First published online April 25, 2002; 10.1104/pp.010815
Plant Physiol, June 2002, Vol. 129, pp. 551-564
Signals Involved in Arabidopsis Resistance to
Trichoplusia ni Caterpillars Induced by Virulent and
Avirulent Strains of the Phytopathogen Pseudomonas
syringae1
Jianping
Cui,
Georg
Jander,2
Lisa R.
Racki,
Paul D.
Kim,3
Naomi E.
Pierce, and
Frederick M.
Ausubel*
Department of Organismic and Evolutionary Biology, Harvard
University, Cambridge, Massachusetts 02138 (J.C., L.R.R., P.D.K.,
N.E.P.); Department of Genetics, Harvard Medical School, Boston,
Massachusetts 02115 (G.J., F.M.A.); and Department of Molecular
Biology, Massachusetts General Hospital, Boston, Massachusetts 02114 (G.J., F.M.A.)
Plants have evolved different but interconnected strategies
to defend themselves against herbivorous insects and microbial pathogens. We used an Arabidopsis/Pseudomonas syringae
pathosystem to investigate the impact of pathogen-induced defense
responses on cabbage looper (Trichoplusia ni) larval
feeding. Arabidopsis mutants [npr1,
pad4, eds5, and
sid2(eds16)] or transgenic plants (nahG)
that are more susceptible to microbial pathogens and are compromised in
salicylic acid (SA)-dependent defense responses exhibited reduced
levels of feeding by T. ni compared with wild-type plants.
Consistent with these results, Arabidopsis mutants that are more
resistant to microbial pathogens and have elevated levels of SA
(cpr1 and cpr6) exhibited enhanced levels
of T. ni feeding. These experiments suggested an inverse
relationship between an active SA defense pathway and insect feeding.
In contrast to these results, there was increased resistance to
T. ni in wild-type Arabidopsis ecotype Columbia plants that
were infected with P. syringae pv.
maculicola strain ES4326 (Psm ES4326)
expressing the avirulence genes avrRpt2 or
avrB, which elicit a hypersensitive response, high
levels of SA accumulation, and systemic acquired resistance to
bacterial infection. Similar results were obtained with other ecotypes,
including Landsberg erecta, Cape Verdi Islands, and
Shakdara. When infected with Psm
ES4326(avrRpt2) or Psm
ES4326(avrB), nahG transgenic and
npr1 mutant plants (which are more susceptible to
virulent and avirulent P. syringae strains) failed to
show the increased insect resistance exhibited by wild-type plants. It
was surprising that wild-type plants, as well as nahG
and npr1 plants, infected with Psm ES4326
not expressing avrRpt2 or avrB, which
elicits disease, became more susceptible to T. ni. Our
results suggest two potentially novel systemic signaling pathways: a
systemic response elicited by HR that leads to enhanced T. ni resistance and overrides the SA-mediated increase in T. ni susceptibility, and a SA-independent systemic response induced
by virulent pathogens that leads to enhanced susceptibility to T. ni.
1
This work was supported by the Department of
Organismic and Evolutionary Biology (Harvard University Graduate
Student Grant to J.C.) and by the National Institutes of Health (grant
no. GM48707 to F.M.A.).
2
Present address: 45 Sidney Street, Cereon
Genomics, Cambridge, MA 02139.
3
Present address: 630 West 168th Street, College of
Physicians and Surgeons, Columbia University, New York, NY 10032.
*
Corresponding author; e-mail ausubel{at}molbio.mgh.harvard.edu;
fax 617-726-5949.
© 2002 American Society of Plant Physiologists
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