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Plant Physiol, June 2000, Vol. 123, pp. 487-496
Ozone Sensitivity in Hybrid Poplar Correlates with Insensitivity
to Both Salicylic Acid and Jasmonic Acid. The Role of Programmed Cell
Death in Lesion Formation1
Jennifer Riehl
Koch,
Robert A.
Creelman,2
Steven M.
Eshita,
Mirjana
Seskar,
John E.
Mullet, and
Keith R.
Davis*
Department of Molecular Genetics (J.R.K.) and Department of Plant
Biology and the Plant Biotechnology Center (K.R.D.), The Ohio State
University, Columbus, Ohio 43210-1002; Forestry Sciences Laboratory,
United States Department of Agriculture Northeastern Research Station,
Delaware, Ohio 43015-8640 (J.R.K., S.M.E.); Department of Biochemistry
and Biophysics Crop Biotechnology Center, Texas A&M University, College
Station, Texas 77843-0001 (R.A.C., J.E.M.); and Biotechnology Center
for Agriculture and the Environment, Rutgers University, New Brunswick,
New Jersey 08901-1190 (M.S.)
Our earlier studies demonstrated that the ozone-sensitive hybrid
poplar clone NE-388 displays an attenuated level of ozone-, wound-, and
phytopathogen-induced defense gene expression. To determine if this
reduced gene activation involves signal transduction pathways dependent
on salicylic acid (SA) and/or jasmonic acid (JA), we compared the
responses of NE-388 and an ozone-tolerant clone, NE-245, to these
signal molecules. JA levels increased in both clones in response to
ozone, but only minimal increases in SA levels were measured for either
clone. Treatment with SA and methyl jasmonate induced defense gene
expression only in NE-245, indicating that NE-388 is insensitive to
these signal molecules. DNA fragmentation, an indicator of programmed
cell death (PCD), was detected in NE-245 treated with either ozone or
an avirulent phytopathogen, but was not detected in NE-388. We conclude
that these clones undergo two distinct mechanisms of ozone-induced lesion formation. In NE-388, lesions appear to be due to toxic cell
death resulting from a limited ability to perceive and subsequently activate SA- and/or JA-mediated antioxidant defense responses. In
NE-245, SA-dependent PCD precedes lesion formation via a process related to the PCD pathway activated by phytopathogenic bacteria. These
results support the hypothesis that ozone triggers a hypersensitive response.
1
This work was supported in part by a cooperative
agreement with the Northeastern Research Station of the Forest Service,
by the U.S. Department of Agriculture (K.R.D.), by a National Science Foundation grant (no. MCB-9514034 to J.E.M.), and by a U.S. Department of Agriculture National Research Initiative Competitive Grants Program
grant (no. 95-37304-2440 to J.E.M.).
2
Present address: Mendel Biotechnology, 21375 Cabot Boulevard, Hayward, CA 94545.
*
Corresponding author; e-mail kdavis{at}paragen.com; fax
919- 544-8094.
© 2000 American Society of Plant Physiologists
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