Due to soil changes, high density planting, and the use of straw-returning methods, wheat common root rot (spot blotch), Fusarium crown rot (FCR), and sharp eyespot (sheath blight) have become severe threats to global wheat production. Only a few wheat genotypes show moderate resistance to these root and crown rot fungal diseases, and the genetic determinants of wheat resistance to these devastating diseases are poorly understood. This review summarizes recent results of genetic studies of wheat resistance to common root rot, Fusarium crown rot, and sharp eyespot. Wheat germplasm with relatively higher resistance are highlighted and genetic loci controlling the resistance to each disease are summarized.
NPR1 is a key regulator of systemic acquired resistance (SAR) in plant species. In our previous study, we identified a conserved fungal effector PNPi from Puccinia striiformis f. sp. tritici (Pst) that can suppress acquired resistance in local leaf by directly targeting the wheat NPR1 protein. In this investigation, we identified and validated a novel protein interaction between PNPi and wheat pathogenesis-related TaPR1a in the apoplastic space. TaPR1a-overexpressing wheat lines exhibited enhanced resistance to both Pst and Puccinia triticina (Pt). We further determined that exogenous expression of PNPi RNA in transgenic wheat lines reduced the degree of acquired resistance to Magnaporthe oryzae isolate P131 in the region adjacent to Pseudomonas syringae pv. tomato DC3000 infection area. Additionally, when PNPi was overexpressed, the expression levels of two plant defense responsive genes were suppressed upon P. syringae DC3000 infection in the local infiltration region. These findings established the mechanism of a single rust effector that can suppress multiple defense responses in wheat plants by targeting different components.
Plant apoplast serves as the frontier battlefield of plant defense in response to different types of pathogens. Many pathogenesis-related (PR) proteins are accumulated in apoplastic space during the onset of plant–pathogen interaction, where they act to suppress pathogen infection. In this study, we found the expression of Triticum aestivum lipid transfer protein 3 (TaLTP3) gene was unregulated during incompatible interaction mediated by leaf rust resistance genes Lr39/41 at the early infection stage. Stable transgenic wheat lines overexpressing TaLTP3 exhibited enhanced resistance to leaf rust pathogen Puccinia triticina. Transcriptome analysis revealed that overexpression of TaLTP3 specifically activated the transcription of pathogenesis-related protein 1a (TaPR1a) and multiple plant hormone pathways, including salicylic acid (SA), jasmonic acid (JA), and auxin, in response to the infection of the model bacterial pathogen Pseudomonas syringae pv. tomato DC3000. Further investigation indicated that TaLTP3 physically associated with wheat TaPR1a protein in the apoplast. Transgenic wheat lines overexpressing TaLTP3 and TaPR1a showed higher accumulations of reactive oxygen species (ROS) during plant defense responses. All these findings suggested that TaLTP3 is involved in wheat resistance against leaf rust pathogen infection and forming a TaLTP3-TaPR1a complex in apoplast against this pathogen, which provides new insights into the functional roles of PR proteins.
Due to the field soil changes, high density planting, and straw-returning methods, wheat common root rot (spot blotch) and Fusarium crown rot (FCR) have become severe threatens to global wheat productions. Only a few wheat genotypes show moderate resistance to these root and crown rot fungal diseases, and the genetic determinants of wheat resistance to these two devastating diseases have been poorly understood. This review summarizes the recent progress of genetic studies on wheat resistance to common root rot and Fusarium crown rot. Wheat germplasms with relative higher resistance are highlighted and genetic loci controlling the resistance to each of the disease are summarized.
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