Global H-NS counter-silencing by LuxR activates quorum sensing gene expression
| Autor: | Julia C. van Kessel, Laura C Miller Conrad, Ryan R. Chaparian, Minh L N Tran, Douglas B. Rusch |
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| Rok vydání: | 2019 |
| Předmět: |
DNA
Bacterial Transcription Genetic Repressor Biology 03 medical and health sciences Bacterial Proteins Transcription (biology) Gene expression Escherichia coli Genetics Gene Silencing Promoter Regions Genetic Gene Transcription factor Vibrio 030304 developmental biology Regulation of gene expression 0303 health sciences Chemistry Activator (genetics) Sequence Analysis RNA 030306 microbiology Gene regulation Chromatin and Epigenetics Quorum Sensing food and beverages Promoter Gene Expression Regulation Bacterial biochemical phenomena metabolism and nutrition Bacterial Load Cell biology DNA-Binding Proteins Repressor Proteins Luminescent Proteins Quorum sensing Trans-Activators bacteria Autoinducer |
| Zdroj: | Nucleic Acids Research |
| ISSN: | 1362-4962 0305-1048 |
| DOI: | 10.1093/nar/gkz1089 |
| Popis: | Bacteria coordinate cellular behaviors using a cell-cell communication system termed quorum sensing. In Vibrio harveyi, the master quorum sensing transcriptional 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. |
| Databáze: | OpenAIRE |
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