Comparative transcriptome profiling of two maize near-isogenic lines differing in the allelic state for bacterial brown spot disease resistance
2015
WU Xiao-jun, Xu Li, ZHAO Pan-feng, LI Na, WU Lei, HE Yan, WANG Shou-cai (State Key Laboratory for Agrobiotechnology/Beijing Key Laboratory of Crop Genetic Improvement/Key Laboratory of Crop Heterosis Research Utilization, Department of Plant Genetics Breeding, China Agricultural University, Beijing 100193, P.R.China)
The bacterial brown spot disease (BBS), caused primarily by Pseudomonas syringae pv. syringae van Hall (Pss), reduces plant vigor, yield and quality in maize. To reveal the nature of the defense mechanisms and identify genes involved in the effective host resistance, the dynamic changes of defense transcriptome triggered by the infection of Pss were investigated and compared between two maize near-isogenic lines (NILs). We found that Pss infection resulted in a sophisticated transcriptional reprogramming of several biological processes and the resistant NIL employed much faster defense responses than the susceptible NIL. Numerous genes encoding essential components of plant basal resistance would be able to be activated in the susceptible NIL, such as PEN1, PEN2, PEN3, and EDR1, however, in a basic manner, such resistance might not be sufficient for suppressing Pss pathogenesis. In addition, the expressions of a large number of PTI-, ETI-, PR-, and WRKY-related genes were pronouncedly activated in the resistant NIL, suggesting that maize employ a multitude of defense pathways to defend Pss infection. Six R-gene homologs were identified to have significantly higher expression levels in the resistant NIL at early time point, indicating that a robust surveillance system (gene-to-gene model) might operate in maize during Pss attacks, and these homolog genes are likely to be potential candidate resistance genes involved in BBS disease resistance. Furthermore, a holistic group of novel pathogen-responsive genes were defined, providing the repertoire of candidate genes for further functional characterization and identification of their regulation patterns during pathogen infection.
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