Prfa: A Transcriptional Activator Protein of Facultative Bacterium Listeria Monocytogenes

PrfA is a transcriptional activator protein of facultative bacterium, Listeria monocytogenes. This microbe is an opportunistic intracellular pathogen mainly responsible for human foodborne infections worldwide.1 The pathogen especially causes Listerosis in humans upon invasion and is found in wild and domestic animals, water and soil.2 PrfA, is a27 kDa DNA binding protein and belongs to Crp/Fnr family of transcriptional activators.3 It is very specific in recognizing PrfA-dependent promoters that contain a 14-bp palindrome ,PrfA box.4 The PrfA protein is homologous to Escherichia coli cyclic AMP (cAMP) receptor protein (Crp) in structure and function.5

PrfA gene is considered as the main contributor of L. monocytogenes pathogenesis Its depletion from the bacterial strains was also reported to result in non- virulence in mouse models of infection. 6, 7

PrfA gene which encodes PrfA protein is controlled by three unique promoters namely, prfAP1, prfAP2 and plcA.8-10 PrfA is thought to mainly interact with plcA promoter and undergoes a positive self –regulated expression. This results in prfA–plcA transcript formation and an increased PrfA synthesis that becomes pivotal for the bacterial intracellular spread and virulence.9,10

PrfA serves as a virulence regulator as it coordinates and differentially controls the cascade of events in the infection process. These are eukaryotic cell internalization, phagosome lysis, host cytoplasmic multiplication and motility, intracellular distribution and final double-membrane vacuole lysis during neighboring cell entry.11

Interestingly, this diverse regulatory action of PrfA has not been given adequate research focus in the recent years. Therefore, this has drawn our attention to carry out a revie...

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...ht to be altered differently by mutations19. Scientists have identified mutations like PrfA G155S,PrfA E77K ,19 prfA Y63C/Y154C,30,31 and prfA P219S.25 This implies tthat mutation studies may have good future implications for further understanding the differential PrfA gene activity and its impact on virulence gene expression. Most importantly, problem s like poor bacterial resistance could be studied and solution could be sought through novel approaches that target the PrfA protein functional activity.

Conclusion:

In conclusion, PrfA protein essential for Listeriosis appears to rely on a given environmental stimuli. This could trigger a necessity of factors like additional regulatory components, metabolic shifts, mutant driven activity for differential regulation of bacterial virulence gene products. Further studies are suggestive for strengthening this concept.