What if our textbooks aren't quite correct, and the plant cell wall isn't just the purely structural organ it's thought to be? That's the theory Shauna Somerville of Stanford's Carnegie Institution described yesterday (February 11) in her talk at the Keystone joint meeting on plant signaling and innate immunity in Keystone, Co.

Somerville studies powdery mildew, a fungal disease that infects as many as 9,000 different species of plants. The pathogen attacks by building a haustorium, an extension that breaches the plant's cell wall, enabling it to siphon off its host's nutrients. The haustorium is the key to the pathogen's success, she explained in her talk - the fungus itself has only enough nutrients to reach that stage of infection, and if it can't access those of the plant, it won't survive. But Somerville believes that the fungal bite out of the cell wall may also signal to the plant that it's under attack.

Using a mutant screen, her group identified three Arabidopsis mutants that were resistant to powdery mildew. One, called pmr4, turned out to be deficient in callose, a substance that forms plugs in the cell wall when the plant is infected or under attack; the Pmr4 gene coded for the enzyme that synthesizes callose. Logically, an absence of callose should make the plant more susceptible to infection, but Somerville was surprised to find that another effect of the mutation: the plants' salicylic acid signaling pathway, a plant defense mechanism, was on overdrive - accounting for their ability to fight off the fungal infection. Somehow, then, a mutation in the cell wall structure was causing changes in defense signaling.

In the question/answer session, someone mentioned another Arabidopsis mutant called cev1, which makes less cellulose than wild type plants and also has elevate levels of jasmonic acid, another major defense signal - another suggestion of a direct link between cell wall structure and defense signaling cascades, Somerville later explained to me.

The two other mutants Somerville described in her talk, pmr5 and pmr6, small and showed constrained cell expansion. Both have altered cell wall compositions due to a change in the composition of pectin, a structural molecule that creates crosslinking between other cell wall components, thereby influencing nutrient exchange between the host and pathogen. Preliminary experiments suggest that genes related to pathogen defense responses are constitutively upregulated in these mutants, suggesting again that structural mutations have direct effects on defense signaling.

Somerville believes that signaling via cell wall cues is a novel defense mechanism. In her mutants, she said, it's the genetic change in cell structure that produces signaling effects. But in a wild-type plant, such effects would be induced as part of a wound detection system. Her work harkens back to a plant chemist named Peter Albersheim, she said, who proposed a few decades ago that the cell wall's complex structure plays a role in signaling. So far, she said, her data doesn't yet prove the existence of a communication system between the cell wall and the plant's defense systems. But, she said, "It's time to revisit this idea."