Microbial Mechanisms of Heat Sensing

Abstract

Temperature is one of the ubiquitous signals that control both the development as well as virulence of various microbial species. Therefore their survival is dependent upon initiating appropriate response upon temperature fluctuations. In particular, pathogenic microbes exploit host-temperature sensing mechanisms for triggering the expression of virulence genes. Many studies have revealed that the biomolecules within a cell such as DNA, RNA, lipids and proteins help in sensing change in temperature, thereby acting as thermosensors. This review shall provide an insight into the different mechanisms of thermosensing and how they aid pathogenic microbes in host invasion.

Keywords: Microbes; Pathogen; Temperature; Thermosensors; Virulence.

Fig. 1

Schematic diagram depicting the role of various thermosensors present inside the cell upon heat stress. The increase in temperature such as 37 °C not only acts as heat stress signal for microbes but also serves as a good indicator of host invasion in case of pathogenic microbes. The increase in temperature often leads to the protein unfolding inside the cell which activates the chaperones such as DnaK and DnaJ which assist in protein folding. High temperature also activates other DNA binding proteins such as CtsR and RovA and leads to the transcription of Hsps and invasion proteins required for pathogenesis respectively. Increase in temperature also affects the local DNA structures and thus the binding of regulatory proteins such as H-NS. This causes the expression of genes such as VirF which is required for virulence. Moreover, stability of RNA thermometers present in the UTR of genes like Hsps and tviA is affected by heat stress thereby leading to translation of Hsps and tviA protein. tviA functions as a transcriptional regulator of virulence factors. Certain microbes synthesize modified lipids such as lipid A upon change in temperature to protect itself from host immune response

Fig. 2

Functioning of various thermosensors inside the cell. a DNA thermosensor. H-NS proteins affects the DNA bending and transcription process, as increase in temperature disables the formation of higher-order oligomers, thereby leading to opening of bent DNA and allowing RNA Polymerase to proceed transcription. b RNA thermosensor. The formation of RNA thermometer at low temperatures leads to the pairing of the Shine Dalgarno sequence and the AUG start codon. The rise in temperatures causes melting of the structure which permits the binding of the ribosome (30S and 50S) and allows translation. c Protein thermosensor. The repressor proteins forms dimmer and bind to the DNA at normal temperatures, thereby blocking its transcription. Upon heat shock, these proteins lose their conformation and dissociate from the DNA, allowing transcription to occur