Temperature Control of psaA Expression by PsaE and PsaF in Yersinia pestis

• Published in: Journal of bacteriology 2019-08, Vol.201 (16)
• Main Authors: Quinn, Joshua D, Weening, Eric H, Miner, Taryn A, Miller, Virginia L
• Format: Article
• Language: English
• Subjects: Antibodies; Antigens; Bacteriology; Bubonic plague; Gene expression; Gene regulation; High temperature; pH effects; Plague; Post-transcription; Pseudotuberculosis; Spotlight; Stability; Temperature control; Temperature effects; Temperature requirements; Translation; Virulence; Yersinia pestis
• ISSN: 0021-9193; 1098-5530
• DOI: 10.1128/JB.00217-19

PsaA, the subunit of the fimbria originally referred to as the "pH 6 antigen," is required for full virulence of during bubonic plague. The expression of is dependent upon specific environmental signals, and while the signals (high temperature and acidic pH) are defined, the mechanisms underlying this regulation remain unclear. In the closely related species , transcription requires two regulatory genes, and , and it is speculated that posttranscriptional regulation of PsaE and/or PsaF contributes to the regulation of transcription. Few studies have examined the regulation of expression in , and prior to this work, the roles of and in had not been defined. The data presented here show that both and are required for transcription in and that the impact of temperature and pH is mediated through discrete posttranscriptional effects on PsaE and PsaF. By generating antibodies that recognize endogenous PsaE and PsaF, we determined that the levels of both proteins are impacted by temperature and pH. High temperature is required for and translation via discrete mechanisms mediated by the mRNA 5' untranslated region (UTR) upstream of each gene. Additionally, levels of PsaE and PsaF are impacted by pH. We show that PsaF enhances the stability of PsaE, and thus, both PsaE and PsaF are required for transcription. Our data indicate that the environmental signals (temperature and pH) impact the expression of by affecting the translation of and and the stability of PsaE and PsaF. is a Gram-negative bacterial pathogen that causes bubonic plague. As a vector-borne pathogen, fluctuates between an arthropod vector (flea) and mammalian host. As such, must recognize environmental signals encountered within each host environment and respond by appropriately regulating gene expression. PsaA is a key mammalian virulence determinant that forms fimbriae. Our work provides evidence that utilizes multiple posttranscriptional mechanisms to regulate the levels of two PsaA regulatory proteins in response to both temperature and pH. This study offers insight into mechanisms that bacteria utilize to sense environmental cues and regulate the expression of determinants required for mammalian disease.