The biofilm-forming phenotype of 14 isolates from four 'nonmain' subspecies of Yersinia pestis was compared with eight isolates from the more commonly studied 'main' or epidemic subspecies of Y. pestis in this study. The four nonmain subspecies are more geographically limited, and are associated with certain mammalian hosts and regions of the Caucasus and Central Asia, whereas the main subspecies spread worldwide during the historic plague pandemics. With the main subspecies pestis, pigmentation on Congo red medium (CR(+)) correlated with biofilm formation on both abiotic and biotic surfaces. Main subspecies pestis strains that do not produce pigmentation on Congo red medium (CR(-)) have a deletion that includes the hmsF and hmsS genes known to be required for biofilm formation. CR(-) strains of the nonmain subspecies, altaica and ulegeica, differed however from pestis and, while defective for biofilms on the two surfaces, both had intact hmsF and hmsS genes. The presence of rcsA was also investigated and results showed that it occurred with a 30-bp insertion in all forms of the subspecies. These findings suggest that biofilms are regulated differently in altaica and ulegeica than they are in pestis and also indicate that the rcsA pseudogene arose early in Y. pestis evolution, increasing the ability of the strain to form biofilm and thereby increasing its effective transmission.
Carried out was structural and functional analysis of nap genes coding for a significant diagnostic feature - nitrate reduction in main and non-main subspecies of Yersinia pestis. The presence of a single nucleotide substitution (A for T in position 631) in gene napA was determined to be the reason for the lack of nitrate reduction in part of the main subspecies strains. Other mutation - single nucleotide substitution G for A in position 1021 of napA is not the reason for absence of this diagnostic feature in non-main subspecies and biovar microtus as this substitution is present in denitrifying and nondenitrifying strains.
In non-pigmented and plasmid-deprived mutants-isogenic variants of highly virulent Yersinia pestis 231 strain-studied is the mechanism of biofilm formation on biotic surfaces, both in vitro (on the laboratory model of nematode Caenorhabdiitis elegans) and in vivo (inside the alimentary tract of Nosopsyllus laeviceps flea). It is determined that spontaneous loss of ability to form biofilms and generate pigmented colonies in the mutants is probably caused not only by the deletion of the whole chromosome pigmentation fragment, but also by a point(single base) mutation in structural hms operon. It is demonstrated that the absence of pCad, pFra or pPst plasmids does not have an impact on the ability of plasmid-deprived mutants to form biofilm on the cuticle of nematode C. elegans.
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