Global H-NS counter-silencing by LuxR activates quorum sensing gene expression.
Nucleic Acids Res, 2020/01/10;48(1):171-183.
Chaparian RR[1], Tran MLN[2], Miller Conrad LC[2], Rusch DB[3], van Kessel JC[1]
Affiliations
PMID: 31745565DOI: 10.1093/nar/gkz1089
Impact factor: 19.16
Abstract
Bacteria coordinate cellular behaviors using a cell-cell communication system termed quorum sensing. In Vibrio harveyi, the master quorum sensing transcription factor LuxR directly regulates >100 genes in response to changes in population density. Here, we show that LuxR derepresses quorum sensing loci by competing with H-NS, a global transcriptional repressor that oligomerizes on DNA to form filaments and bridges. We first identified H-NS as a repressor of bioluminescence gene expression, for which LuxR is a required activator. In an hns deletion strain, LuxR is no longer necessary for transcription activation of the bioluminescence genes, suggesting that the primary role of LuxR is to displace H-NS to derepress gene expression. Using RNA-seq and ChIP-seq, we determined that H-NS and LuxR co-regulate and co-occupy 28 promoters driving expression of 63 genes across the genome. ChIP-PCR assays show that as autoinducer concentration increases, LuxR protein accumulates at co-occupied promoters while H-NS protein disperses. LuxR is sufficient to evict H-NS from promoter DNA in vitro, which is dependent on LuxR DNA binding activity. From these findings, we propose a model in which LuxR serves as a counter-silencer at H-NS-repressed quorum sensing loci by disrupting H-NS nucleoprotein complexes that block transcription.
MeSH terms
Bacterial Load; Bacterial Proteins; DNA, Bacterial; DNA-Binding Proteins; Escherichia coli; Gene Expression Regulation, Bacterial; Gene Silencing; Luminescent Proteins; Promoter Regions, Genetic; Quorum Sensing; Repressor Proteins; Sequence Analysis, RNA; Trans-Activators; Transcription, Genetic; Vibrio
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