Bacteriocinogenia, un sistema de antagonismo bacteriano / Bacteriocinogenia, a system for bacterial antagonism

ABSTRACT

Bacterial antagonism depends on many factors. Among others, for example we have competition for an essential nutrient, the production of toxic metabolites or the release of antibiotic substances. The production of bacteriocines by "killer" strains correspons to the latrer, being determined by plasmidial or chromosomal genes. On the other hand, the susceptibility to a given bacteriocine depends on the presence of surface recptors that are codified by the cellular DNA. The bacteriocine particles correspond to protein conglomerates which are sometimes associated with glucolipids. With the death of the productive cell, these particles are livated motivated by synthesis. The similarities which they share with the bacteriophage are many. However, their fundamental differences are that they lack nuclic acid and their incapcity to transmit themselves. Cellular death caused by the action of the bacteriocine is extremely quck, acting on the permeability of the plasmatic membrane, on the macromolecular syntesis (DNA, RNA an proteins) and on cellular oxidation. The wide range of bacteriocine and their respective spectre of action over the more or less related strains are excellent parameters to detect, identify and classify the productive bacteria and the susceptible ones. With only a few exceptions, the bacteriocines not lethal to their own productive cell nor to taxonomically distant species. This has led to intersting ecological and epidemiological outlooks. The amplitude of this phenomenon in Gram+ and Gram- bacteria has led to the study of fine mechanisms which have triggered the genetic expression to elaborate bacteriocines, determining the one responsible for this are the genes and localized signals in transmissible episomes or in chromosomal operons