Abstract
Guide RNA molecules (crRNA) produced from clustered regularly interspaced short palindromic repeat (CRISPR) arrays, altogether with effector proteins (Cas) encoded by cognate cas (CRISPR associated) genes, mount an interference mechanism (CRISPR-Cas) that limits acquisition of foreign DNA in Bacteria and Archaea. The specificity of this action is provided by the repeat intervening spacer carried in the crRNA, which upon hybridization with complementary sequences enables their degradation by a Cas endonuclease. Moreover, CRISPR arrays are dynamic landscapes that may gain new spacers from infecting elements or lose them for example during genome replication. Thus, the spacer content of a strain determines the diversity of sequences that can be targeted by the corresponding CRISPR-Cas system reflecting its functionality. Most Escherichia coli strains possess either type I-E or I-F CRISPR-Cas systems. To evaluate their impact on the pathogenicity of the species, we inferred the pathotype and pathogenic potential of 126 strains of this and other closely related species and analyzed their repeat content. Our results revealed a negative correlation between the number of I-E CRISPR units in this system and the presence of pathogenicity traits: the median number of repeats was 2.5-fold higher for commensal isolates (with 29.5 units, range 0–53) than for pathogenic ones (12.0, range 0–42). Moreover, the higher the number of virulence factors within a strain, the lower the repeat content. Additionally, pathogenic strains of distinct ecological niches (i.e., intestinal or extraintestinal) differ in repeat counts. Altogether, these findings support an evolutionary connection between CRISPR and pathogenicity in E. coli.
Highlights
CRISPR-Cas systems are composed of at least one array of clustered regularly interspaced short palindromic repeats (CRISPR) and a set of cas (CRISPR-associated) genes [1,2]
D9 and those ECOR strains not previously characterized was inferred following the criteria described in Materials and Methods. The robustness of these criteria was demonstrated by the high degree of coincidence between the pathotype described for categorized strains and the one predicted after the detection of the selected pathogenicity markers in the genomes of such strains (S1 Table)
The most striking difference involved strain EC23, which showed hemolytic activity in our tests and papG was amplified, even though these UPEC genes had not been detected in a previous Southern analysis [40]. This inconsistency might be due to low sequence conservation in this strain of the probes used in the Southern blot analyses. Another somehow unexpected result was the finding of some UPEC traits in several strains that had been deemed to be commensal E. coli (CEC) or EnPEC (S1 Table), which could be attributed to the great genome plasticity found in E. coli and the fact that genes, while present, may not necessarily be expressed [56,57]
Summary
CRISPR-Cas systems are composed of at least one array of clustered regularly interspaced short palindromic repeats (CRISPR) and a set of cas (CRISPR-associated) genes [1,2]. Several CRISPR-Cas types (denoted I, II and III) and subtypes (identified with an additional letter) are distinguished according to the identity of the associated cas genes [3]. Diverse tentative functions were initially postulated for particular systems [4,5,6,7], it has been demonstrated. CRISPR Impact on Pathogenicity in E. coli
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