooperative benefit of this approach to evading the immune response for the bacterial community. She then tested the effect on the community of adding a single strain that provoked an immune response. She found that growth of all bacteria was suppressed. Effectors can thus act as against the community when they trigger an immune response.

Desveaux is excited by how this revelation changes our view of virulence. “You can have a single pathogen that is a one-man band of virulence, but we’ve shown that virulence can come from a symphony of individually ineffective strains that together cause virulence and evade immune detection.”

The full details are available at “Cooperative virulence via the collective action of secreted pathogen effectors