Ithaca, New York
December 8, 2003
Scientists
have found the gene that sends a signal through plant immune
systems, saying, in effect: "Take two aspirin and call out the
troops -- we're under attack !"
Discovery
of the salicylic acid-binding protein 2 (SABP2) gene, by
scientists at Boyce Thompson
Institute for Plant Research (BTI) at
Cornell University, is
being called an important step toward new strategies to boost
plants' natural defenses against disease and for reducing the
need for agricultural pesticides.
Salicylic
acid, the chemical compound found naturally in most plants (as
well as in the most-used medication, aspirin), is a plant
hormone produced at elevated levels in response to attack by
microbial pathogens. According to a report on the Web today in
the Proceedings of the National Academy of Sciences (PNAS
Early Edition, week of Dec. 7, 2003) by BTI's Dhirendra Kumar
and Daniel F. Klessig, the aspirin-like hormone is perceived by
the SABP2 protein and a message is transmitted, via a
lipid-based signal, to activate the plant's defense arsenal.
Says
Klessig, "Now that we know a key signaling protein in plant
immune systems, we can work on ways to enhance the signal and
help plants fight disease without using potentially harmful
pesticides."
The PNAS
authors say SABP2 plays an important role in restricting
infections by inducing host cells at the site of infection to
undergo programmed cell death and sacrifice themselves for the
benefit of the rest of the plant.
SABP2 also
plays a critical role in activating the innate immune system in
other parts of the plant to guard against further attack or
spread by the same pathogen -- and even against unrelated
pathogens. (Innate immune systems, which mount an immediate
defense against infections, are found in all plants and animals.
But only vertebrates, including humans and other mammals, have
additional levels of defense -- the antibody-producing B cell
and T cell-mediated acquired immunity for a delayed response
that can take weeks to develop.) The Klessig laboratory
discovered the presence of the SABP2 protein in plants in 1997.
But it took five years to purify the protein, which occurs
naturally in "excruciatingly small amounts," then to clone the
gene that encodes it, and finally to assess the role of SABP2 in
disease resistance. The PNAS article tells how the researchers
proved that SABP2 is a key player in innate immunity by
silencing the SABP2 gene and watching the plant immune system
fail.
Although
the salicylic acid-signaling experiments were done with tobacco
plants -- because tobacco is a well-known plant species for
studying disease resistance -- similar salicylic acid-binding
proteins are found in other plant species, the BTI researchers
say, making their results applicable to other crop plants.
And the
finding might even help immunologists understand evolutionarily
related signaling pathways in vertebrates, including humans,
according to another BTI researcher and professor of plant
pathology at Cornell, Gregory B. Martin. In a 2001 research
article, he suggested that some molecular mechanisms involved in
innate immunity in mammalian and insect systems "are remarkably
similar to the molecular mechanisms underlying plant
disease-resistance responses." Innate immunity in all kinds of
living things, Martin and his co-authors added, "might be an
evolutionarily ancient system of host defense."
When
tobacco mosaic virus attacks a tobacco plant, the PNAS authors
report, the immediate visible effect of SABP2 is to enable
salicylic acid to induce the so-called hypersensitive resistance
response. "We see programmed cell death at the site of the
attack as plant cells sacrifice themselves for the overall
survival of the plant," Klessig explains. "We believe programmed
cell death helps restrict the infection to a small part of the
plant. Something similar happens in animal systems, when
virus-infected cells or cells with defective growth control that
could become cancerous undergo programmed cell death," he says,
noting that aspirin has been found to have a protective effect
against cancer.
Even as the
infection is being contained, the plant begins to signal other
parts of itself that it is undergoing attack. "This leads to
long-lasting, broad-spectrum systemic resistance to infections
against the initial attacking pathogen and also against other
viral, bacterial and fungal pathogens," Klessig says. "Systemic
acquired resistance can last throughout most of the life of an
annual plant."
Earlier
this year the Klessig research group announced (in the May 16,
2003, issue of the journal Cell) their discovery of a plant gene
for nitric oxide synthase, the enzyme that rapidly produces
nitric oxide (NO) after infection. This is one of the earliest
responses to pathogen attack.
"With
nitric oxide synthase and now with SABP2, as well as other
defense-signaling pathway components that have already or are
sure to be discovered, we are beginning to see some effective
and sustainable alternatives to pesticides," Klessig says,
suggesting two possible strategies: Genetic manipulation could
enhance a crop plant's ability to make more of a scarce
defense-signaling compound or a limiting receptor needed to
transmit this signaling compound. Alternatively, crops could be
treated with a functional mimic of the signaling compound itself
when plant disease is anticipated.
"Either
way, we are utilizing and enhancing a plant's own natural
defenses," Klessig says. "That should be a better way, both
because it will be much more difficult for pathogenic organisms
to develop resistance and because we can avoid contaminating the
environment."
He adds
that an attack by a plant pathogen "marks the start of a war. If
the plant can recognize the pathogen and activate its defense
arsenal in time, the plant usually wins. But if the pathogen
circumvents detection or the defenses themselves, the plant is
in trouble. The more we learn about plant immune systems, the
better are the chances we can help important crop plants win
their war -- without the collateral damage from chemical
pesticides."
Klessig is
president of BTI, an independent, not-for-profit organization
located on the Cornell campus, and an adjunct professor of plant
pathology; Kumar is a
BTI research associate. The salicylic acid-binding protein
research was supported by the National Science Foundation and by
a plants and human health grant from the Triad Foundation.
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