<i>Blufensin1</i>Negatively Impacts Basal Defense in Response to Barley Powdery Mildew

Oxford University Press (OUP) - Tập 149 Số 1 - Trang 271-285 - 2009
Yan Meng1, Matthew Moscou1, Roger P. Wise1
1Department of Plant Pathology and Center for Plant Responses to Environmental Stresses, Iowa State University, Ames, Iowa 50011–1020 (Y.M., M.J.M., R.P.W.); Bioinformatics and Computational Biology Graduate Program, Iowa State University, Ames, Iowa 50011–1020 (M.J.M., R.P.W.); and Corn Insects and Crop Genetics Research, U.S. Department of Agriculture-Agricultural Research Service, Iowa State Un

Tóm tắt

AbstractPlants have evolved complex regulatory mechanisms to control the defense response against microbial attack. Both temporal and spatial gene expression are tightly regulated in response to pathogen ingress, modulating both positive and negative control of defense. BLUFENSIN1 (BLN1), a small peptide belonging to a novel family of proteins in barley (Hordeum vulgare), is highly induced by attack from the obligate biotrophic fungus Blumeria graminis f. sp. hordei (Bgh), casual agent of powdery mildew disease. Computational interrogation of the Bln1 gene family determined that members reside solely in the BEP clade of the Poaceae family, specifically, barley, rice (Oryza sativa), and wheat (Triticum aestivum). Barley stripe mosaic virus-induced gene silencing of Bln1 enhanced plant resistance in compatible interactions, regardless of the presence or absence of functional Mla coiled-coil, nucleotide-binding site, Leu-rich repeat alleles, indicating that BLN1 can function in an R-gene-independent manner. Likewise, transient overexpression of Bln1 significantly increased accessibility toward virulent Bgh. Moreover, silencing in plants harboring the Mlo susceptibility factor decreased accessibility to Bgh, suggesting that BLN1 functions in parallel with or upstream of MLO to modulate penetration resistance. Collectively, these data suggest that the grass-specific Bln1 negatively impacts basal defense against Bgh.

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Oxford University Press (OUP)

Tập 149 Số 1

271-285

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