Where Does the Peanut Smut Pathogen, Thecaphora frezii, Fit in the Spectrum of Smut Diseases?

Smut fungi, such as Ustilago maydis, have been studied extensively as a model for plant-pathogenic basidiomycetes. However, little attention has been paid to smut diseases of agronomic importance that are caused by species of the genus Thecaphora, probably due to their more localized distribution. Peanut smut incited by Thecaphora frezii has been reported only in South America, and Argentina is the only country where this disease has been noted in commercial peanut production. In this work, important advances in deciphering T. frezii specific biology/pathobiology in relation to potato (T. solani), wheat (U. tritici), and barley (U. nuda) smuts are presented. We summarize the state of knowledge of fungal effectors, functionally characterized to date in U. maydis and most recently in T. thlaspeos, as well as the potential to be present in other Thecaphora species involved in dicot-host interactions like T. frezii-peanut. We also discuss applicability and limitations of currently available methods for identification of smut fungi in different situations and management strategies to reduce their impact on agri-food quality. We conclude by describing some of the challenges in elucidating T. frezii strategies that allow it to infect the host and tolerate or evade plant immune defense mechanisms, and assessing other aspects related to pest control and their implications for human health.

The aflatoxin B1 -fumonisin B1 toxicity in BRL-3A hepatocytes is associated to induction of cytochrome P450 activity and arachidonic acid metabolism.

Human oral exposure to aflatoxin B1 (AFB1 ) and fumonisin B1 (FB1 ) is associated with increased hepatocellular carcinoma. Although evidence suggested interactive AFB1 -FB1 hepatotoxicity, the underlying mechanisms remain mostly unidentified. This work was aimed at evaluating the possible AFB1 -FB1 interplay to induce genetic and cell cycle toxicities in BRL-3A rat hepatocytes, reactive oxygen species (ROS) involvement, and the AFB1 metabolizing pathways cytochrome P450 (CYP) and arachidonic acid (ArAc) metabolism as ROS contributors. Flow cytometry of stained BRL-3A hepatocytes was used to study the cell cycle (propidium iodide), ROS intracellular production (DCFH-DA, HE, DAF-2 DA), and phospholipase A activity (staining with bis-BODIPY FL C11-PC). The CYP1A activity was assessed by the 7-ethoxyresorufin-O-deethylase (EROD) assay. Despite a 48-h exposure to FB1 (30 µM) not being genotoxic, the AFB1 (20 µM)-induced micronucleus frequency was overcome by the AFB1 -FB1 mixture (MIX), presumably showing toxin interaction. The mycotoxins blocked G1/S-phase, but only MIX caused cell death. Overall, the oxidative stress led these alterations as the pretreatment with N-acetyl-l-cysteine reduced such toxic effects. While AFB1 had a major input to the MIX pro-oxidant activity, with CYP and ArAc metabolism being ROS contributors, these pathways were not involved in the FB1 -elicited weak oxidative stress. The MIX-induced micronucleus frequency in N-acetyl-l-cysteine pretreated cells was greater than that caused by AFB1 without antioxidants, suggesting enhanced AFB1 direct genotoxicity probably owing to the higher CYP activity and ArAc metabolism found in MIX. The metabolic pathways modulation by AFB1 -FB1 mixtures could raise its hepatocarcinogenic properties.

Synergistic effect of chickpea plants and Mesorhizobium as a natural system for chromium phytoremediation.

The presence of chromium in soils not only affects the physiological processes of plants but also the microbial rhizosphere composition and metabolic activities of microorganisms. Hence, the inoculation of plants with Cr(VI)-tolerant rhizospheric microorganisms as an alternative to reduce Cr phytotoxicity was studied. In this work, chickpea germination was reduced by Cr(VI) concentrations of 150 and 250 mg/L (6 and 33%, respectively); however lower Cr(VI) concentrations negatively affected the biomass. On the other hand, its symbiont, Mesorhizobium ciceri, was able to grow and remove different Cr(VI) concentrations (5-20 mg/L). The inoculation of chickpea plants with this strain exposed to Cr(VI) showed a significantly enhanced plant growth. In addition, inoculated plants accumulated higher Cr concentration in roots than those noninoculated. It is important to note that Cr was not translocated to shoots independently of inoculation. These results suggest that Mesorhizobium's capability to remove Cr(VI) could be exploited for bioremediation. Moreover, chickpea plants would represent a natural system for phytoremediation or phytostabilization of Cr in situ that could be improved with M. ciceri inoculation. This strategy would be considered as a phytoremediation tool with great economic and ecological relevance.