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6. mecanismos de resistencia a bacteriófagos
Programmed genetic variation increases the diversity of the bacterial innate and adaptive immune response, allowing bacteria to resist rapid-evolving phages. Here we review three bacterial immunity mechanisms that are subjected to programmed genetic variation: first, the modification of surface elements that serve as phage receptors, second, thediversification of restriction–modification (RM) systems that attack phage genomes, and third, the generation of an arsenal of antiphage sequences in CRISPR loci.

_ their host range is most of the time limited to only a few strains of a given bacterial species. They thus rely on the specific binding of cell surface receptors to inject their DNA productively in appropriate host cells. Bacteria canprevent phage docking by mutating cell surface receptors. Early experiments on the coliphage lambda have shown that missense mutations in the phage receptor gene (lamB) can affect phage absorption and lead to tight resistance. . Phase variation enables bacteria to switch between different types of surface receptors at high frequencies to generate immunity against bacteriophages.

_RM : Theyconsist of two or more genes encoding a sequence-specific restriction endonuclease that cleaves exogenous dsDNA, and a DNA methylase that modifies specific bases of the bacterial genetic material to protect it from the restriction endonuclease. RM systems frequently differ between strains of the same bacterial species due to their presence on mobile genetic elements. Bacteriophages that attemptpropagation in different strains lack the protective DNA methylation pattern of the new host; therefore, their genomic DNA becomes substrate for restriction endonucleases and the cell is protected from infection.
http://www.sciencedirect.com.biblioteca.uniandes.edu.co:8080/science/article/pii/S0952791511001518


bacteria use a system, apparently akin to the RNA interference (RNAi) system of higherorganisms, to block phage reproduction, thus making them resistant to infection.
first biological evidence for a function of so-called CRISPR sequences. These sequences, formally known by the descriptive name of “clustered regularly interspaced short palindromic repeats” because of the way they are arranged in the genome, are widely distributed in the genomes of both Bacteria and Archaea.Accompanying the CRISPR sequences are a suite of perhaps four to 10 cas (CRISPR-associated) genes.
In a second analysis, published by Biology Direct on 16 March of last year, Makarova, Koonin, and colleagues proposed that the Cas proteins and CRISPR spacer sequences, which were presumably picked up by the bacteria during prior phage infections, together constitute a bacterial immune system that worksby a mechanism similar to that of RNAi in higher organisms. The idea is that the spacers make short RNA sequences that can bind to complementary sequences in messenger RNAs made by invading phages. This would block their translation into proteins and mark them for degradation by Cas proteins, some of which resemble those known to be involved in RNAi.
In addition to matching phage, the spacersalso match chromosomal and plasmid sequences,” he notes, and thus they might help control normal bacterial gene activity.
http://www.sciencemag.org.biblioteca.uniandes.edu.co:8080/content/315/5819/1650.1.full?sid=1e3c318c-99dc-4836-b181-038449b6f5e7
CRISPR-mediated adaptive immunity. CRISPR immunity can be divided into two distinct phases. During CRISPR adaptation new spacer sequences (coloredbars) are introduced in the repeat array. These sequences are present in bacteriophages and plasmids that invade the bacterium. It is hypothesized that foreign DNA is cut by the Cas1 endonuclease and integrated into the CRISPR locus. Spacer incorporation always occurs at the end proximal to the leader sequence (white box) and is accompanied by the replication of a repeat (black bars). During the...