Bovicins: The Bacteriocins of Streptococci and Their Potential in Methane Mitigation

Probiotics and Antimicrobial Proteins - Bovicin is a type AII lantibiotic, possessing two β-methyllanthionine and a disulfide bridge encoded by bovA gene hitherto unknown a couple of decades...     

The continuing story of class IIa bacteriocins.

Many bacteria produce antimicrobial peptides, which are also referred to as peptide bacteriocins. The class IIa bacteriocins, often designated pediocin-like bacteriocins, constitute the most dominant group of antimicrobial peptides produced by lactic acid bacteria. The bacteriocins that belong to this class are structurally related and kill target cells by membrane permeabilization. Despite their structural similarity, class IIa bacteriocins display different target cell specificities. In the search for new antibiotic substances, the class IIa bacteriocins have been identified as promising new candidates and have thus received much attention. They kill some pathogenic bacteria (e.g., Listeria) with high efficiency, and they constitute a good model system for structure-function analyses of antimicrobial peptides in general. This review focuses on class IIa bacteriocins, especially on their structure, function, mode of action, biosynthesis, bacteriocin immunity, and current food applications. The genetics and biosynthesis of class IIa bacteriocins are well understood. The bacteriocins are ribosomally synthesized with an N-terminal leader sequence, which is cleaved off upon secretion. After externalization, the class IIa bacteriocins attach to potential target cells and, through electrostatic and hydrophobic interactions, subsequently permeabilize the cell membrane of sensitive cells. Recent observations suggest that a chiral interaction and possibly the presence of a mannose permease protein on the target cell surface are required for a bacteria to be sensitive to class IIa bacteriocins. There is also substantial evidence that the C-terminal half penetrates into the target cell membrane, and it plays an important role in determining the target cell specificity of these bacteriocins. Immunity proteins protect the bacteriocin producer from the bacteriocin it secretes. The three-dimensional structures of two class IIa immunity proteins have been determined, and it has been shown that the C-terminal halves of these cytosolic four-helix bundle proteins specify which class IIa bacteriocin they protect against.     

Factors and genetics of pathogenicity of group B Streptococci

In this review data on the pathogenicity factors of streptococci and their genetic control are presented. Attention is paid mainly to protein antigens alpha and beta, C5a peptidase, CAMP factor, R, Rib and X proteins. The problems of making the genetic and physical charts of the genome of group B streptococci, the genetic regulation of the synthesis of pathogenicity factors and the specific features of the damaging action of the infective agent are discussed.     

Classification and mode of action of membrane-active bacteriocins produced by gram-positive bacteria

Bacteriocins are ribosomally synthesized antimicrobial peptides produced by microorganisms belonging to different eubacterial taxonomic branches. Most of them are small cationic membrane-active compounds that form pores in the target cells, disrupting membrane potentials and causing cell death. The production of small cationic peptides with antibacterial activity is a defense strategy found not only in bacteria, but also in plants and animals. Bacteriocins are classified according to different criteria by different authors; in this review, we will summarize the principal bacteriocin classifications, highlight their main physical and chemical characteristics, and describe the mechanism of some selected bacteriocins that act at the membrane level.     

The ecology and evolution of bacteriocins

In this review we focus on the ecological and evolutionary forces that determine the frequency and diversity of colicins inEscherichia coli. To begin, we describe that this killing phenotype is ubiquitous inE. coli, with as many as 50% of the isolates from a population producing colicin toxins, and that each population sampled has its own unique distribution of the more than 20 known colicin types. Next, we explore the dynamics of colicinogeny, which exhibits a typical form of frequency dependence, where the likelihood of successful colicin invasion into a population increases as the initial density of colicinogenic cells increases. We then incorporate thoughts on the evolution of chromosomal resistance to colicins and describe how resistance might influence the dynamics of colicinogen invasion and maintenance and the resulting colicin diversity. The final section deals with a genetic and phylogenetic characterization of colicins and a discussion of the evolutionary mechanisms responsible for generating colicin diversity. In this final section we provide details of the different molecular mechanisms known to play a role in generating colicin diversity, including the two most dominant forces in colincin evolution: recombination and positive, deversifying, selection.     

Transmission of Bacteriocinogenicity by Conjugation in Group D Streptococci

Seventy-seven out of eighty-one group D streptococcal strains isolated from humans and animals were found to produce bacteriocins that were active on other streptococcal strains of gorup A and D, but inactive on their own cells. On the bases of the spectra of indicator strains, and the sensitivities to heat, chloroform, and trypsin, seven types of bacteriocins were classified. Streptococcus faecalis var. liquefaciens strain 4532 or strain A (liq-A) was UV-irradiated, and mutants which lost bacteriocin- as well as the β-hemolysin-forming activities (Bact^–.Hem^–) were obtained. Cells of the type I bacteriocin producer (SM^r.TC^r.Bact-I⁺.Hem⁺) and nonproducer 2025 (PC^r.Bact-I^–.Hem^–), both belonging to S. faecalis var. liquefaciens, were mixed and incubated in broth. Recombinants (PC^r.-SM^s.TC^s.Bact-I⁺.Hem⁺) were obtained at a high frequency (5.8% preinoculum size of PC^r.-Bact-I^–.Hem^–), and the character was stable for at least ten transfers. In the mixed culture, a marked decrease in the recipient 2025 cell number was observed. The occurrence of recombinants was not inhibited by deoxyribonuclease. A cell-free filtrate of Bact⁺.Hem⁺ cells mixed with Bact^–.Hem^– cells did pot cause a mutation of the latter combined characters. The transfer of a genetic marker is discussed as an event of the cell-to-cell contact.