Ozone sensitivity in hybrid poplar correlates with insensitivity to both salicylic acid and jasmonic acid. The role of programmed cell death in lesion formation

Our earlier studies demonstrated that the ozone-sensitive hybrid poplar clo ne NE-388 displays an attenuated level of ozone-, wound-, and phytopathogen -induced defense gene expression. To determine if this reduced gene activat ion 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 w ere measured for either clone. Treatment with SA and methyl jasmonate induc ed defense gene expression only in NE-245, indicating that NE-388 is insens itive to these signal molecules. DNA fragmentation, an indicator of program med cell death (PCD), was detected in NE-245 treated with either ozone or a n avirulent phytopathogen, but was not detected in NE-388. We conclude that these clones undergo two distinct mechanisms of ozone-induced lesion forma tion. In NE-388, lesions appear to be due to toxic cell death resulting fro m a limited ability to perceive and subsequently activate SA- and/or JA-med iated antioxidant defense responses. Ln NE-245, SA-dependent PCD precedes l esion formation via a process related to the PCD pathway activated by phyto pathogenic bacteria. These results support the hypothesis that ozone trigge rs a hypersensitive response.