Relationship Exploration Of Mobile Element Mediated Drug-resistance And CRISPR Loci

Enterococcus faecalis is gram-positive spherical cocci. It have been neglected because of being a natural member of the digestive microflora in humans and many other animals. Subsequently, the bacterium was known as the most important pathogen resulted in nosocomialtion and multidrug. For many bacteria, including the opportunistically pathogenic enterococci, antibiotic resistance is mediated by acquisition of new DNA and is frequently encoded on mobile DNA elements such as plasmids and transposons. Certain enterococcal lineages have recently emerged that are characterized by abundant mobile DNA, including numerous viruses (phage), and plasmids and transposons encoding multiple antibiotic resistances. These mobile elemens constitute up to25%of the genome of multidrug-resistant (MDR) enterococci. These lineages cause hospital infection outbreaks around the world. The striking influx of mobile DNA into these lineages is in contrast to what would be expected if a self (genome)-defense system was present. Clustered, regularly interspaced short palindromic repeat (CRISPR) defense is a discovered mechanism of prokaryotic self-defense that provides a type of acquired immunity recently.The results of this assay indicated that no significance difference have been observed between CRISPR loci and attendance of multidrug resistance gene mediated by mobile elements, that is to say, the strain which contain CRISPR loci have a low carrying rate of multidrug resistance genes. On the other hand, the strains which contain CRISPR loci have low recall rate of drug-resistance phenotype. So we can conclude that the new spacer of CRISPR loci generated maybe not at the time of attacking by foreign gene, but at the time of transcription of foreign gene. That is to say, when the foreign gene transcript to mRNA. RNAi will degradate to siRNA, and the siRNA will be integrated into CRISPR loci as a new spacer. On the other hand, the length of siRNA and spacer of CRISP loci are all20-30bp, maybe this is a proof to our conclusion. But whether this presume is right, more data are needed to prove.