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Senescence-Associated Gene Expression during Ozone-Induced Leaf Senescence in Arabidopsis1

Jennifer D. Miller, Richard N. Arteca, and Eva J. Pell*

Intercollege Graduate Program in Plant Physiology (J.D.M., R.N.A., E.J.P.), Department of Horticulture (R.N.A.), and Department of Plant Pathology and Environmental Resources Research Institute (E.J.P.), The Pennsylvania State University, University Park, Pennsylvania 16802

The expression patterns of senescence-related genes were determined during ozone (O3) exposure in Arabidopsis. Rosettes were treated with 0.15 µL L-1 O3 for 6 h d-1 for 14 d. O3-treated leaves began to yellow after 10 d of exposure, whereas yellowing was not apparent in control leaves until d 14. Transcript levels for eight of 12 senescence related genes characterized showed induction by O3. SAG13 (senescence-associated gene), SAG21, ERD1 (early responsive to dehydration), and BCB (blue copper-binding protein) were induced within 2 to 4 d of O3 treatment; SAG18, SAG20, and ACS6 (ACC synthase) were induced within 4 to 6 d; and CCH (copper chaperone) was induced within 6 to 8 d. In contrast, levels of photosynthetic gene transcripts, rbcS (small subunit of Rubisco) and cab (chlorophyll a/b-binding protein), declined after 6 d. Other markers of natural senescence, SAG12, SAG19, MT1 (metallothionein), and Atgsr2 (glutamine synthetase), did not show enhanced transcript accumulation. When SAG12 promoter-GUS (beta -glucuronidase) and SAG13 promoter-GUS transgenic plants were treated with O3, GUS activity was induced in SAG13-GUS plants after 2 d but was not detected in SAG12-GUS plants. SAG13 promoter-driven GUS activity was located throughout O3-treated leaves, whereas control leaves generally showed activity along the margins. The acceleration of leaf senescence induced by O3 is a regulated event involving many genes associated with natural senescence.


1   External funding for this research was provided by the Environmental Protection Agency (grant no. U915212-01-1) and by the U.S. Department of Agriculture (grant no. 93-38420-8742). This research was also supported in part by the Pennsylvania Agricultural Experiment Station and the Environmental Resources Research Institute. It is contribution no. 2064 from the Department of Plant Pathology, The Pennsylvania State University.
*   Corresponding author; e-mail ejp{at}psu.edu; fax 814-863-7217.

Plant Physiol. (1999) 120: 1015-1024
Copyright Clearance Center:   0032-0889/99/120//10
© 1999 American Society of Plant Physiologists




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