Boron deficiency results in induction of pathogenesis-related proteins from the PR-10 family during the legume-rhizobia interaction

被引:22
|
作者
Reguera, Maria [1 ]
Bonilla, Ildefonso [1 ]
Bolanos, Luis [1 ]
机构
[1] Univ Autonoma Madrid, Fac Ciencias, Dept Biol, E-28049 Madrid, Spain
关键词
ABR17; Boron; Legume-rhizobia interaction; Pathogenesis-related proteins; Symbiosis; PEA ROOT-NODULES; PISUM-SATIVUM-L; APHANOMYCES-EUTEICHES; RESPONSIVE PROTEINS; PLANT DEFENSE; INFECTION; EXPRESSION; SYMBIOSIS; RIBONUCLEASE; GENES;
D O I
10.1016/j.jplph.2009.11.017
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Boron (B) deficiency has a strong effect on molecular and cellular plant-bacteria interactions during the development of the legume-rhizobia symbiosis, leading to reduced infection and early necrosis of nodules, resembling a pathogenic-like rather than a symbiotic interaction. Therefore, induction of pathogenesis-related (PRs) proteins was investigated here in legume root nodules. Following two-dimensional electrophoresis and MALDI-TOF spectrometry analysis of proteins extracted from Pisum sativum B-sufficient (+B) or B-deficient (-B) root nodules, two proteins from the family PR10, ABR17 and PR10.1, were identified as highly induced in -B nodules. Analysis of gene expression and the use of anti-ABR17 confirmed that induction occurred in B-deficient young nodules and increased during nodule development. ABR17 was also induced in -B nodules of Phaseolus vulgaris. Boron deficiency did not significantly increase the expression of these PR10 in uninfected plant tissues. Moreover, independent of B, induction was detected in senescent tissues, although at a level weaker than in B nodules. The immunochemical study of ABR17 antigen distribution showed that it was localized in all tissues of poorly invaded B-deficient nodules and accumulated around bacteria, which showed advanced degradation. These results suggest that, under B deficiency, the rhizobia-legume dialogue fails and the bacterium is recognized as a pathogen by the plant, which reacts to prevent infection by inducing at least these two identified PR10 proteins. (C) 2010 Elsevier GmbH. All rights reserved.
引用
收藏
页码:625 / 632
页数:8
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