Relocating immune receptors

Daniel Schwen / commons.wikimedia.org

The paper:

Q.H. Shen et al., "Nuclear activity of MLA immune receptors links isolate-specific and basal disease–resistance responses," Science, 315:1098–1103, 2007. (Cited in 76 papers)

The finding:

After staining the nuclei of barley cells, Paul Schulze-Lefert and his colleagues at the Max Planck Institute for Plant Breeding Research in Cologne discovered something unexpected—trace amounts of the cytoplasmic immune protein, mildew A receptor (MLA). They thought it was an artifact, but when they forced all of the MLA out of the nucleus by attaching a nuclear export signal to the protein, the plant was no longer able to stave off infection, indicating that MLA must be in the nucleus in order to function.

The surprise:

"Everyone in the field presumed that these proteins acted in the cytoplasm" rather than the nucleus, says Shulze-Lefert. He suspects that MLA may be "shuttling" between the cytoplasm and the nucleus to instigate cell suicide and protect cells from neighboring infections.

The mechanism:

Using fluorescence lifetime imaging to visualize protein-protein interactions, Shulze-Lefert's team showed that the receptor interacts directly with a genetic repressor in the nucleus to trigger an immune response.

The future:

"The field is hot on the trail of generalizing those findings," says Jeffery Dangl of the University of North Carolina at Chapel Hill. "There are 120 to 140 of these [receptors] in Arabidopsis," he says, "but there's no rule to say they have to act the same way."