Polyoxins resistance

Recently, Nishimura et at. (47) have reported the discovery of polyoxin resistant strains of A. kikuehiana in some orchards of Tottori Prefecture, Japan. Hori et at. (48) suggested that the resistance is caused by a lowered permeability of the antibiotic through the cell membrane into the site of chitin synthesis. 

Polyoxins such as polyoxin A, B and D which block the biosynthesis of chitin are competitive inhibitors of uridine diphosphate-N-acetylglucosamine [65]. In resistant isolates of Altemaria kikuchiana, no uptake of dipeptides was observed suggesting that altered dipeptide permease may be responsible for polyoxin resistance [65]. 

Polyoxins are used in the control of several pathogens, notably sheath blight of rice (Rhizoctonia solani). Polyoxin is specific to Alternaria, Botrytis, and powdery mildew. Differences in activity between members of the polyoxin group probably reflect dissimilar uptake characteristics, which are governed by specific peptides. Different peptides may limit polyoxin activity at the level of the uptake mechanism and may also determine their resistance traits. 

Polyoxlns. The polyoxin antibiotics are effective against fungi that contain chitin in their cell walls. The resistance to polyoxlns in some fungi of this type appears to be related to a permeability factor rather than to a change in the site of action (14). Polyoxlns competitively inhibit chitin synthetase and thus prevent the incorporation of uridinediphospho-N-acetylglucosamine into the chitin polymer (14). 

Prior to the 1980s, bacterially produced antibiotics were the mainstay of control of pathogenic organisms in humans (P-lactams, chloramphenicol, tetracyclines, erythromycin, streptomycin, gentamicin, rifamycin, vancomycin, lincomycin), in foods (nisin), in animals (monensin) and in plants (polyoxins). However, new antibiotics were clearly needed because of (1) the development of resistance in pathogens (2) the evolution of new... 

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