Last night's session (February 12) on hormones networks at the joint Keystone meeting on plant signaling and immunity in Keystone, Co, began with Charlie Chaplin. Specifically, the audience was treated to a video clip of the scene in Modern Times where Chaplin, a worker on a factory assembly line, becomes curious about the gears that drive the machinery, and to the horror of other workers, dives onto the assembly line and down the chute to explore.

It was a clear metaphor for what's going on in the field. Over the past decade, as researchers first began identifying receptors of key plant signaling molecules such as auxins, gibberellins, and brassinosteroids, they've taken a fairly linear view of the pathways involved, the session's organizer, Jennifer Nemhauser of the University of Washington, explained. But increasingly, the level of complexity in these pathways, and the crosstalk between them, is becoming clear.

I caught up with Joanne Chory of the Salk Institute, one of the organizers of the hormones and signaling component of the meeting, who highlighted one of the key differences between plant and animal signaling. While mammalian signaling systems can be thought of as "top-down," plants are "bottom-up," because many of the molecules work in parallel, impacting the same processes. Take auxins, for example: The plant has two ways of synthesizing the main endogenous auxin, indole-3-acetic acid (IAA) from tryptophan, and neither can compensate for the other. "So that means there are multiple pools of auxins acting independently," she said. Unlike like G-protein coupled receptors in mammals, which are associated with specific signaling molecules, unraveling a system in which most players wear several hats poses a challenge. (Which may have been what prompted another speaker yesterday to start his talk with the assertion that "auxin signaling is a mess.")

Teasing out the complexity is going to require new approaches, Chory said. Identifying signaling molecules from mutant phenotypes has taken the field a long way, but many phenotypes are likely to be lethal, she said, so it's time to move beyond genetics, and towards better biochemistry and cell biology techniques to directly probe signaling interactions. "We really need to get hardcore about mechanisms."