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Transcriptional response of Pseudomonas aeruginosa to the prebiotic Fructooligosaccharide

ABSTRACT: Transcriptional response of Pseudomonas aeruginosa to the prebiotic Fructooligosaccharide

PROVIDER: PRJNA512099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8377190.fastq.gz	Fastqsanger.gz
	SRR8377191.fastq.gz	Fastqsanger.gz
	SRR8377186.fastq.gz	Fastqsanger.gz
	SRR8377187.fastq.gz	Fastqsanger.gz
	SRR8377188.fastq.gz	Fastqsanger.gz

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Transcriptional response of Pseudomonas aeruginosa to the prebiotic Fructooligosaccharide

Project description:The bifidogenic effect of the prebiotic inulin and its hydrolysed form (fructoligosaccharide, FOS) is well established since they promote the growth of specific beneficial (probiotic) gut bacteria such as bifidobacteria. Previous studies of the opportunistic nosocomial pathogen Pseudomonas aeruginosa PAO1 have shown that inulin and FOS reduce growth, biofilm formation, through decrease of its ability to motility and exotoxin secretion. However, the transcriptional basis for these phenotypic alterations remains unclear. To address this question we conducted RNA-sequence analysis. In most cases changes in the transcript level induced by inulin and FOS were similar. However, a set of transcripts were increased in expression response to inulin, but reduced in the presence of FOS. In the presence of inulin or FOS 260 and 217 transcript levels, respectively, were altered as compared to the control to which no polysaccharide was added. Importantly, changes in transcript levels of 57 and 83 genes were found to be specific for either inulin or FOS, respectively, indicating that both compounds trigger different changes. Gene pathway analysis of different exposure genes (DEG) revealed a specific FOS-mediated reduction in transcript levels of genes that participate in several canonical pathways involved in metabolism and growth, motility, biofilm formation, β-lactam resistance and in the modulation of type III and VI secretion system which were supported by real time quantitative PCR measurements. These results may provide solid information to suggest that FOS selectively modulates the P. aeruginosa PAO1 pathogenecity through distinct signaling pathways.

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