Stage-specific suppression of basal defense discriminates barley plants containing fast- and delayed-acting Mla powdery mildew resistance alleles

被引:64
作者
Caldo, Rico A.
Nettleton, Dan
Peng, Jiqing
Wise, Roger P. [1 ]
机构
[1] Iowa State Univ, Dept Plant Pathol, USDA, ARS,Corn Insects & Crop Genet Unit, Ames, IA 50011 USA
[2] Iowa State Univ, Ctr Plant Responses Environm Stresses, USDA, ARS,Corn Insects & Crop Genet Unit, Ames, IA 50011 USA
[3] Iowa State Univ, Dept Stat, USDA, ARS,Corn Insects & Crop Genet Unit, Ames, IA 50011 USA
[4] Iowa State Univ, GeneChip Facil,Off Biotechnol, USDA, ARS,Corn Insects & Crop Genet Unit, Ames, IA 50011 USA
关键词
innate immunity; pathogen-associated molecular patterns; timing of resistance response;
D O I
10.1094/MPMI-19-0939
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nonspecific recognition of pathogen-derived general elicitors triggers the first line of plant basal defense, which in turn, preconditions the host towards resistance or susceptibility. To elucidate how basal defense responses influence the onset of Mla (mildew resistance locus a)-specified resistance, we performed a meta-analysis of GeneChip mRNA expression for 155 basal defense-related genes of barley (Hordeum vulgare) challenged with Blumeria graminis f. sp. hordei, the causal agent of powdery mildew disease. In plants containing the fast-acting Mla1, Mla6, or Mla13 alleles, transcripts hyper-accumulated from 0 to 16 h after inoculation (hai) in both compatible and incompatible interactions. Suppression of basal defense-related transcripts was observed after 16 hai only in compatible interactions, whereas these transcripts were sustained or increased in incompatible interactions. By contrast, in plants containing wild-type and mutants of the delayed-acting Mla12 allele, an early hyper-induction of transcripts from 0 to 8 hai was observed, but the expression of many of these genes is markedly suppressed from 8 to 16 hai. These results suggest that the inhibition of basal defense facilitates the development of haustoria by the pathogen, consequently delaying the onset of host resistance responses. Thus, we hypothesize that the regulation of basal defense influences host-cell accessibility to the fungal pathogen and drives allelic diversification of gene-specific resistance phenotypes.
引用
收藏
页码:939 / 947
页数:9
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