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Alterations by a defect in a rice G protein α subunit in probenazole and pathogen‐induced responses

Alterations by a defect in a rice G protein α subunit in probenazole and pathogen‐induced responses ABSTRACT The rice dwarf1 (d1) mutant, which is deficient in an α subunit (Gα) of heterotrimeric G protein, was used to obtain specific evidence on the functions of Gα protein in defence signalling in rice. Using proteome analysis, a probenazole‐inducible protein (PBZ1) was detected in the cytosolic fraction of leaf blade of the wild type, but not the d1 mutant. After treatment with probenazol, PBZ1 reached maximal levels at 72 h in the wild type but 96 h in the d1 mutant. The induction of PBZ1 by probenazole treatment was inhibited by protein kinase inhibitors. A 48‐kDa putative mitogen‐activated protein kinase (MAPK) and a 55‐kDa putative Ca2+‐dependent protein kinase (CDPK) showed lower activities in the cytosolic fraction of the d1 mutant than that of the wild type. The activities of these protein kinases were enhanced at 24 h in the wild type and 48 h in the d1 mutant after probenazole treatment. Although the d1 mutant responded to the rice blast fungus similarly to the wild type, the d1 mutant developed rice blight symptoms earlier than the wild type when infected with Xoo. In addition, the blight symptoms were more severe on the mutant than on the wild type, and wilting was frequently observed in the d1 mutant. Furthermore, induction by the bacterial infection of the 48‐kDa putative MAPK and PBZ1 was delayed by 2 and 4 d, respectively, in the d1 mutant compared with the wild type. These results indicate that the Gα protein plays a role in the induction of PBZ1 and protein kinases by probenazole and Xoo, and suggest that the 48‐kDa putative MAPK may be involved in a signalling pathway for resistance to bacterial infection. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Cell & Environment Wiley

Alterations by a defect in a rice G protein α subunit in probenazole and pathogen‐induced responses

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References (41)

Publisher
Wiley
Copyright
Copyright © 2004 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0140-7791
eISSN
1365-3040
DOI
10.1111/j.1365-3040.2004.01202.x
Publisher site
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Abstract

ABSTRACT The rice dwarf1 (d1) mutant, which is deficient in an α subunit (Gα) of heterotrimeric G protein, was used to obtain specific evidence on the functions of Gα protein in defence signalling in rice. Using proteome analysis, a probenazole‐inducible protein (PBZ1) was detected in the cytosolic fraction of leaf blade of the wild type, but not the d1 mutant. After treatment with probenazol, PBZ1 reached maximal levels at 72 h in the wild type but 96 h in the d1 mutant. The induction of PBZ1 by probenazole treatment was inhibited by protein kinase inhibitors. A 48‐kDa putative mitogen‐activated protein kinase (MAPK) and a 55‐kDa putative Ca2+‐dependent protein kinase (CDPK) showed lower activities in the cytosolic fraction of the d1 mutant than that of the wild type. The activities of these protein kinases were enhanced at 24 h in the wild type and 48 h in the d1 mutant after probenazole treatment. Although the d1 mutant responded to the rice blast fungus similarly to the wild type, the d1 mutant developed rice blight symptoms earlier than the wild type when infected with Xoo. In addition, the blight symptoms were more severe on the mutant than on the wild type, and wilting was frequently observed in the d1 mutant. Furthermore, induction by the bacterial infection of the 48‐kDa putative MAPK and PBZ1 was delayed by 2 and 4 d, respectively, in the d1 mutant compared with the wild type. These results indicate that the Gα protein plays a role in the induction of PBZ1 and protein kinases by probenazole and Xoo, and suggest that the 48‐kDa putative MAPK may be involved in a signalling pathway for resistance to bacterial infection.

Journal

Plant Cell & Environment – Wiley

Published: Jul 1, 2004

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