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Loss of SigB in Listeria monocytogenes strains EGD-e and 10403S leads to hypersensitivity to hydrogen peroxide in stationary phase under aerobic conditions

Boura, M., Keating, C., Royet, K., Paudyal, R., O’Donoghue, B., O'Byrne, C. P. and Karatzas, K. A. G. (2016) Loss of SigB in Listeria monocytogenes strains EGD-e and 10403S leads to hypersensitivity to hydrogen peroxide in stationary phase under aerobic conditions. Applied and Environmental Microbiology, 82 (15). pp. 4584-4591. ISSN 0099-2240

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To link to this item DOI: 10.1128/AEM.00709-16

Abstract/Summary

SigB is the main stress gene regulator in L. monocytogenes affecting the expression of more than 150 genes and thus contributing in multiple stress resistance. Despite its clear role in most stresses, its role in oxidative stress is uncertain as results accompanying the loss of sigB range from hyperresistance to hypersensitivity. Previously, these differences have been attributed to strain variation. In this study, we show conclusively that in contrast to all other stresses, loss of sigB results in hyperresistance against H2O2 (more than 8 log CFU ml-1 compared to the wild type) in aerobically-grown stationary phase cultures of 10403S and EGD-e.. Furthermore, growth at 30°C resulted in higher resistance to oxidative stress than at 37°C. Oxidative stress resistance seemed to be higher with higher levels of oxygen. Under anaerobic conditions, loss of SigB in 10403S did not affect survival against H2O2 while in EGD-e it resulted in a sensitive phenotype. During exponential phase, minor differences occurred as expected due to the absence of sigB transcription. Catalase tests were performed under all conditions and stronger catalase results corresponded well with higher survival underpinning the important role of catalase in this phenotype. Furthermore, we assessed the catalase activity in protein lysates which corresponded with the catalase tests and survival. In addition, RT-PCR showed no differences in transcription between the wild type and the ΔsigB in various oxidative stress genes. Further investigation of the molecular mechanism behind this phenotype and its possible consequences for the overall phenotype of L. monocytogenes are underway.

Item Type:Article
Refereed:Yes
Divisions:Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > Department of Food and Nutritional Sciences > Food Microbial Sciences Research Group
ID Code:66100
Publisher:American Society for Microbiology

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