Interaction-Dependent Gene Expression inMla-Specified Response to Barley Powdery Mildew[W]
Author:
Caldo Rico A.1, Nettleton Dan2, Wise Roger P.13
Affiliation:
1. Department of Plant Pathology and Center for Plant Responses to Environmental Stresses, Iowa State University, Ames, Iowa 50011-1020 2. Department of Statistics, Iowa State University, Ames, Iowa 50011-1210 3. Corn Insects and Crop Genetics Research, U.S. Department of Agriculture-Agricultural Research Service, Iowa State University, Ames, Iowa 50011-1020
Abstract
AbstractPlant recognition of pathogen-derived molecules influences attack and counterattack strategies that affect the outcome of host–microbe interactions. To ascertain the global framework of host gene expression during biotrophic pathogen invasion, we analyzed in parallel the mRNA abundance of 22,792 host genes throughout 36 (genotype × pathogen × time) interactions between barley (Hordeum vulgare) and Blumeria graminis f. sp hordei (Bgh), the causal agent of powdery mildew disease. A split-split-plot design was used to investigate near-isogenic barley lines with introgressed Mla6, Mla13, and Mla1 coiled-coil, nucleotide binding site, Leu-rich repeat resistance alleles challenged with Bgh isolates 5874 (AvrMla6 and AvrMla1) and K1 (AvrMla13 and AvrMla1). A linear mixed model analysis was employed to identify genes with significant differential expression (P value < 0.0001) in incompatible and compatible barley-Bgh interactions across six time points after pathogen challenge. Twenty-two host genes, of which five were of unknown function, exhibited highly similar patterns of upregulation among all incompatible and compatible interactions up to 16 h after inoculation (hai), coinciding with germination of Bgh conidiospores and formation of appressoria. By contrast, significant divergent expression was observed from 16 to 32 hai, during membrane-to-membrane contact between fungal haustoria and host epidermal cells, with notable suppression of most transcripts identified as differentially expressed in compatible interactions. These findings provide a link between the recognition of general and specific pathogen-associated molecules in gene-for-gene specified resistance and support the hypothesis that host-specific resistance evolved from the recognition and prevention of the pathogen's suppression of plant basal defense.
Publisher
Oxford University Press (OUP)
Subject
Cell Biology,Plant Science
Reference113 articles.
1. Abramovitch, R.B., Kim, Y.J., Chen, S., Dickman, M.B., and Martin, G.B. (2003). Pseudomonas type III effector AvrPtoB induces plant disease susceptibility by inhibition of host programmed cell death. EMBO J. 22 , 60–69. 2. Ahn, H.J., Yang, J.K., Lee, B.I., Yoon, H.J., Kim, H.W., and Suh, S.W. (2003). Crystallization and preliminary X-ray crystallographic studies of chorismate synthase from Helicobacter pylori. Acta. Crystallogr. D. Biol. Crystallogr. 59 , 569–571. 3. Axtell, M.J., and Staskawicz, B.J. (2003). Initiation of RPS2-specified disease resistance in Arabidopsis is coupled to the AvrRpt2-directed elimination of RIN4. Cell 112 , 369–377. 4. Azevedo, C., Sadanandom, A., Kitagawa, K., Freialdenhoven, A., Shirasu, K., and Schulze-Lefert, P. (2002). The RAR1 interactor SGT1, an essential component of R gene-triggered disease resistance. Science 295 , 2073–2076. 5. Bohlmann, J., Lins, T., Martin, W., and Eilert, U. (1996). Anthranilate synthase from Ruta graveolens. Duplicated AS alpha genes encode tryptophan-sensitive and tryptophan-insensitive isoenzymes specific to amino acid and alkaloid biosynthesis. Plant Physiol. 111 , 507–514.
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