Functional analysis of endo-1,4-ß-glucanases in response to Botrytis cinerea and Pseudomonas syringae reveals their involvement in plant-pathogen interactions.
Functional analysis of endo-1,4-ß-glucanases in response to Botrytis cinerea and Pseudomonas syringae reveals their involvement in plant-pathogen interactions.
复制标题
对灰霉病菌和丁香假单胞菌反应的内切 1,4-α-葡聚糖酶的功能分析揭示了它们参与植物-病原体相互作用。
DOI:
10.1111/j.1438-8677.2012.00701.x
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发表时间:
2013
期刊:
影响因子:
--
通讯作者:
Finiti I
中科院分区:
文献类型:
--
作者:
Finiti I
Plant cell wall modification is a critical component in stress responses. Endo‐1,4‐β‐glucanases (EGs) take part in cell wall editing processes,e.g. elongation, ripening and abscission. Here we studied the infection response ofSolanum lycopersicumandArabidopsis thalianawith impaired EGs. TransgenicTomCel1andTomCel2tomato antisense plants challenged withPseudomonas syringaeshowed higher susceptibility, callose priming and increased jasmonic acid pathway marker gene expression. These two EGs could be resistance factors and may act as negative regulators of callose deposition, probably by interfering with the defence‐signalling network. A study of a set ofArabidopsisEG T‐DNA insertion mutants challenged withP. syringaeandBotrytis cinerearevealed that the lack of other EGs interferes with infection phenotype, callose deposition, expression of signalling pathway marker genes and hormonal balance. We conclude that a lack of EGs could alter plant response to pathogens by modifying the properties of the cell wall and/or interfering with signalling pathways, contributing to generate the appropriate signalling outcomes. Analysis of microarray data demonstrates that EGs are differentially expressed upon many different plant–pathogen challenges, hormone treatments and many abiotic stresses. We found someArabidopsisEG mutants with increased tolerance to osmotic and salt stress. Our results show that impairing EGs can alter plant–pathogen interactions and may contribute to appropriate signalling outcomes in many different biotic and abiotic plant stress responses.