Location: Corn Insects and Crop Genetics Research
Title: Flor revisited (again): eQTL and mutational analysis of NB-LRR mediated immunity to powdery mildew in barley Authors
|Surana, Priyanka -|
|Xu, Ruo -|
|Mistry, Divya -|
|Dickerson, Julie -|
|Nettleton, Dan -|
Submitted to: Journal of Integrative Agriculture
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 30, 2012
Publication Date: February 1, 2014
Citation: Wise, R.P., Surana, P., Fuerst, G.S., Xu, R., Mistry, D., Dickerson, J., Nettleton, D. 2014. Flor revisited (again): eQTL and mutational analysis of NB-LRR mediated immunity to powdery mildew in barley. Journal of Integrative Agriculture. 13(2):237-243. Interpretive Summary: ARS researchers identify core set of genes that defend against powdery mildew attack. The barley powdery mildew pathogen is a devastating foliar pathogen causing losses in grain yield as well as grain quality. Barley has traditionally been considered a model for plant genetic research, closely related to the most widely grown crop, hexaploid wheat. Barley genomic resources have increased rapidly in the last several years, enabling new research to be performed that was previously not possible, including new approaches to broaden the germplasm base, facilitate new breeding strategies and accelerate rates of genetic gain. In this manuscript, we combine several bioinformatic approaches to identify core sets of genes that are activated upon infection by the barley powdery mildew pathogen, facilitating the ongoing search for the molecular mechanisms underlying plant immunity. Impact: Because common themes govern all plant-pathogen interactions, this finding provides new knowledge of broad significance to plant scientists, and to growers who utilize disease resistance to protect their crops.
Technical Abstract: Genes encoding early signaling events in pathogen defense often are identified only by their phenotype. Such genes involved in barley-powdery mildew interactions include Mla, specifying race-specific resistance; Rar1 (Required for Mla12-specified resistance1), and Rom1 (Restoration of Mla-specified resistance1). The HSP90-SGT1-RAR1 complex appears to function as chaperone in MLA-specified resistance, however, much remains to be discovered regarding the precise signaling underlying plant immunity. Genetic analyses of fast-neutron mutants derived from CI 16151 (Mla6) uncovered a novel locus, designated Rar3 (Required for Mla6-specified resistance3). Rar3 segregates independent of Mla6 and Rar1, and rar3 mutants are susceptible to Blumeria graminis f. sp. hordei (Bgh) isolate 5874 (AVRa6), whereas, wild-type progenitor plants are resistant. Comparative expression analyses of the rar3 mutant vs. its wild-type progenitor were conducted via Barley1 GeneChip and GAIIx paired-end RNA-Seq. Whereas Rar1 affects transcription of relatively few genes; Rar3 appears to influence thousands, notably in genes controlling ATP binding, catalytic activity, transcription, and phosphorylation; possibly membrane bound or in the nucleus. eQTL analysis of a segregating doubled haploid population identified over two-thousand genes as being regulated by Mla (FDR<0.001%), a subset of which are significant in Rar3 interactions. The intersection of datasets derived from mla-loss-of-function mutants, Mla-associated eQTL, and rar3-mediated transcriptome reprogramming are narrowing the focus on essential genes required for Mla-specified immunity.