|
PageContent
Inter-chromosomal transfer of immune response during barley-powdery mildew interactions R. WISE (1), P. Surana (2), D. Mistry (2), R. Xu (3), A. Chapman (2), G. Fuerst (1), J. Dickerson (2), D. Nettleton (2) (1) USDA-ARS / Iowa State University, U.S.A.; (2) Iowa State University, U.S.A.; (3) Google Inc., U.S.A.
Powdery mildews infect over 9,500 plant species, causing critical yield loss. Barley powdery mildew, caused by Blumeria graminis f. sp. hordei (Bgh), is an emerging model for the interactions among obligate biotrophic fungi and their cereal hosts. Host ML (mildew) immune receptors sense Bgh effectors, triggering defense networks comprising thousands of genes. Genome-wide transcriptome analysis of the barley Q21861 X SM89010 doubled haploid population identified significant clusters of trans eQTL (expression quantitative trait loci) hotspots on chromosomes 2HL and 1HS. Embedded within these clusters are the resistance loci, MlLa and Mla, which associate with the altered expression of 961 and 3,296 genes, respectively, corresponding to Bgh penetration and haustorial growth (q-value <= 1e-3). Moreover, of the 961 genes regulated by MlLa during penetration, control of 299 of these was transferred to Mla during haustorial development. Time-course pattern analysis of these transcripts discerned two opposing scenarios: The first represents host defense genes that are suppressed by pathogen effectors in compatible interactions, as opposed to corresponding incompatible interactions. In contrast, the second represents a situation where the pathogen continues to induce defense in compatible interactions, and may co-opt these host genes for its own purposes. Annotations uniquely assigned to the first pattern were associated with vesicle transport, secondary metabolism, and hormone signaling, whereas genes associated with the second pattern were annotated as abiotic stress, RNA synthesis, and RNA processing. We postulate that the functions of genes regulated by alternate chromosomal positions are repurposed as part of a conserved immune complex to respond to different pathogen attack scenarios.
Abstract Number:
P11-384 Session Type:
Poster
|
|
|