The glyoxalase system is ubiquitous among all forms of life owing to its central role in relieving the cell from the accumulation of methylglyoxal, a toxic metabolic byproduct. In higher plants, this system is upregulated under diverse metabolic stress conditions, such as in the defence response to infection by pathogenic microorganisms. Despite their proven fundamental role in metabolic stresses, plant glyoxalases have been poorly studied. In this work, glyoxalase I from Zea mays has been characterized both biochemically and structurally, thus reporting the first atomic model of a glyoxalase I available from plants. The results indicate that this enzyme comprises a single polypeptide with two structurally similar domains, giving rise to two lateral concavities, one of which harbours a functional nickel(II)-binding active site. The putative function of the remaining cryptic active site remains to be determined.

Fusarium verticillioides causes ear rot and grain mycotoxins in maize (Zea mays L.), which are harmful to human and animal health. Breeding and growing less susceptible plant genotypes is one alternative to reduce these detrimental effects. A better understanding of the resistance mechanisms would facilitate the implementation of strategic molecular agriculture to breeding of resistant germplasm. Our aim was to identify genes and metabolites that may be related to the Fusarium reaction in a resistant (L4637) and a susceptible (L4674) inbred. Gene expression data were obtained from microarray hybridizations in inoculated and non-inoculated kernels from both inbreds. Fungal inoculation did not produce considerable changes in gene expression and metabolites in L4637. Defense-related genes changed in L4674 kernels, responding specifically to the pathogen infection. These results indicate that L4637 resistance may be mainly due to constitutive defense mechanisms preventing fungal infection. These mechanisms seem to be poorly expressed in L4674; and despite the inoculation activate a defense response; this is not enough to prevent the disease progress in this susceptible line. Through this study, a global view of differential genes expressed and metabolites accumulated during resistance and susceptibility to F. verticillioides inoculation has been obtained, giving additional information about the mechanisms and pathways conferring resistance to this important disease in maize.

The aim of this work was to investigate the role of pericarp phenylpropanoids as resistance factors to F. verticillioides in eleven maize genotypes. Disease severity and kernel fumonisin accumulation were measured after inoculation with F. verticillioides and related to contents of pericarp phenylpropanoids in field trials conducted during 2 years. Grain fumonisin concentrations were highly dependant on disease severity of the genotypes (r00.88). A detailed analysis of pericarp phenylpropanoids indicated the presence of trans-ferulic acid (tFA), cis-ferulic acid (cFA), pcoumaric acid (pCA), and five diferulates (DFAs). The most prominent diferulates were 8,5′-diferulic acid benzofuram form (8,5′-DFAbz), followed by 8,5′-DFA and 8,8′-DFA. Except for cFA, the most resistant genotypes exhibited high levels of phenylpropanoids which were related to low levels of disease severity and grain fumonisin concentration (−0.61 > r>−0.90).A stepwise regression analysis revealed that total diferulates was the best explanatory parameter for variability of disease severity (r 2 00.71). Grain fumonisin concentration was well depicted by contents of total diferulates, 8,5′DFAbz and pCA (r 2 00.82). Our findings suggest that high level of phenylpropanoids in the kernel pericarp is a trait associated to less disease severity and fumonisin accumulation caused by F. verticillioides. Further research is in progress to map quantitative trait loci for these cell wall components in bi-parental populations derived by crossing resistant and susceptible genotypes included in this study.

Fusarium verticillioides and F. graminearum cause ear rots in maize (Zea mays L.) that reduce yield and contaminate the grain with mycotoxins produced by the fungi. To map QTLs for resistance to these ear rots, a F 5 mapping population, consisting of 298 recombinant inbreds obtained by randomly selfing of the cross between LP4637 (moderately resistant) and L4674 (susceptible), was genotyped with 250 single nucleotide polymorphism markers and phenotyped 2 years for disease severity after silk inoculation with conidial suspensions of F. verticillioides and F. graminearum. Four QTLs were mapped in chromosomes 2, 3 and 5, bins 2.03, 3.05, 3.07 and 5.07, explaining ranges of 11.2-11.8, 3.4-5.1, 6.2-7.6 and 3.8-5.0 of phenotypic variances (%), respectively, depending on year and fungus. Additive effects of each QTL ranged from 5.0 to 11.9 % of ear area covered by mold and no epistatic interactions were observed. The four QTLs were effective for both Fusarium species and environments indicating that LP4637 is a source of broad resistance to Fusarium stable across environments. These results are consistent with previous research reporting QTLs for ear rot resistance in the same chromosome regions from sources of resistance growing in North America, Africa, Europe and China.

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