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dc.contributor.authorDuru, Ilhan Cem
dc.contributor.authorBucur, Florentina Ionela
dc.contributor.authorAndreevskaya, Margarita
dc.contributor.authorNikparvar, Bahareh
dc.contributor.authorYlinen, Anne
dc.contributor.authorGrigore-Gurgu, Leontina
dc.contributor.authorRode, Tone Mari
dc.contributor.authorCrauwels, Peter
dc.contributor.authorLaine, Pia
dc.contributor.authorPaulin, Lars
dc.contributor.authorLøvdal, Trond Karsten
dc.contributor.authorRiedel, Christian U.
dc.contributor.authorBar, Nadav
dc.contributor.authorBorda, Daniela
dc.contributor.authorNicolau, Anca Loana
dc.contributor.authorAuvinen, Petri
dc.description.abstractBackground: High-pressure processing (HPP) is a commonly used technique in the food industry to inactivate pathogens, including L. monocytogenes. It has been shown that L. monocytogenes is able to recover from HPP injuries and can start to grow again during long-term cold storage. To date, the gene expression profiling of L. monocytogenes during HPP damage recovery at cooling temperature has not been studied. In order identify key genes that play a role in recovery of the damage caused by HPP treatment, we performed RNA-sequencing (RNAseq) for two L. monocytogenes strains (barotolerant RO15 and barosensitive ScottA) at nine selected time points (up to 48 h) after treatment with two pressure levels (200 and 400 MPa). Results: The results showed that a general stress response was activated by SigB after HPP treatment. In addition, the phosphotransferase system (PTS; mostly fructose-, mannose-, galactitol-, cellobiose-, and ascorbate-specific PTS systems), protein folding, and cobalamin biosynthesis were the most upregulated genes during HPP damage recovery. We observed that cell-division-related genes (divIC, dicIVA, ftsE, and ftsX) were downregulated. By contrast, peptidoglycan-synthesis genes (murG, murC, and pbp2A) were upregulated. This indicates that cell-wall repair occurs as a part of HPP damage recovery. We also observed that prophage genes, including anti-CRISPR genes, were induced by HPP. Interestingly, a large amount of RNA-seq data (up to 85%) was mapped to Rli47, which is a noncoding RNA that is upregulated after HPP. Thus, we predicted that Rli47 plays a role in HPP damage recovery in L. monocytogenes. Moreover, gene-deletion experiments showed that amongst peptidoglycan biosynthesis genes, pbp2A mutants are more sensitive to HPP. Conclusions: We identified several genes and mechanisms that may play a role in recovery from HPP damage of L. monocytogenes. Our study contributes to new information on pathogen inactivation by HPP.en_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleHigh-pressure processing-induced transcriptome response during recovery of Listeria monocytogenesen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.source.journalBMC Genomicsen_US
dc.description.localcode© The Author(s). 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.en_US

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