Comparative genomic analysis of Myroides odoratimimus isolates.

Myroides odoratimimus is an important nosocomial pathogen. Management of M. odoratimimus infection is difficult owing to the multidrug resistance and the unknown pathogenesis mechanisms. Based on our previous genomic sequencing data of M. odoratimimus PR63039 (isolated from a patient with the urinary tract infection), in this study, we further performed comparative genomic analysis for 10 selected Myroides strains. Our results showed that these Myroides genome contexts were very similar and phylogenetically related. Various prophages were identified in the four clinical isolate genomes, which possibly contributed to the genome evolution among the Myroides strains. CRISPR elements were only detected in the two clinical (PR63039 and CCUG10230) isolates and two environmental (CCUG12700 and H1bi) strains. With more stringent cutoff parameters in CARD analysis, the four clinical M. odoratimimus contained roughly equal antibiotic resistance genes, indicating their similar antibiotic resistance profiles. The three clinical (CCUG10230, CCUG12901, CIP101113) and three environmental (CCUG12700, L41, H1bi) M. odoratimimus strains were speculated to carry the indistinguishable virulent factors (VFs), which may involve in the similar pathogenesis mechanism. Moreover, some VFs might confer to the high capacity of dissemination, attacking tissue cells and induction of autoimmune complications. Our results facilitate the research of antibiotic resistance and the development of therapeutic regimens for the M. odoratimimus infections.

Colcemid inhibits the rejoining of the nucleotide excision repair of UVC-induced DNA damages in Chinese hamster ovary cells.

In our previous study, we found that colcemid, an inhibitor of mitotic spindle, promotes UVC-induced apoptosis in Chinese hamster ovary cells (CHO.K1). In this study, a brief treatment of colcemid on cells after but not before UV irradiation could synergistically reduce the cell viability. Although colcemid did not affect the excision of UV-induced DNA damages such as [6-4] photoproducts or cyclobutane pyrimidine dimers, colcemid accumulated the DNA breaks when it was added to cells following UV-irradiation. This colcemid effect required nucleotide excision repair (NER) since the same accumulation of DNA breaks was barely or not detected in two NER defective strains of CHO cells, UV5 or UV24. Furthermore, the colcemid effect was not due to semi-conservative DNA replication or mitosis since the colcemid-caused accumulation of DNA breaks was also seen in non-replicating cells. Moreover, colcemid inhibited rejoining of DNA breaks accumulated by hydroxyurea/cytosine arabinoside following UV irradiation. Nevertheless, colcemid did not affect the unscheduled DNA synthesis as assayed by the incorporation of bromodeoxyuridine. Taken together, our results suggest that colcemid might inhibit the step of ligation of NER pathways.