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Entry URI http://metadb.riken.jp/db/SciNetS_ria224i/cria224u4ria224u16415066i
Entry name Kobae Yoshihiro et al. 2006 Mar. Plant Cell Physiol. 47(3):309-18.
Title Loss of AtPDR8, a plasma membrane ABC transporter of Arabidopsis thaliana, causes hypersensitive cell death upon pathogen infection.
Authors Kobae Yoshihiro|Maeshima Masayoshi|Martinoia Enrico|Nakagawa Tsuyoshi|Sekino Tetsuro|Yoshioka Hirofumi
Abstract 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 beta-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, VPEgamma, 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.
Pubmed ID 16415066
Journal Plant & cell physiology
Volume 47
Issue 3
Pages 309-18
Publication date 2006 Mar
Num of phenotype gene 0