The effects of antibacterial compounds produced by Saccharomyces cerevisiae in Koumiss on pathogenic Escherichia coli O₈ and its cell surface characteristics were investigated.  S. cerevisiae isolated from Koumiss produced antibacterial compounds which were active against pathogenic E. coli O₈ as determined by the Oxford cup method.  The aqueous phases from S. cerevisiae at pH=2.0 (S2) and pH=8.0 (S8) were extracted and tested, respectively.  The organic acids of S2 and S8 were determined by high performance liquid chromatography (HPLC), and the concentrations of killer toxins were determined by enhanced bicinchoninic acid (BCA) Protein Assay Kit.  The minimum inhibition concentration (MIC) and the minimum bactericidal concentration (MBC) of S2 and S8 on E. coli O₈ were determined by the broth microdilution method.  The effects of S2 and S8 on the growth curve of E. coli O₈ were determined by turbidimetry, and the hydrophobicities of E. coli O₈ cell surface were determined using the microbial adhesion to solvents method, the permeation of E. coli O₈ cell membrane were determined by the o-nitrophenyl-β-D-galactoside (ONPG) method.  Aqueous phases at pH 2.0 and 8.0 had larger inhibition zones and then S2 and S8 were obtained by freeze-drying.  The main component in S2 was citric acid and it was propanoic acid in S8.  Other organic acids and killer toxins were also present.  Both the MICs of S2 and S8 on E. coli O₈ were 0.025 g mL^–1, the MBCs were 0.100 and 0.200 g mL^–1, respectively.  The normal growth curve of E. coli O₈ was S-shaped, however, it changed after addition of S2 and S8.  E. coli O₈ was the basic character, and had a relatively hydrophilic surface.  The hydrophobicity of E. coli O₈ cell surface and the permeation of E. coli O₈ cell membrane were increased after adding S2 and S8.  The present study showed that S2 and S8 inhibit the growth of pathogenic E. coli O₈ and influence its cell surface characteristics.

    The pleiotropic drug resistance (PDR) sub-family of adenosine triphosphate (ATP)-binding cassette (ABC) transporter had been reported to participate in diverse biological processes of plant. In this study, we cloned three novel PDR genes in Fusarium head blight (FHB) resistant wheat cultivar Ning 7840, which were located on wheat chromosomes 6A, 6B and 6D. In phylogeny, these genes were members of cluster I together with AePDR7 and BdPDR7. Subcellular localization analysis showed that TaPDR7 was expressed on the plasmalemma. The quantitative real time PCR (RT-PCR) analysis showed that this gene and its probable orthologues in chromosomes 6B and 6D were both up-regulated sharply at 48 h after infected by Fusarium graminearum and trichothecene deoxynivalenol (DON) in spike. When knocking down the transcripts of all TaPDR7 members by barely stripe mosaic virus-induced gene silencing (BSMV-VIGS) system, it could promote the F. graminearum hyphae growth and made larger pathogen inoculation points in Ning 7840, which suggested that TaPDR7 might play an important role in response to F. graminearum. Although salicylic acid (SA), methyl jasmonate (MeJA) and abscisic acid (ABA) had been reported to possibly regulate wheat FHB resistance, here, we found that the three members of TaPDR7 were negatively regulated by these three hormones but positively regulated by indoleacetic acid (IAA).

Fusarium head blight (FHB), caused primarily by Fusarium graminearum, is a destructive disease of wheat throughout the world. However, the mechanisms of host resistance to FHB are still largely unclear. Deoxynivalenol (DON) produced by F. graminearum which enhances the pathogen to spread could be converted into inactive form D3G by UDP-glycosyltransferases (UGTs). A DON responsive UGT gene, designated as TaUGT4, was first cloned from wheat in this study. The putative open reading frame (ORF) of TaUGT4 was 1 386 bp, encoding 461 amino acids protein. TaUGT4 was placed on chromosome 2D using a set of nulli-tetrasomic lines of wheat cultivar Chinese Spring (CS). When fused with eGFP at C terminal, TaUGT4 was shown to localize in cytoplasm of the transformed tobacco cells. The transcriptional analysis revealed that TaUGT4 was strongly induced by F. graminearum or DON in both of FHB-resistant cultivar Sumai 3 and susceptible cultivar Kenong 199, especially in Sumai 3 under DON treatment. Similar increase of TaUGT4 expression was observed in Sumai 3 and Kenong 199 in response to salicylic acid (SA) treatment. But interestingly, the transcripts level of TaUGT4 in Sumai 3 showed significantly higher than that in Kenong 199 after treated with methyl jasmonate (MeJA). According to the expression patterns, TaUGT4 might lead to different effects between FHB-resistant genotype and susceptible genotype in the process against F. graminearum inoculation. It had also been discussed in this paper that JA signaling pathway might play a significant role in the resistance against F. graminearum compared to SA signaling pathway.