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CpxAR of Actinobacillus pleuropneumoniae Contributes to Heat Stress Response by Repressing Expression of Type IV Pilus Gene apfA

ABSTRACT: CpxAR of Actinobacillus pleuropneumoniae Contributes to Heat Stress Response by Repressing Expression of Type IV Pilus Gene apfA

PROVIDER: PRJNA883725 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21685465_1.fastq.gz	Fastqsanger.gz
	SRR21685465_2.fastq.gz	Fastqsanger.gz
	SRR21685466_1.fastq.gz	Fastqsanger.gz
	SRR21685466_2.fastq.gz	Fastqsanger.gz
	SRR21685467_1.fastq.gz	Fastqsanger.gz

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CpxAR of Actinobacillus pleuropneumoniae Contributes to Heat Stress Response by Repressing Expression of Type IV Pilus Gene apfA

Project description:Acute pleuropneumonia in swine, caused by Actinobacillus pleuropneumoniae (APP), is characterized by a high and sustained fever. Fever creates an adverse environment for many bacteria leading to reduced bacterial proliferation; however, most pathogenic bacteria can tolerate higher temperatures. CpxAR is a two-component regulation system, ubiquitous among Gram-negative bacteria, which senses and responds to envelope alterations that are mostly associated with protein misfolding in the periplasm. Our previous study showed that CpxAR is necessary for the optimal growth of Actinobacillus pleuropneumoniae (APP) under heat stress. Here, we showed that mutation of the type IV pilin gene apfA rescued the growth defect of the cpxAR deletion strain under heat stress. RNA-seq analyses revealed that 265 genes were differentially expressed in the ∆cpxAR strains grown at 42°C, including genes involved in type IV pilus biosynthesis. We also demonstrated direct binding of the CpxR protein to the promoter of the apf operon by an electrophoretic mobility shift assay, and identified the binding site by a DNase I footprinting assay. In conclusion, our results revealed the important role of CpxAR in APP resistance to heat stress by directly suppressing the expression of ApfA.

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