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The role of TolB in Francisella tularensis Erythrocyte Invasion Caleb Martin#, Deanna Schmitt#, Alec Florjanczyk#, Edward Beaumont III#, Devin Sindeldecker#, Donald Primerano *, James Denvir *, and Joseph Horzempa# # Department of Natural Sciences and Mathematics, West Liberty University, West Liberty, WV * Genomics and Bioinformatics Core Facility, Marshall University, Huntington, WV Background and Objectives Francisella tularensis is the causative agent of a disease called tularemia. In the murine model of tularemia, F. tularensis bacteria invade erythrocytes. The bacteria do not replicate within erythrocytes. However, residing within these cells allows for increased colonization of the tick vector following acquisition of a blood meal – a situation that presumably increases transmission. We hypothesized that F. tularensis genes involved in erythrocyte invasion would be upregulated during exposure to these host cells. Methods RNAseq was used to identify differentially expressed F. tularensis genes in response to erythrocytes. Deletion of F. tularensis LVS tolB was generated via homologous recombination. Gentamicin protection assays were used to evaluate erythrocyte invasion. Results RNAseq revealed that approximately 7% of the F. tularensis genes were induced when exposed to erythrocytes. One of the most highly upregulated genes, tolB, encodes a protein responsible for the detection of environmental signals in other bacteria. Deletion of tolB significantly reduced the ability of F. tularensis to invade erythrocytes. Discussion and Conclusions Erythrocyte cues stimulate expression of F. tularensis genes required for erythrocyte invasion. TolB is required for erythrocyte invasion by F. tularensis. Supported by NIH Grant P20GM103434 to the West Virginia IDeA Network for Biomedical Research Excellence and through the WV Research Challenge Fund [HEPC.dsr.14.13]