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.

Fusarium head blight (FHB) is a devastating disease worldwide, affecting wheat and other small grains. To identify key wheat genes involved in FHB pathogenesis, 406 FHB-related wheat expressed sequence tags functionally identified in Sumai 3 were investigated for their association with FHB-resistance quantitative trait loci (QTL) Fhb1 and Fhb_6BL in 2010 and 2011. A total of 47 candidate genes were identified by bulk analysis, near-isogenic screening and expression QTL mapping, and were finally mapped to their carrier chromosomes with Chinese Spring nulli-tetra deficiency lines. One gene, designated WFhb1_c1 (wheat Fhb1 candidate gene 1), was both functionally associated with and physically located within Fhb1 and was found to be weakly similar (E = 5e+0) to an Arabidopsis gene encoding pectin methyl esterase inhibitor. Two other genes, designated WFI_6BL1 and WFI_6BL2 (wheat-Fusarium interaction genes 6BL1 and 6BL2), were functionally associated with Fhb_6BL but physically mapped on chromosomes 7D and 5A, respectively. WFI_6BL1 was annotated as a 13- lipoxygenase gene and WFI_6BL2 might encode a PR-4-like protein. Our data suggested that i) Fhb1 seems to contribute to FHB resistance by reducing susceptibility in the first 60 h, ii) Fhb_6BL makes its contribution via the jasmonate-mediated pathways, and iii) wheat seems to activate its defense mechanism in the biotrophic phase of FHB pathogenesis.

Fusarium head blight (FHB) is a highly detrimental disease of wheat. A quantitative trait locus for FHB resistance, Qfhb1, is the most utilized source of resistance in wheat-breeding programs, but very little is known about its resistance mechanism. In this study, we elucidated a prospective FHB resistance mechanism by investigating the proteomic signatures of Qfhb1 in a pair of contrasting wheat near-isogenic lines (NIL) after 24 h of inoculation of wheat florets by Fusarium graminearum. Statistical comparisons of the abundances of protein spots on the 2D-DIGE gels of contrasting NILs (fhb1+ NIL = Qfhb1 present; fhb1- NIL = Qfhb1 absent) enabled us to select 80 high-ranking differentially accumulated protein (DAP) spots. An additional evaluation confirmed that the DAP spots were specific to the spikelet from fhb1- NIL (50 spots), and fhb1+ NIL (seven spots). The proteomic data also suggest that the absence of Qfhb1 makes the fhb1- NIL vulnerable to Fusarium attack by constitutively impairing several mechanisms including sucrose homeostasis by enhancing starch synthesis from sucrose. In the absence of Qfhb1, Fusarium inoculations severely damaged photosynthetic machinery; altered the metabolism of carbohydrates, nitrogen and phenylpropanoids; disrupted the balance of proton gradients across relevant membranes; disturbed the homeostasis of many important signaling molecules induced the mobility of cellular repair; and reduced translational activities. These changes in the fhb1- NIL led to strong defense responses centered on the hypersensitive response (HSR), resulting in infected cells suicide and the consequent initiation of FHB development. Therefore, the results of this study suggest that Qfhb1 largely functions to either alleviate HSR or to manipulate the host cells to not respond to Fusarium infection.

Fusarium head blight (FHB) is a severe disease of wheat (Triticum aestivum L.). Qfhb1 is the most important quantitative trait locus (QTL) for FHB resistance. We previously identified wheat gene WFhb1-1 (aka WFhb1-c1) as a candidate for FHB resistance gene. Here we report that WFhb1-1 has been cloned. The gene (GenBank # KU304333.1) consists of a single exon, encoding a putative membrane protein of 127 amino acids. WFhb1-1 protein produced in Pichia pastoris inhibits growth of both F. graminearum and P. pastoris in culture. Western Blotting with anti- WFhb1-1 antibody revealed a significant decrease (p < 0.01) in WFhb1-1 accumulation, 12 hours post Fusarium inoculation in non-Qfhb1-carrier wheat but not in Qfhb1-carrier wheat. Overexpressing WFhb1-1 in non-Qfhb1-carrier wheat led to a significant decrease (p < 0.01) in Fusarium-damaged rachis rate, Fusarium-diseased kernel rate and DON content in harvested kernels, while silencing WFhb1-1 in Qfhb1-carrier wheat resulted in a significant increase (p < 0.01) in FHB severity. Therefore, WFhb1-1 is an important FHB resistance gene with a potential antifungal function and probably a key functional component of Qfhb1 in wheat. A model regarding how WFhb1-1 functions in FHB resistance/susceptibility is hypothesized and discussed.