Coexistence of and interaction relationships between an aflatoxin-producing fungus and a bacterium.

The interactions between aflatoxin-producing fungi and bacteria have opened up a new avenue for identifying biological agents suitable for controlling aflatoxin contamination. In this study, we analysed the interactions between A. flavus and the bacterium Burkholderia gladioli M3 that coexist in rice that is naturally contaminated with A. flavus. Our results showed that a cell-free culture filtrate (CCF) and the metabolite bongkrekic acid of the M3 strain potently suppressed the mycelial growth and spore production, and then affected the production of aflatoxin of A. flavus. Bongkrekic acid secreted by the M3 strain exhibited higher antifungal activity than did analogues. The CCF of the M3 strain and its metabolite bongkrekic acid can inhibit the growth of A. flavus, but the metabolites of A. flavus, aflatoxins, exerted no inhibitory effect on the growth of the M3 strain. Furthermore, we determined that the M3 cells could use the dead mycelia of A. flavus as energy sources for reproduction, while A. flavus could not grow in a solution containing dead M3 cells. In summary, these results indicated that B. gladioli has a competitive advantage in survival when it coexists with its fungal partner A. flavus.

Bisulfite sequencing reveals that Aspergillus flavus holds a hollow in DNA methylation.

Aspergillus flavus first gained scientific attention for its production of aflatoxin. The underlying regulation of aflatoxin biosynthesis has been serving as a theoretical model for biosynthesis of other microbial secondary metabolites. Nevertheless, for several decades, the DNA methylation status, one of the important epigenomic modifications involved in gene regulation, in A. flavus remains to be controversial. Here, we applied bisulfite sequencing in conjunction with a biological replicate strategy to investigate the DNA methylation profiling of A. flavus genome. Both the bisulfite sequencing data and the methylome comparisons with other fungi confirm that the DNA methylation level of this fungus is negligible. Further investigation into the DNA methyltransferase of Aspergillus uncovers its close relationship with RID-like enzymes as well as its divergence with the methyltransferase of species with validated DNA methylation. The lack of repeat contents of the A. flavus' genome and the high RIP-index of the small amount of remanent repeat potentially support our speculation that DNA methylation may be absent in A. flavus or that it may possess de novo DNA methylation which occurs very transiently during the obscure sexual stage of this fungal species. This work contributes to our understanding on the DNA methylation status of A. flavus, as well as reinforces our views on the DNA methylation in fungal species. In addition, our strategy of applying bisulfite sequencing to DNA methylation detection in species with low DNA methylation may serve as a reference for later scientific investigations in other hypomethylated species.

CYP1A1, GSTs and mEH polymorphisms and susceptibility to esophageal carcinoma: study of population from a high- incidence area in north China.

AIM: To characterize cytochrome P4501A1 (CYP1A1), glutathione S-transferases (GSTs) and microsomal epoxide hydrolase (mEH) polymorphisms in Chinese esophageal cancer patients. METHODS: Multiplex polymerase chain reaction (PCR) and PCR based restriction fragment length polymorphisms (PCR-RFLP) were used to detect polymorphism changes of CYP, GSTs and mEH on esophageal cancerous and precancerous lesions as well as in case control group. All the examination samples were obtained from Linzhou (formerly Linxian), Henan Province, the highest incidence area for esophageal cancer. RESULTS: The frequency of CYP1A1 3' polymorphism in case control group (26/38, 68 %) was significantly higher than in esophageal squamous cell carcinoma group (ESCC) (29/62, 47 %) (P<0.05). A significant difference in the incidence of mEH slow allele variant was observed between case control group (15/38, 39 %) and esophageal dysplasia group (22/32, 69 %) or ESCC group (39/62, 63 %) (P<0.05). However, no significant difference was observed among different groups in the polymorphisms of CYP1A1 exon 7, GSTM1, GSTT1, GSTP1 and mEH fast allele. CONCLUSION: The present results suggest that CYP1A1 3' polymorphism may be one of the promising protective factors and its wild gene type may be an indicator for higher susceptibility to esophageal cancer. mEH slow allele variant, associated with the progression of esophageal precancerous lesions, may contribute to the high susceptibility to esophageal carcinoma.