Journal article
Bacterial sensing: A putative amphipathic helix in RsiV is the switch for activating σV in response to lysozyme
PLoS genetics, Vol.14(7), pp.e1007527-e1007527
07/2018
DOI: 10.1371/journal.pgen.1007527
PMCID: PMC6066255
PMID: 30020925
Abstract
Extra Cytoplasmic Function (ECF) σ factors are a diverse group of alternate σ factors bacteria use to respond to changes in the environment. The Bacillus subtilis ECF σ factor σV responds to lysozyme. In the absence of lysozyme, σV is held inactive by the anti-σ factor, RsiV. In the presence of lysozyme RsiV is degraded via regulated intramembrane proteolysis, which results in the release of σV and thus activation of lysozyme resistance genes. Signal peptidase is required to initiate degradation of RsiV. Previous work indicated that RsiV only becomes sensitive to signal peptidase upon direct binding to lysozyme. We have identified a unique domain of RsiV that is responsible for protecting RsiV from cleavage by signal peptidase in the absence of lysozyme. We provide evidence that this domain contains putative amphipathic helices. Disruption of the hydrophobic surface of these helices by introducing positively charged residues results in constitutive cleavage of RsiV by signal peptidase and thus constitutive σV activation. We provide further evidence that this domain contains amphipathic helices using a membrane-impermeable reagent. Finally, we show that upon lysozyme binding to RsiV, the hydrophobic face of the amphipathic helix becomes accessible to a membrane-impermeable reagent. Thus, we propose the amphipathic helices protect RsiV from cleavage in the absence of lysozyme. Additionally, we propose the amphipathic helices rearrange to form a suitable signal peptidase substrate upon binding of RsiV to lysozyme leading to the activation of σV.
Details
- Title: Subtitle
- Bacterial sensing: A putative amphipathic helix in RsiV is the switch for activating σV in response to lysozyme
- Creators
- Lincoln T Lewerke - Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA, United States of AmericaPaige J Kies - Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA, United States of AmericaUte Müh - Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA, United States of AmericaCraig D Ellermeier - Graduate Program in Genetics, University of Iowa, Iowa City, IA, United States of America
- Resource Type
- Journal article
- Publication Details
- PLoS genetics, Vol.14(7), pp.e1007527-e1007527
- DOI
- 10.1371/journal.pgen.1007527
- PMID
- 30020925
- PMCID
- PMC6066255
- NLM abbreviation
- PLoS Genet
- ISSN
- 1553-7390
- eISSN
- 1553-7404
- Publisher
- Public Library Science
- Grant note
- R01 AI087834 / NIAID NIH HHS
- Language
- English
- Date published
- 07/2018
- Academic Unit
- Microbiology and Immunology
- Record Identifier
- 9984083877402771
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