fumonisin-b1 and Disease-Resistance

Verticillium wilt caused by Verticillium dahliae is a major disease of cotton. Acidic protein-lipopolysaccharide complexes are thought to be the toxins responsible for its symptoms. Here, we determined that the sphingolipid biosynthesis inhibitor fumonisin B1 (FB1) acts as a toxin and phenocopies the symptoms induced by V. dahliae. Knocking out genes required for FB1 biosynthesis reduced V. dahliae pathogenicity. Moreover, we showed that overexpression of a FB1 and V. dahliae both downregulated gene, GhIQD10, enhanced verticillium wilt resistance by promoting the expression of brassinosteroid and anti-pathogen genes. Our results provide a new strategy for preventing verticillium wilt in cotton.

Topics: Disease Resistance; Fumonisins; Gene Expression Regulation, Plant; Gossypium; Plant Diseases; Sphingolipids; Verticillium

Fumonisin B1 (FB1) and Alternaria alternate f. sp. lycopersici (AAL)-toxin are classified as sphinganine analog mycotoxins (SAMTs), which induce programmed cell death (PCD) in plants and pose health threat to humans who consume the contaminated crop products. Herein, Fumonisin B1 Resistant41 (FBR41), a dominant mutant allele, was identified by map-based cloning of Arabidopsis FB1-resistant mutant fbr41, then ectopically expressed in AAL-toxin sensitive tomato (Solanum lycopersicum) cultivar. FBR41-overexpressing tomato plants exhibited less severe cell death phenotype upon AAL-toxin treatment. Analysis of free sphingoid bases showed that both fbr41 and FBR41-overexpressing tomato plants accumulated less sphinganine and phytosphingosine upon FB1 and AAL-toxin treatment, respectively. Alternaria stem canker is a disease caused by AAL and responsible for severe economic losses in tomato production, and FBR41-overexpressing tomato plants exhibited enhanced resistance to AAL with decreased fungal biomass and less cell death, which was accompanied by attenuated accumulation of free sphingoid bases and jasmonate (JA). Taken together, our results indicate that FBR41 is potential in inhibiting SAMT-induced PCD and controlling Alternaria stem canker in tomato.

Topics: Alternaria; Cell Death; Disease Resistance; Fumonisins; Genes, Plant; Mycotoxins; Plant Diseases; Solanum lycopersicum

Fusarium verticillioides is an important pathogen in maize that causes various diseases affecting all stages of plant development worldwide. The fungal pathogen could be seed borne or survive in soil and penetrate the germinating seed. Most F. verticillioides strains produce fumonisins, which are of concern because of their toxicity to animals and possibly humans, and because they enhance virulence against seedlings of some maize genotypes. In this work, we studied the action of fumonisin B1 (FB1) on the activity of maize β-1,3-glucanases involved in plant defense response. In maize embryos, FB1 induced an acidic isoform while suppressing the activity of two basic isoforms. This acidic isoform was induced also with 2,6-dichloroisonicotinic acid, an analog of salicylic acid. Repression of the basic isoforms suggested a direct interaction of the enzymes with the mycotoxin as in vitro experiments showed that pure FB1 inhibited the basic β-1,3-glucanases with an IC(50) of 53 μM. When germinating maize embryos were inoculated with F. verticillioides the same dual effect on β-1,3-glucanase activities that we observed with the pure toxin was reproduced. Similar levels of FB1 were recovered at 24 h germination in maize tissue when they were treated with pure FB1 or inoculated with an FB1-producing strain. These results suggest that β-1,3-glucanases are a relevant physiological target and their modulation by FB1 might contribute to F. verticillioides colonization.

Topics: Adjuvants, Immunologic; Chitinases; Disease Resistance; Fumonisins; Fusarium; Glucan 1,3-beta-Glucosidase; Mycotoxins; Plant Proteins; Seeds; Zea mays

Long chain bases (LCBs) are sphingolipid intermediates acting as second messengers in programmed cell death (PCD) in plants. Most of the molecular and cellular features of this signaling function remain unknown. We induced PCD conditions in Arabidopsis thaliana seedlings and analyzed LCB accumulation kinetics, cell ultrastructure and phenotypes in serine palmitoyltransferase (spt), mitogen-activated protein kinase (mpk), mitogen-activated protein phosphatase (mkp1) and lcb-hydroxylase (sbh) mutants. The lcb2a-1 mutant was unable to mount an effective PCD in response to fumonisin B1 (FB1), revealing that the LCB2a gene is essential for the induction of PCD. The accumulation kinetics of LCBs in wild-type (WT) and lcb2a-1 plants and reconstitution experiments with sphinganine indicated that this LCB was primarily responsible for PCD elicitation. The resistance of the null mpk6 mutant to manifest PCD on FB1 and sphinganine addition and the failure to show resistance on pathogen infection and MPK6 activation by FB1 and LCBs indicated that MPK6 mediates PCD downstream of LCBs. This work describes MPK6 as a novel transducer in the pathway leading to LCB-induced PCD in Arabidopsis, and reveals that sphinganine and the LCB2a gene are required in a PCD process that operates as one of the more effective strategies used as defense against pathogens in plants.

Topics: Arabidopsis; Arabidopsis Proteins; Cell Death; Chloroplasts; Disease Resistance; DNA Fragmentation; Fumonisins; Genotype; Mitogen-Activated Protein Kinases; Mutagenesis, Insertional; Phenotype; Protein Tyrosine Phosphatases; Pseudomonas syringae; Seedlings; Serine C-Palmitoyltransferase; Signal Transduction; Sphingolipids; Sphingosine