An investigation of the role of FTL_1711 in erythrocyte invasion by Francisella tularensis.

• DOI: 10.55632/pwvas.v97i2.1120
• Publication Date: 2025-04-08T15:27:00Z
• Authors: Audrey Blust; Joseph Horzempa
• Keywords: Tularemia; Francisella

Francisella tularensis is a pathogenic intracellular bacterium and the causative agent of zoonotic disease tularemia. The CDC classifies F. as Tier 1 select due to its potential for misuse biological weapon, given low infectious dose capacity produce fatal pneumonic infection. Furthermore, naturally occurring subspecies are known cause numerous human infections through exposure various blood-sucking arthropods contaminated animal hosts. Prior research conducted in our laboratory has demonstrated that FTL_1199 serves putative transcriptional regulator necessary erythrocyte invasion. Comprehensive transcriptome analysis further elucidated FTL_1711 an open reading frame regulated by FTL_1199. We hypothesize plays role invasion tularensis. In pursuit this objective, we will generate deletion mutant FTL_1711. During process, DNA flanking be cloned into unstable plasmid, pJH1. After integration chromosome homologous recombination, merodiploid resolved introducing pGUTS. This plasmid encodes enzyme force double-stranded break near target gene, facilitating Upon confirmation mutagenesis, evaluate ability strain invade erythrocytes, thereby revealing significance red blood cell