By Susan Lang
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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