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Flavobacterium covae

ABSTRACT: Flavobacterium covae overview

PROVIDER: PRJNA1059736 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR19406464_1.fastq.gz	Fastqsanger.gz
	SRR19406464_2.fastq.gz	Fastqsanger.gz
	SRR19406465_1.fastq.gz	Fastqsanger.gz
	SRR19406465_2.fastq.gz	Fastqsanger.gz

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Project description:Columnaris disease, caused by Flavobacterium covae, is one of three primary bacterial diseases that cause significant mortality and economic losses in farmed catfish (Ictalurus spp.). The quorum sensing gene luxR was reported to be upregulated in F. covae biofilm-grown cells stimulated with channel catfish (I. punctatus) mucus. To understand LuxR’s contributions to F. covae virulence, a F. covae C#2 luxR deletion mutant (ΔluxR) was created along with a complemented luxR (ΔluxR + pCE1). Channel catfish fingerlings challenged with the wild type or ΔluxR + pCE1 were observed to have 100% or 90% mortality, respectively; in contrast, only 2% mortality was observed for catfish fingerlings challenged with ΔluxR, indicating the important role for LuxR-regulated genes in F. covae virulence. A transcriptomic analysis indicated that LuxR-regulated genes in F. covae encode many functions including those associated with virulence, bacterial growth and metabolism, and survival during a fish infection. A decrease in biofilm formation was observed for ΔluxR relative to the wild-type and the complemented mutant, but only when mannose was included in the growth medium. The results of this study indicated that LuxR is a critical regulator of F. covae quorum sensing and virulence, warranting further research to identify and describe the relative contributions of LuxR-regulated virulence factors.

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