Plants have developed a complex defense system against diverse pests and pathogens. Once pathogens overcome mechanical barriers to infection, plant receptors initiate signaling pathways driving the expression of defense response genes. Plant immune systems rely on their ability to recognize enemy molecules, carry out signal transduction, and respond defensively through pathways involving many genes and their products. Pathogens actively attempt to evade and interfere with response pathways, selecting for a decentralized, multicomponent immune system. Recent advances in molecular techniques have greatly expanded our understanding of plant immunity, largely driven by potential application to agricultural systems. Here, we review the major plant immune system components, state of the art knowledge, and future direction of research on plant–pathogen interactions. In our review, we will discuss how the decentralization of plant immune systems have provided both increased evolutionary opportunity for pathogen resistance, as well as additional mechanisms for pathogen inhibition of such defense responses. We conclude that the rapid advances in bioinformatics and molecular biology are driving an explosion of information that will advance agricultural production and illustrate how complex molecular interactions evolve.

A toxin, designated SnTox1, was partially purified from culture filtrates of isolate Sn2000 of Stagonospora nodorum, the causal agent of wheat leaf and glume blotch. The toxin showed selective action on several different wheat genotypes, indicating that it is a host-selective toxin (HST). The toxic activity was reduced when incubated at 50 degrees C and activity was eliminated when treated with proteinase K, suggesting that the HST is a protein. The synthetic hexaploid wheat W-7984 and hard red spring wheat Opata 85, the parents of the International Triticeae Mapping Initiative (ITMI) mapping population, were found to be sensitive and insensitive, respectively, to SnTox1. The ITMI mapping population was evaluated for toxin reaction and used to map the gene conditioning sensitivity. This gene, designated Snn1, mapped to the distal end of the short arm of chromosome 1B. The wheat cv. Chinese Spring (CS) and all CS nullisomic-tetrasomic lines were sensitive to the toxin, with the exception of N1BT1D. Insensitivity also was observed when the 1B chromosome of CS was substituted with the 1B chromosome of an insensitive accession of Triticum dicoccoides. In addition, a series of 1BS chromosome deletion lines were used to physically localize the sensitivity gene. Physical mapping indicated that Snn1 lies within a major gene-rich region on 1BS. This is the first report identifying a putative proteinaceous HST from S. nodorum and the chromosomal location of a host gene conferring sensitivity.

Stagonospora nodorum leaf blotch is an economically important foliar disease in the major wheat-growing areas of the world. In related work, we identified a host-selective toxin (HST) produced by the S. nodorum isolate Sn2000 and determined the chromosomal location of the host gene (Snn1) conditioning sensitivity to the toxin using the International Triticeae Mapping Initiative mapping population and cytogenetic stocks. In this study, we used the same plant materials to identify quantitative trait loci (QTL) associated with resistance to fungal inoculations of Sn2000 and investigate the role of the toxin in causing disease. Disease reactions were scored at 5, 7, and 10 days postinoculation to evaluate changes in the degree of effectiveness of individual QTL. A major QTL was identified on the short arm of chromosome 1B, which coincided with the snn1 toxin-insensitivity gene. This locus explained 58% of the phenotypic variation for the 5-day reading but decreased to 27% for the 10-day reading, indicating that the toxin is most effective in the early stages of the interaction. In addition, relatively minor QTL were identified on chromosomes 3AS, 3DL, 4AL, 4BL, 5DL, 6AL, and 7BL, but not all minor QTL were significant for all readings and their effects varied. Multiple regression models explained from 68% of the phenotypic variation for the 5-day reading to 36% for the 10-day reading. The Chinese Spring nullisomic 1B tetrasomic 1D line and the Chinese Spring-Triticum dicoccoides disomic 1B chromosome substitution line, which were insensitive to SnTox1, were more resistant to the fungus than the rest of the nullisomictetrasomic and disomic chromosome substitution lines. Our results indicate that the toxin produced by isolate Sn2000 is a major virulence factor.

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The fungus Pyrenophora tritici-repentis, cause of tan spot of wheat, is an important foliar pathogen worldwide. Genetic variation in the fungal population prevalent in the Great Plains was studied by analysis of 270 single-spore isolates of P. tritici-repentis recovered from wheat, durum, and 10 noncereal grasses: Alti wild rye, barnyard grass, crested wheatgrass, intermediate wheatgrass, needle and thread grass, quackgrass, smooth bromegrass, sand reedgrass, slender wheatgrass, and wild barley. The isolates were grouped into five known races based on necrosis and/or chlorosis induction on standard differentials with two additional wheat genotypes ND495 and M-3. The isolates recovered from wheat were races 1, 2, and 4, while those from durum were races 1 and 5. Isolates from noncereal grasses were all race 4, except for the recovery of two isolates of race 1 from smooth bromegrass. Race 3 was not found in this study. This is the first record of barnyard grass and slender wheatgrass as alternative hosts for P. tritici-repentis. The recovery from noncereal grasses suggests that the fungus has a fairly wide host range; however, predominance of a race that is avirulent on wheat on these grasses tends to eliminate their significance in the disease epidemiology of wheat. The results indicate that P. tritici-repentis has a diverse population on wheat and noncereal grasses. For durable resistance, wheat lines should be tested against all virulent races found in the field.

Tan spot, caused by Pyrenophora tritici-repentis, is an important foliar disease of wheat (Triticum aestivum) worldwide. In a preliminary study, P. tritici-repentis isolates from Arkansas were shown to vary in virulence relative to isolates from other regions of the United States. Therefore, the aim of the current study was to characterize both pathogenic and molecular variations in P. tritici-repentis isolates from Arkansas. The virulence of 93 isolates of P. tritici-repentis was evaluated by inoculating five differential wheat cultivars/lines. Based on virulence phenotypes, 63 isolates were classified as race 1, and 30 isolates were assigned to race 3. A subset of 42 isolates was selected for molecular characterization with the presence or absence of the ToxA and ToxB genes. The results showed that 36 isolates out of 42 tested by polymerase chain reaction (PCR) and Southern analysis lacked the ToxA and ToxB genes. Six isolates harboring the ToxA and ToxB genes induced necrosis and chlorosis on Glenlea and 6B365, respectively. Thirteen ToxA gene-deficient isolates also caused necrosis and chlorosis on Glenlea and 6B365, respectively; however, they did not fit current race classification. In contrast, the remaining 23 ToxA gene-deficient isolates did not cause necrosis, but induced chlorosis on 6B365, showing a disease profile for race 3. When the virulence of AR LonB2 (an isolate with unclassified race) was compared with known races 1, 3, and 5 of P. tritici-repentis on 20 winter wheat cultivars from Arkansas, the virulence phenotypes differed substantially. Taken together, the ToxA and ToxB gene-deficient isolates of P. tritici-repentis that induce necrosis and/or chlorosis may produce a novel toxin(s) on wheat.

Spot blotch (SB) caused by Cochliobolus sativus (anamorph: Bipolaris sorokiniana) is an economically important disease of wheat worldwide. Under a severe epidemic condition, the disease can cause yield losses up to 70%. Previous approaches like bi-parental mapping for identifying SB resistant genes/QTLs exploited only a limited portion of the available genetic diversity with a lower capacity to detect polygenic traits, and had a lower marker density. In this study, we performed genome-wide association study (GWAS) for SB resistance in hard winter wheat association mapping panel (HWWAMP) of 294 genotypes. The HWWAMP was evaluated for response to B. sorokiniana (isolate SD40), and a range of reactions was observed with 10 resistant, 38 moderately resistant, 120 moderately resistant- moderately susceptible, 111 moderately susceptible, and 15 susceptible genotypes. GWAS using 15,590 high-quality SNPs and 294 genotypes we identified six QTLs (p = <0.001) on chromosomes 2D, 3A, 4A, 4B, 5A, and 7B that collectively explained 30% of the total variation for SB resistance. Highly associated SNPs were identified for all six QTLs, QSb.sdsu-2D.1 (SNP: Kukri_c31121_1460, R2 = 4%), QSb.sdsu-3A.1 (SNP: Excalibur_c46082_440, R2 = 4%), QSb.sdsu-4A.1 (SNP: IWA8475, R2 = 5.5%), QSb.sdsu-4B.1 (SNP: Excalibur_rep_c79414_306, R2 = 4%), QSb.sdsu-5A.1 (SNP: Kukri_rep_c104877_2166, R2 = 6%), and QSb.sdsu-7B.1 (SNP: TA005844-0160, R2 = 6%). Our study not only validates three (2D, 5A, and 7B) genomic regions identified in previous studies but also provides highly associated SNP markers for marker assisted selection. In addition, we identified three novel QTLs (QSb.sdsu-3A.1, QSb.sdsu-4A.1, and QSb.sdsu-4B.1) for SB resistance in wheat. Gene annotation analysis of the candidate regions identified nine NBS-LRR and 38 other plant defense-related protein families across multiple QTLs, and these could be used for fine mapping and further characterization of SB resistance in wheat. Comparative analysis with barley indicated the SB resistance locus on wheat chromosomes 2D, 3A, 5A, and 7B identified in our study are syntenic to the previously identified SB resistance locus on chromosomes 2H, 3H, 5H, and 7H in barley. The 10 highly resistant genotypes and SNP markers identified in our study could be very useful resources for breeding of SB resistance in wheat.

Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F(2)-derived F(6) recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. Kulm with the toxin-insensitive, disease-resistant cv. Erik segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritability estimates suggested the presence of four to five genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild-type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.