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Plant and Cell Physiology Advance Access originally published online on January 13, 2006
Plant and Cell Physiology 2006 47(3):309-318; doi:10.1093/pcp/pcj001
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Loss of AtPDR8, a Plasma Membrane ABC Transporter of Arabidopsis thaliana, Causes Hypersensitive Cell Death Upon Pathogen Infection

Yoshihiro Kobae1, Tetsuro Sekino1, Hirofumi Yoshioka2, Tsuyoshi Nakagawa3, Enrico Martinoia4 and Masayoshi Maeshima1,*

1 Laboratory of Cell Dynamics, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601 Japan
2 Laboratory of Defense in Plant–Pathogen Interactions, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601 Japan
3 Department of Molecular and Functional Genomics, Shimane University, Matsue, 690-8504 Japan
4 Zürich-Basel Plant Science Center, University of Zürich, Institute of Plant Biology, Molecular Plant Physiology, Zollikerstrasse 107, CH-8008 Zürich, Switzerland

* Corresponding author: E-mail, maeshima{at}agr.nagoya-u.ac.jp; Fax, +81-52-789-4096.

Plants contain a large number of ATP-binding cassette (ABC) transporters belonging to different subclasses. AtPDR8 is the only member of the pleiotropic drug resistance (PDR) ABC transporter subclass in Arabidopsis that is constitutively highly expressed. In transgenic Arabidopsis plants harboring the AtPDR8 promoter fused to ß-glucuronidase (GUS), reporter expression was shown to be strong in the stomata and hydathode. In the stomata, transcripts of AtPDR8 were particularly frequent in the cells surrounding air spaces. Subcellular fractionation and immunochemical analysis showed that AtPDR8 was localized in the plasma membrane. When a knockout mutant of AtPDR8 (atpdr8) was infected with bacterial and oomycete pathogens, the plants exhibited chlorotic lesions and a hypersensitive response (HR)-like cell death. Cell death was detected in the atpdr8 mutants within 10 h of infection with the virulent bacterial pathogen, Pseudomonas syringae. As a result, the growth of P. syringae in the leaves of the atpdr8 mutant was reduced to 1% of that in the wild type. The defense response genes, PR-1, PR-2, PR-5, VPE{gamma}, AtrbohD and AtrbohF were highly expressed when the mutant plants were grown under non-sterile conditions. The expression of the AtPDR8 gene was enhanced by infection of virulent and avirulent bacterial pathogens. Our results indicate that AtPDR8 is a key factor controlling the extent of cell death in the defense response and suggest that AtPDR8 transports some substance(s) which is closely related to the response of plants to pathogens.

(Received November 26, 2005; Accepted December 27, 2005)
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