The Pleiotropic Phenotypes Caused by an Hfq Null Mutation in Vibrio Harveyi

Hfq is a global regulator and can be involved in multiple cellular processes by assisting small regulatory RNAs (sRNAs) to target mRNAs. To gain insight into the virulence regulation of Hfq in Vibrio harveyi, the hfq null mutant, ∆hfq, was constructed in V. harveyi strain 345. Compared with the wild-type strain, the mortality of pearl gentian sharply declined from 80% to 0% in ∆hfq when infected with a dose that was 7.5-fold the median lethal dose (LD50). Additionally, ∆hfq led to impairments of bacterial growth, motility, and biofilm formation and resistance to reactive oxygen species, chloramphenicol, and florfenicol. A transcriptome analysis indicated that the expression of 16.39% genes on V. harveyi 345 were significantly changed after the deletion of hfq. Without Hfq, the virulence-related pathways, including flagellar assembly and bacterial chemotaxis, were repressed. Moreover, eleven sRNAs, including sRNA0405, sRNA0078, sRNA0419, sRNA0145, and sRNA0097, which, respectively, are involved in chloramphenicol/florfenicol resistance, outer membrane protein synthesis, electron transport, amino acid metabolism, and biofilm formation, were significantly down-regulated. In general, Hfq contributes to the virulence of V. harveyi 345 probably via positively regulating bacterial motility and biofilm formation. It is involved in flagellar assembly and bacterial chemotaxis by binding sRNAs and regulating the target mRNAs.