The Role of the sigB Gene in the General Stress Response of Listeria monocytogenes Varies between a Strain of Serotype 1/2a and a Strain of Serotype 4c

2003 ◽  
Vol 46 (6) ◽  
pp. 461-466 ◽  
Author(s):  
Sandra M. Moorhead ◽  
Gary A. Dykes
2011 ◽  
Vol 193 (23) ◽  
pp. 6629-6638 ◽  
Author(s):  
A. Kaczmarczyk ◽  
S. Campagne ◽  
F. Danza ◽  
L. C. Metzger ◽  
J. A. Vorholt ◽  
...  

Structure ◽  
2016 ◽  
Vol 24 (8) ◽  
pp. 1237-1247 ◽  
Author(s):  
Sébastien Campagne ◽  
Sebastian Dintner ◽  
Lisa Gottschlich ◽  
Maxence Thibault ◽  
Miriam Bortfeld-Miller ◽  
...  

2011 ◽  
Vol 39 (5) ◽  
pp. 1514-1519 ◽  
Author(s):  
Matthias Müller ◽  
Andreas S. Reichert

Autophagy is a fundamental cellular process promoting survival under various environmental stress conditions. Selective types of autophagy have gained much interest recently as they are involved in specific quality control mechanisms removing, for example, aggregated proteins or dysfunctional mitochondria. This is considered to counteract the development of a number of neurodegenerative disorders and aging. Here we review the role of mitophagy and mitochondrial dynamics in ensuring quality control of mitochondria. In particular, we provide possible explanations why mitophagy in yeast, in contrast with the situation in mammals, was found to be independent of mitochondrial fission. We further discuss recent findings linking these processes to nutrient sensing pathways and the general stress response in yeast. In particular, we propose a model for how the stress response protein Whi2 and the Ras/PKA (protein kinase A) signalling pathway are possibly linked and thereby regulate mitophagy.


2016 ◽  
Vol 82 (13) ◽  
pp. 4017-4027 ◽  
Author(s):  
Beth O'Donoghue ◽  
Kerrie NicAogáin ◽  
Claire Bennett ◽  
Alan Conneely ◽  
Teresa Tiensuu ◽  
...  

ABSTRACTListeria monocytogenessenses blue light via the flavin mononucleotide-containing sensory protein Lmo0799, leading to activation of the general stress response sigma factor SigB (σB). In this study, we investigated the physiological response of this foodborne pathogen to blue light. We show that blue light (460 to 470 nm) doses of 1.5 to 2 mW cm−2cause inhibition of growth on agar-based and liquid culture media. The inhibitory effects are dependent on cell density, with reduced effects evident when high cell numbers are present. The addition of 20 mM dimethylthiourea, a scavenger of reactive oxygen species, or catalase to the medium reverses the inhibitory effects of blue light, suggesting that growth inhibition is mediated by the formation of reactive oxygen species. A mutant strain lacking σB(ΔsigB) was found to be less inhibited by blue light than the wild type, likely indicating the energetic cost of deploying the general stress response. When a lethal dose of light (8 mW cm−2) was applied to cells, the ΔsigBmutant displayed a marked increase in sensitivity to light compared to the wild type. To investigate the role of the blue-light sensor Lmo0799, mutants were constructed that either had a deletion of the gene (Δlmo0799) or alteration in a conserved cysteine residue at position 56, which is predicted to play a pivotal role in the photocycle of the protein (lmo0799C56A). Both mutants displayed phenotypes similar to the ΔsigBmutant in the presence of blue light, providing genetic evidence that residue 56 is critical for light sensing inL. monocytogenes. Taken together, these results demonstrate thatL. monocytogenesis inhibited by blue light in a manner that depends on reactive oxygen species, and they demonstrate clear light-dependent phenotypes associated with σBand the blue-light sensor Lmo0799.IMPORTANCEListeria monocytogenesis a bacterial foodborne pathogen that can cause life-threatening infections in humans. It is known to be able to sense and respond to visible light. In this study, we examine the effects of blue light on the growth and survival of this pathogen. We show that growth can be inhibited at comparatively low doses of blue light, and that at higher doses,L. monocytogenescells are killed. We present evidence suggesting that blue light inhibits this organism by causing the production of reactive oxygen species, such as hydrogen peroxide. We help clarify the mechanism of light sensing by constructing a “blind” version of the blue-light sensor protein. Finally, we show that activation of the general stress response by light has a negative effect on growth, probably because cellular resources are diverted into protective mechanisms rather than growth.


2021 ◽  
Author(s):  
Duarte Guerreiro ◽  
M. Graciela Pucciarelli ◽  
Teresa Tiensuu ◽  
Diana Gudynaite ◽  
Aoife Boyd ◽  
...  

The general stress response (GSR) in Listeria monocytogenes plays a critical role in the survival of this pathogen in the host gastrointestinal tract. The GSR is regulated by the alternative sigma factor B (σB), whose role in protection against acid stress is well established. However, the mechanisms leading to its activation by low pH are unknown. Here, we investigated the involvement of the stressosome, a sensory organelle, in transducing low pH signals to induce the GSR. Mild acid shock (15 min at pH 5.0) activated σB and conferred protection against a subsequent lethal pH challenge. A mutant strain where the stressosome subunit RsbR1 was present but its remaining paralogues were genetically inactivated retained the ability to induce σB activity at pH 5.0. The role of stressosome phosphorylation in signal transduction was investigated by mutating the putative phosphorylation sites in the core stressosome proteins RsbR1 (rsbR1 T175A, T209A, T241A) and RsbS (rsbS S56A), or in the active site of the stressosome kinase RsbT (rsbT N49A). The rsbS S56A and rsbT N49A mutations abolished the response to low pH. The rsbR1 T175A variant, retained a near-wild type phenotype. The rsbR1 T209A and rsbR1 T241A mutants displayed constitutive σB activity. Mild acid shock upregulates invasion genes and stimulates epithelial cell invasion, effects that were abolished in mutants with an inactive or overactive stressosome. Overall, the results show that the stressosome is required for acid-induced activation of σB in L. monocytogenes. Furthermore, RsbR1 can function independently of its paralogues and that signal transduction requires RsbT-mediated phosphorylation of RsbS on S56 and RsbR1 on T209. These insights shed light on the mechanisms of signal transduction that activate the GSR in L. monocytogenes in response to acidic environments, and highlight the role this sensory process in the early stages of the infectious cycle.


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