Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection
The virus–host interaction requires a complex interplay between the phage strategy of reprogramming the host machinery to produce and release progeny virions, and the host defense against infection. Using RNA sequencing, we investigated the phage–host interaction to resolve the phenomenon of improve...
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doaj-5717c8c6dacc4f598dee73ed72fb09fb2021-06-30T23:32:45ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-06-01226159615910.3390/ijms22116159Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> InfectionGrzegorz M. Cech0Agnieszka Szalewska-Pałasz1Katarzyna Potrykus2Anna Kloska3Department of Bacterial Molecular Genetics, University of Gdańsk, Wita Stwosza 59, 80-308 Gdańsk, PolandDepartment of Bacterial Molecular Genetics, University of Gdańsk, Wita Stwosza 59, 80-308 Gdańsk, PolandDepartment of Bacterial Molecular Genetics, University of Gdańsk, Wita Stwosza 59, 80-308 Gdańsk, PolandDepartment of Medical Biology and Genetics, University of Gdańsk, Wita Stwosza 59, 80-308 Gdańsk, PolandThe virus–host interaction requires a complex interplay between the phage strategy of reprogramming the host machinery to produce and release progeny virions, and the host defense against infection. Using RNA sequencing, we investigated the phage–host interaction to resolve the phenomenon of improved lytic development of P1<i>vir</i> phage in a DksA-deficient <i>E. coli</i> host. Expression of the <i>ant1</i> and <i>kilA</i> P1<i>vir</i> genes in the wild-type host was the highest among all and most probably leads to phage virulence. Interestingly, in a DksA-deficient host, P1<i>vir</i> genes encoding lysozyme and holin are downregulated, while antiholins are upregulated. Gene expression of RepA, a protein necessary for replication initiating at the phage <i>oriR</i> region, is increased in the <i>dksA</i> mutant; this is also true for phage genes responsible for viral morphogenesis and architecture. Still, it seems that P1<i>vir</i> is taking control of the bacterial protein, sugar, and lipid metabolism in both, the wild type and <i>dksA<sup>−</sup></i> hosts. Generally, bacterial hosts are reacting by activating their SOS response or upregulating the heat shock proteins. However, only DksA-deficient cells upregulate their sulfur metabolism and downregulate proteolysis upon P1<i>vir</i> infection. We conclude that P1<i>vir</i> development is enhanced in the <i>dksA</i> mutant due to several improvements, including replication and virion assembly, as well as a less efficient lysis.https://www.mdpi.com/1422-0067/22/11/6159P1<i>vir</i> bacteriophageDksARNA-seq analysisphage developmenthost-virus interactiontranscriptomics |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Grzegorz M. Cech Agnieszka Szalewska-Pałasz Katarzyna Potrykus Anna Kloska |
spellingShingle |
Grzegorz M. Cech Agnieszka Szalewska-Pałasz Katarzyna Potrykus Anna Kloska Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection International Journal of Molecular Sciences P1<i>vir</i> bacteriophage DksA RNA-seq analysis phage development host-virus interaction transcriptomics |
author_facet |
Grzegorz M. Cech Agnieszka Szalewska-Pałasz Katarzyna Potrykus Anna Kloska |
author_sort |
Grzegorz M. Cech |
title |
Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection |
title_short |
Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection |
title_full |
Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection |
title_fullStr |
Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection |
title_full_unstemmed |
Virus–Host Interaction Gets <i>Curiouser and Curiouser</i>. PART II: Functional Transcriptomics of the <i>E. coli</i> DksA-Deficient Cell upon Phage P1<i>vir</i> Infection |
title_sort |
virus–host interaction gets <i>curiouser and curiouser</i>. part ii: functional transcriptomics of the <i>e. coli</i> dksa-deficient cell upon phage p1<i>vir</i> infection |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1661-6596 1422-0067 |
publishDate |
2021-06-01 |
description |
The virus–host interaction requires a complex interplay between the phage strategy of reprogramming the host machinery to produce and release progeny virions, and the host defense against infection. Using RNA sequencing, we investigated the phage–host interaction to resolve the phenomenon of improved lytic development of P1<i>vir</i> phage in a DksA-deficient <i>E. coli</i> host. Expression of the <i>ant1</i> and <i>kilA</i> P1<i>vir</i> genes in the wild-type host was the highest among all and most probably leads to phage virulence. Interestingly, in a DksA-deficient host, P1<i>vir</i> genes encoding lysozyme and holin are downregulated, while antiholins are upregulated. Gene expression of RepA, a protein necessary for replication initiating at the phage <i>oriR</i> region, is increased in the <i>dksA</i> mutant; this is also true for phage genes responsible for viral morphogenesis and architecture. Still, it seems that P1<i>vir</i> is taking control of the bacterial protein, sugar, and lipid metabolism in both, the wild type and <i>dksA<sup>−</sup></i> hosts. Generally, bacterial hosts are reacting by activating their SOS response or upregulating the heat shock proteins. However, only DksA-deficient cells upregulate their sulfur metabolism and downregulate proteolysis upon P1<i>vir</i> infection. We conclude that P1<i>vir</i> development is enhanced in the <i>dksA</i> mutant due to several improvements, including replication and virion assembly, as well as a less efficient lysis. |
topic |
P1<i>vir</i> bacteriophage DksA RNA-seq analysis phage development host-virus interaction transcriptomics |
url |
https://www.mdpi.com/1422-0067/22/11/6159 |
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