Members of Shewanella are ubiquitous in aquatic environments, some of which have been implicated in human infections. The progenitors of antibiotic resistance genes with clinical relevance, such as qnrA genes, have been identified in Shewanella. qnrA code for a pentapeptide repeat protein that protects type II topoisomerases, decreasing susceptibility to quinolones and fluoroquinolones. In this study, 248 genomes of 49 Shewanella species were analysed as well as 33 environmental isolates belonging to 10 Shewanella species. The presence of the qnrA gene was detected in 22.9% of the genomes and 15.2% of the isolates. The gene was more often detected in Shewanella algae , but was also detected in Shewanella carassii , Shewanella chilikensis , Shewanella haliotis and Shewanella indica . The identified genes encoded the previously described variants QnrA3 (in 22 genomes of one species), QnrA2 (eight genomes and three species), QnrA1 (six genomes and two species), QnrA7 (five genomes and two species), QnrA10 (two genomes of one species) and QnrA4 (one genome). In addition, 11 novel variants with 3 to 7 amino acid substitutions were identified (in 13 genomes and one environmental isolate). The presence of this gene appears to be species-specific although within some species several variants were detected. The study presents a previously unknown diversity of qnrA in Shewanella , highlighting the role of this genus as progenitor and reservoir of these genes. Further studies are needed to determine the phenotypes conferred by the new variants and the mechanisms that may mediate the transfer of these genes to new hosts.
Peptidyl‐prolyl cis‐trans isomerase C (Ppic) is expressed in several bone marrow (BM) hematopoietic progenitors and in T‐cell precursors. Since the expression profile of Ppic in the hematoimmune system was suggestive that it could play a role in hematopoiesis and/or T lymphocyte differentiation, we sought to test that hypothesis in vivo. Specifically, we generated a Ppic‐deficient mouse model by targeting the endogenous locus by CRISPR/Cas9 and tested the requirement of Ppic in hematopoiesis. Several immune cell lineages covering BM progenitors, lymphocyte precursors, as well as mature cells at the periphery were analyzed. While most lineages were unaffected, invariant NKT (iNKT) cells were reduced in percentage and absolute cell numbers in the Ppic‐deficient thymus. This affected the most mature stages in the thymus, S2 and S3, and the phenotype was maintained at the periphery. Additionally, immature transitional T1 and T2 B lymphocytes were increased in the Ppic‐deficient spleen, but the phenotype was lost in mature B lymphocytes. In sum, our data show that Ppic is dispensable for myeloid cells, platelets, erythrocytes, αβ, and γδ T lymphocytes in vivo in the steady state, while being involved in B‐ and iNKT cell differentiation.
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