Ithaca, New York
October 4, 2007
Although plants lack humans' T
cells and other immune-function cells to signal and fight
infection, scientists have known for more than 100 years that
plants still somehow signal that they have been attacked in
order to trigger a plantwide resistance. Now, researchers at the
Boyce Thompson
Institute for Plant Research (BTI) on the Cornell campus
have identified the elusive signal in the process: methyl
salicylate, an aspirin-like compound that alerts a plant's
immune system to shift into high gear.
This phenomenon is called systemic acquired resistance and is
known to require movement of a signal from the site of infection
to uninfected parts of the plant.
The findings are published in the Oct. 5 issue of
Science.
"By finally identifying a signal that moves from an infection
site to activate defenses throughout the plant, as well as the
enzymes that regulate the level of this signal, we may be in a
position to alter the signal in a way that enhances a plant's
ability to defend itself," said BTI senior scientist Daniel F.
Klessig, an adjunct professor in plant pathology at Cornell, who
conducted the work with Sang-Wook Park and other BTI colleagues.
Their approach, using gene technology to enhance plant immunity,
could have wide consequences, boosting crop production and
reducing pesticide use.
Methyl salicylate is a modified form of salicylic acid (SA),
which has been used for centuries to relieve fever, pain and
inflammation, first through the use of willow bark and, since
1889, with aspirin, still the most widely used drug worldwide.
In the 1990s, Klessig's research group reported that SA and
nitric oxide are two critical defense-signaling molecules in
plants, as well as playing important roles in human health.
Then, in 2003 and 2005, the group reported in the Proceedings of
the National Academy of Sciences that an enzyme, salicylic
acid-binding protein 2 (SABP2), is required for systemic
acquired resistance and converts methyl salicylate (which is
biologically inactive as it fails to induce immune responses)
into SA, which is biologically active.
After plants are attacked by a pathogen, the researchers had
previously found, they produce SA at the infection site to
activate their defenses. Some of the SA is converted into methyl
salicylate, which can be converted back into SA by SABP2.
Using plants in which SABP2 function was either normal, turned
off or mutated in the infected leaves or the upper, uninfected
leaves, Klessig's group showed that SABP2 must be active in the
upper, uninfected leaves for systemic acquired resistance to
develop properly. By contrast, SABP2 must be inactivated in the
infected leaves by binding to SA.
"This inactivation allows methyl salicylate to build up,"
explained Klessig. "It then flows through the phloem (or
food-conducting "tubes") to the uninfected tissue, where SABP2
converts it back into active SA, which can now turn on the
plant's defenses."
Klessig said that it is unclear why plants send this hormone to
uninfected tissue in an inactive form, which then must be
activated by removal of the methyl group.
"This research also provides insight into how a hormone like SA
can actively regulate its own structure -- and thereby determine
its own activity -- by controlling the responsible enzyme,"
noted Park, the lead author of the paper.
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