Many fungi in the centre of the group of Fusarium and its teleomorphs were shown to be capable of reducing nitrite anaerobically to form nitric oxide (NO), nitrous oxide (N2O), and/or dinitrogen (N2). Several strains could reduce nitrate as well. Nitrous oxide was the major product of the reduction of nitrate or nitrite. Several fungi could also form N2. When [15]nitrite was used as substrate for the N2‐forming dinitrification, 15N2O, 15NO, and 14N15N were obtained as the products. These results demonstrated that, unexpectedly, many fungi have denitrifying abilities. It was also shown that the fungal system contains a unique reaction, formation of a hybrid dinitrogen.

Many fungi in the centre of the group of Fusarium and its teleomorphs were shown to be capable of reducing nitrite anaerobically to form nitric oxide (NO), nitrous oxide (N2O), and/or dinitrogen (N2). Several strains could reduce nitrate as well. Nitrous oxide was the major product of the reduction of nitrate or nitrite. Several fungi could also form N2. When [15]nitrite was used as substrate for the N2-forming denitrification, 15N2O, 15NO, and 14N15N were obtained as the products. These results demonstrated that, unexpectedly, many fungi have denitrifying abilities. It was also shown that the fungal system contains a unique reaction, formation of a hybrid dinitrogen.

nfxC-type cells of Pseudomonas aeruginosa that produce the MexEF-OprN efflux pump exhibit resistance to fluoroquinolones and chloramphenicol and hypersusceptibility to most classical ␤-lactam antibiotics. We investigated the molecular mechanism of how the nfxC mutation causes ␤-lactam hypersusceptibility. The MexAB-OprM extrusion pump transports and confers resistance to ␤-lactam antibiotics. Interestingly, expression of the mexAB-oprM operon reached the highest level during the mid-stationary growth phase in both wild-type and nfxC-type mutant strains, suggesting that expression of the mexAB-oprM operon may be controlled by cell density-dependent regulation such as quorum sensing. This assumption was verified by demonstrating that exogenous addition of the quorum-sensing autoinducer N-butyryl-L-homoserine lactone (C4-HSL) enhanced the expression of MexAB-OprM, whereas N-(3-oxododecanoyl)-L-homoserine lactone had only a slight effect. Furthermore, this C4-HSL-mediated enhancement of mexAB-oprM expression was repressed by MexT, a positive regulator of the mexEF-oprN operon. It was concluded that ␤-lactam hypersusceptibility in nfxC-type mutant cells is caused by MexT-mediated cancellation of C4-HSL-mediated enhancement of MexABOprM expression.Pseudomonas aeruginosa is an opportunistic pathogen that causes infections in immunocompromised hosts and colonizes the lungs of individuals with cystic fibrosis. This organism shows broad resistance to structurally and functionally dissimilar antibiotics. This type of multidrug resistance is attributable mainly to the expression of the xenobiotic extrusion transporter MexAB-OprM coupled with tight outer membrane permeability (21,23,29). The mexAB-oprM operon encodes three protein subunits (21,26,29): the intrinsic inner membrane protein MexB (9), the inner membrane-associated periplasmic lipoprotein MexA (45), and the outer membrane lipoprotein OprM (13,22,44). The mexAB-oprM operon is negatively regulated by the product of the mexR gene, which is located upstream of the mexAB-oprM genes and is divergently transcribed (1,5,14,34,37). nalB-type mutants caused by the mexR mutation derepress MexAB-OprM production and are highly resistant to fluoroquinolones, chloramphenicol, and most classical ␤-lactam antibiotics (30,32,35,42).Recently, it was reported that the MexAB-OprM transporter exports quorum-sensing mediators, acylhomoserine lactones (AHSLs), which induce the production of cell density-dependent virulence factors, including proteases, rhamnolipids, exotoxin A, exoenzyme S, and pyocyanin (24, 25). The AHSLs control at least two quorum-sensing systems in P. aeruginosa, namely, LasR-LasI and RhlR-RhlI. LasI and RhlI catalyze the last steps in the syntheses of N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) and N-butyryl-L-homoserine lactone (C4-HSL), respectively. LasR and RhlR are specifically activated by the diffusible signaling molecules 3-oxo-C12-HSL and C4-HSL, respectively.Four resistant-nodulation-division efflux pumps (MexABOprM, MexCD-OprJ, MexEF-OprN, ...

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