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Characterization of the Late Response of Neisseria gonorrhoeae F62 to Iron and Fur

ABSTRACT: Characterization of the Late Response of Neisseria gonorrhoeae F62 to Iron and Fur

PROVIDER: PRJNA600738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10874207.fastq.gz	Fastqsanger.gz
	SRR10874208.fastq.gz	Fastqsanger.gz
	SRR10874209.fastq.gz	Fastqsanger.gz
	SRR10874210.fastq.gz	Fastqsanger.gz
	SRR10874211.fastq.gz	Fastqsanger.gz

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Characterization of the Late Response of Neisseria gonorrhoeae F62 to Iron and Fur

Project description:In this study wild-type, fur mutant, and complemented fur mutant strains of the human pathogen Neisseria gonorrhoeae F62 were grown under high (100 uM iron) or low (100 uM desferal) iron conditions to identify genes whose expression was regulated by iron and/or Fur. This study looked at the response 3 hours after the addition of iron or desferal.

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Project description:Previous studies have shown that the MpeR transcriptional regulator produced by Neisseria gonorrhoeae represses expression of mtrF, which encodes a putative inner membrane protein that works with the MtrC-MtrD-MtrE efflux pump to allow gonococci to resist high levels of multiple hydrophobic antimicrobials. Regulation of mpeR has been reported to occur by an iron-dependent mechanism involving Fur (Ferric uptake regulator). Collectively, these observations suggest the presence of an interconnected regulatory system in gonococci that modulates expression of drug efflux pump protein-encoding genes in an iron-responsive manner. Herein, we describe this connection and report that levels of gonococcal resistance to a substrate of the mtrCDE-encoded efflux pump can be modulated by MpeR and the availability of free iron. Using microarray analysis, we found that the mtrR gene, which encodes the direct transcriptional repressor (MtrR) of mtrCDE, is an MpeR-repressed determinant in the late-logarithmic phase of growth when free iron levels would be reduced due to bacterial consumption. MpeR-mediated repression of mtrR appeared to be direct, as judged by DNA-binding analyses, and was enhanced by conditions of iron-limitation, which resulted in increased expression of the mtrCDE efflux pump operon. Taken together, our results indicate that both genetic and physiologic parameters can influence expression of the mtr efflux system and that these can modulate levels of gonococcal susceptibility to efflux pump substrates.

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