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A Small Cysteine-Rich Protein from the Asian Soybean Rust Fungus, Phakopsora pachyrhizi, Suppresses Plant Immunity

Mingsheng Qi, Tobias I. Link, Manuel Müller, Daniela Hirschburger, Ramesh N. Pudake, Kerry F. Pedley, Edward Braun, Ralf T. Voegele, Thomas J. Baum, Steven A. Whitham
PLoS Pathogens 2016 v.12 no.9 pp. -
Glycine max, Phakopsora pachyrhizi, active immunity, disease outbreaks, disease resistance, fungal proteins, genome, host plants, host-pathogen relationships, immune response, plant pathogenic fungi, soybean rust, soybeans, transcription factors, virulence
The Asian soybean rust fungus, Phakopsora pachyrhizi, is an obligate biotrophic pathogen causing severe soybean disease epidemics. Molecular mechanisms by which P. pachyrhizi and other rust fungi interact with their host plants are poorly understood. The genomes of all rust fungi encode many small, secreted cysteine-rich proteins (SSCRP). While these proteins are thought to function within the host, their roles are completely unknown. Here, we present the characterization of P. pachyrhizi effector candidate 23 (PpEC23), a SSCRP that we show to suppress plant immunity. Furthermore, we show that PpEC23 interacts with soybean transcription factor GmSPL12l and that soybean plants in which GmSPL12l is silenced have constitutively active immunity, thereby identifying GmSPL12l as a negative regulator of soybean defenses. Collectively, our data present evidence for a virulence function of a rust SSCRP and suggest that PpEC23 is able to suppress soybean immune responses and physically interact with soybean transcription factor GmSPL12l, a negative immune regulator.