Although 14-3-3 proteins have been reported to be involved in responses to biotic stresses in plants, their functions in rice blast, the most destructive disease in rice, are largely unknown. Only GF14e has been confirmed to negatively regulate leaf blast. We report that GF14b is highly expressed in seedlings and panicles during blast infection. Rice plants overexpressing GF14b show enhanced resistance to panicle blast but are susceptible to leaf blast. In contrast, GF14b-silenced plants show increased susceptibility to panicle blast but enhanced resistance to leaf blast. Yeast one-hybrid assays demonstrate that WRKY71 binds to the promoter of GF14b and modulates its expression. Overexpression of GF14b induces expression of jasmonic acid (JA) synthesis-related genes but suppresses expression of salicylic acid (SA) synthesis-related genes. In contrast, suppressed GF14b expression causes decreased expression of JA synthesis-related genes but activation of SA synthesis-related genes. These results suggest that GF14b positively regulates panicle blast resistance but negatively regulates leaf blast resistance, and that GF14b-mediated disease resistance is associated with the JA- and SA-dependent pathway. The different functions for 14-3-3 proteins in leaf and panicle blast provide new evidence that leaf and panicle blast resistance are controlled by different mechanisms.

We characterized a novel blast resistance gene Pi50 at the Pi2/9 locus; Pi50 is derived from functional divergence of duplicated genes. The unique features of Pi50 should facilitate its use in rice breeding and improve our understanding of the evolution of resistance specificities. Rice blast disease, caused by the fungal pathogen Magnaporthe oryzae, poses constant, major threats to stable rice production worldwide. The deployment of broad-spectrum resistance (R) genes provides the most effective and economical means for disease control. In this study, we characterize the broad-spectrum R gene Pi50 at the Pi2/9 locus, which is embedded within a tandem cluster of 12 genes encoding proteins with nucleotide-binding site and leucine-rich repeat (NBS-LRR) domains. In contrast with other Pi2/9 locus, the Pi50 cluster contains four duplicated genes (Pi50_NBS4_1 to 4) with extremely high nucleotide sequence similarity. Moreover, these duplicated genes encode two kinds of proteins (Pi50_NBS4_1/2 and Pi50_NBS4_3/4) that differ by four amino acids. Complementation tests and resistance spectrum analyses revealed that Pi50_NBS4_1/2, not Pi50_NBS4_3/4, control the novel resistance specificity as observed in the Pi50 near isogenic line, NIL-e1. Pi50 shares greater than 96 % amino acid sequence identity with each of three other R proteins, i.e., Pi9, Piz-t, and Pi2, and has amino acid changes predominantly within the LRR region. The identification of Pi50 with its novel resistance specificity will facilitate the dissection of mechanisms behind the divergence and evolution of different resistance specificities at the Pi2/9 locus.

Ustilaginoidea virens is a flower-infecting fungus that forms false smut balls in rice panicle. Rice false smut has long been considered a minor disease, but recently it occurred frequently and emerged as a major disease in rice production. In vitro co-cultivation of U. virens strain with young rice panicles showed that U. virens enters inside of spikelets from the apex and then grows downward to infect floral organs. In response to U. virens infection, rice host exhibits elevated ROS accumulation and enhanced callose deposition. The secreted compounds of U. virens can suppress rice pollen germination. Examination of sectioning slides of freshly collected smut balls demonstrated that both pistil and stamens of rice flower are infected by U. virens, hyphae degraded the contents of the pollen cells, and also invaded the filaments. In addition, U. virens entered rice ovary through the thin-walled papillary cells of the stigma, then decomposed the integuments and infected the ovary. The invaded pathogen could not penetrate the epidermis and other layers of the ovary. Transverse section of the pedicel just below the smut balls showed that there were no fungal hyphae observed in the vascular bundles of the pedicel, implicating that U. virens is not a systemic flower-infecting fungus.

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Rice bacterial leaf blight is caused by Xanthomonas oryzae pv. oryzae (Xoo) and produces substantial losses in rice yields. Resistance breeding is an effective method for controlling bacterial leaf blight disease. The mutant line H120 derived from the japonica line Lijiangxintuanheigu is resistant to all Chinese Xoo races. To identify and map the Xoo resistance gene(s) of H120, we examined the association between phenotypic and genotypic variations in two F 2 populations derived from crosses between H120/CO39 and H120/IR24. The segregation ratios of F 2 progeny consisted with the action of a single dominant resistance gene, which we named Xa46(t). Xa46(t) was mapped between the markers RM26981 and RM26984 within an approximately 65.34-kb region on chromosome 11. The 12 genes predicted within the target region included two candidate genes encoding the serine/threonine-protein kinase Doa (Loc_Os11g37540) and Calmodulin-2/3/5 (Loc_Os11g37550). Differential expression of H120 was analyzed by RNA-seq. Four genes in the Xa46(t) target region were differentially expressed after inoculation with Xoo. Mapping and expression data suggest that Loc_Os11g37540 allele is most likely to be Xa46(t). The sequence comparison of Xa23 allele between H120 and CBB23 indicated that the Xa46(t) gene is not identical to Xa23. Rice (Oryza sativa) bacterial blight which caused by the pathogen Xanthomonas oryzae pv. oryzae (Xoo) is one of most serious three rice disease in the world, and limits rice productivity each year owing to its high epidemic potential and the lack of effective bactericides 1,2. Xoo causes a systemic infection of the vascular system that results in yellowish brown long strip or offwhite lesions along leaf veins at the maximum booting stage. Rice infected by Xoo can lose 10-20% and even up to 80% of its yield 3,4. Rice bacterial blight disease is usually prevalent in tropical subtropical regions rice-growing regions except North America 5,6. Normally plant disease resistance is divided into qualitative (complete) or quantitative (partial) according to the plant's specific interactions against pathogen invasion 7. Qualitative resistance belongs to pathogen racespecific resistance which controlled by major resistance (MR) genes. Quantitative resistance belongs to pathogen race-nonspecific resistance which is generally mediated by multiple minor genes or quantitative trait loci (QTLs) 8. The rice-Xoo pathosystem as a host-pathogen interactions and co-evolution genetic model was used to dissect plant disease resistance mechanisms 5,9. In the rice-Xoo pathosystem, MR-mediated race-specific resistance usually follows the gene-for-gene relationship 9,10. MR has been widely applied to rice breeding in consideration of its high level of resistance and easy genetic manipulation. Application of resistance variety is firmly believed to be the most effective and environmentfriendly measure to prevent and control bacterial blight disease 1,2. To date, at least 45 race-specific bacterial blight resistance (R) genes to different Xoo r...