Knowing how these pathways of immunity work may one day help researchers breed plants that can better resist a variety of pathogens, said David Mackey, the study's lead author and an assistant professor of horticulture and crop science at Ohio State University .
He and his colleagues explain their findings in the current issue of the journal Cell.
The researchers infected Arabidopsis plants with a bacterial strain of Pseudomonas syringae, a bacterium that usually infects tomato crops. Both Arabidopsis, a plant of the mustard family, and P. syringae are models that researchers commonly use to conduct basic plant research.
One of the immune pathways that interested the researchers recognizes what they call pathogen-associated molecular patterns, or PAMPs. The PAMP pathway appears to be a plant's first line of defense against pathogenic attackers.
"The PAMP path induces a fairly weak immune response," Mackey said. "Even so, there is growing evidence that suggests these kinds of responses are extremely important in restricting the growth of many pathogens."
The other pathway uses disease-resistant proteins, or R-proteins, which can detect certain molecules, called effectors, that are secreted by pathogens. This pathway produces a stronger immune response than the PAMP pathway, Mackey said.
He and his colleagues found that the R-protein pathway steps in when PAMP is rendered useless by a pathogen.
Certain types of bacteria, including P. syringae, make a hypodermic needle-like structure that pierces the outermost membrane of a healthy plant or animal cell. The pathogen uses this conduit to send infectious effector proteins into the host cell.
While P. syringae injects about 40 different varieties of effector molecules into a plant cell, the researchers focused on the actions of two of these molecules – AvrRpt2 and AvrRpm1. Both target a protein key to Arabidopsis health.
The scientists found that both of these effector molecules effectively shut down the PAMP pathway. But the plant's R-proteins detect this, and come to the rescue.
"The R-proteins detect the insidious activity by which the pathogen's effectors block the PAMP pathway," Mackey said. "PAMP defense responses are probably often effective, but they may be blocked by the pathogen's effector proteins. If an R-protein recognizes a pathogen's presence, it usually induces a very strong immune response, in most cases stopping a would-be infection.
"This work further suggests that plants use an active, complex immune system to combat pathogens," he said. "They have complicated surveillance systems that detect various infection-causing molecules and trigger defensive responses."
A next step in this line of work is to look at other pathogen effector proteins and analyze their role in causing infections.
Mackey conducted the study with Ohio State colleagues Min Gab Kim, a graduate student in the department of plant cellular and molecular biology, and graduate student Luis da Cunha and post-doctoral fellow Aidan McFall, both in the department of horticulture and crop science; Youssef Belkhadir and Jeffrey Dangl, both with the department of biology at the University of North Carolina, Chapel Hill; and Sruti DebRoy, formerly of the U.S. Department of Energy Plant Research Laboratory at Michigan State University.
Funding for this work came from the National Science Foundation and the NSF's Arabidopsis Project; Ohio State's Ohio Agricultural and Research Development Center; and the U.S. Department of Energy.
Contact: David Mackey, 614-292-5879; Mackey.86@osu.edu
Written by Holly Wagner, 614-292-8310; Wagner.235@osu.edu
Journal
Cell