Antimicrobial mechanism of lantibiotics

被引:85
作者
Islam, Mohammad R. [1 ]
Nagao, Jun-ichi [2 ]
Zendo, Takeshi [1 ]
Sonomoto, Kenji [1 ,3 ]
机构
[1] Kyushu Univ, Lab Microbial Technol, Div Appl Mol Microbiol & Biomass Chem,Higashi Ku, Dept Biosci & Biotechnol,Fac Agr,Grad Sch, Fukuoka 8128581, Japan
[2] Fukuoka Dent Coll, Sect Infect Biol, Dept Funct Biosci, Sawara Ku, Fukuoka 8140913, Japan
[3] Kyushu Univ, Lab Funct Food Design, Dept Funct Metab Design, Bioarchitecture Ctr,Higashi Ku, Fukuoka 8128581, Japan
基金
日本学术振兴会;
关键词
bacteriocin; cell wall inhibition; lantibiotic; lipid II; pore-forming peptide; PRECURSOR LIPID-II; PORE FORMATION; NUKACIN ISK-1; PEPTIDOGLYCAN BIOSYNTHESIS; MEMBRANE-BINDING; MODEL MEMBRANE; NISIN Z; MERSACIDIN; TARGET; ANTIBIOTICS;
D O I
10.1042/BST20120190
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Lantibiotics are ribosomally synthesized antimicrobial peptides that commonly target the cell wall precursor lipid II during their antimicrobial mechanism and exert their inhibitory activity by (i) inhibition of cell wall biosynthesis, and (ii) stable pore formation in the target membrane. Type-A(I) (i.e. nisin) and two-component (i.e. lacticin 3147) lantibiotics initially interact with lipid II to stabilize the complex, which then proceeds to inhibit cell wall biosynthesis and pore formation. Type-A(II) (i.e. nukacin ISK-1) and type-B (i.e. mersacidin) lantibiotics also use lipid II as a docking molecule, but can only inhibit cell wall biosynthesis without forming pores. In the present paper, we review the antimicrobial mechanism of different types of lantibiotics, their current progress and future prospect.
引用
收藏
页码:1528 / 1533
页数:6
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