Functional genomics reveals the toxin–antitoxin repertoire and AbiE activity in Serratia

Hampton, Hannah G; Smith, Lisa F.; Ferguson, Shaun; Meaden, Sean; Jackson, Simon A.; Fineran, Peter C.

doi:10.1099/mgen.0.000458

Cited by 9 publications

(9 citation statements)

References 80 publications

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“…Recently, a new counter-defence mechanism against CRISPR/Cas has been uncovered, where phage T4 restores the broken genomic material, thereby making progeny phages resistant against future CRISPR attacks [36]. For those interested in more detailed information on anti-phage systems and the phage-bacteria arms race, we refer to some excellent recent reviews [31,35,37,38].…”

Section: Bacterial Defence Mechanisms Against Phagesmentioning

confidence: 99%

Cell wall deficiency as an escape mechanism from phage infection

2021

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The cell wall plays a central role in protecting bacteria from some environmental stresses, but not against all. In fact, in some cases, an elaborate cell envelope may even render the cell more vulnerable. For example, it contains molecules or complexes that bacteriophages recognize as the first step of host invasion, such as proteins and sugars, or cell appendages such as pili or flagella. In order to counteract phages, bacteria have evolved multiple escape mechanisms, such as restriction-modification, abortive infection, CRISPR/Cas systems or phage inhibitors. In this perspective review, we present the hypothesis that bacteria may have additional means to escape phage attack. Some bacteria are known to be able to shed their cell wall in response to environmental stresses, yielding cells that transiently lack a cell wall. In this wall-less state, the bacteria may be temporarily protected against phages, since they lack the essential entities that are necessary for phage binding and infection. Given that cell wall deficiency can be triggered by clinically administered antibiotics, phage escape could be an unwanted consequence that limits the use of phage therapy for treating stubborn infections.

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Section: Bacterial Defence Mechanisms Against Phagesmentioning

confidence: 99%

Cell wall deficiency as an escape mechanism from phage infection

2021

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“…Recently it was demonstrated that AbiEii homo logue MenT 3 from Mycobacterium tuberculosis can trans fer pyrimidines to the acceptor stem of the specific tRNAs [137]. In agreement with this is the fact that over expression of AbiE toxin in Serratia causes growth cessa tion and decrease in the tRNAs levels [138]. In E. coli, the Type II system MazEF interferes with phage P1 propaga tion [139], and the Type I TA system hok/sok reduces the burst size of T4 phage [140].…”

Section: Induced Cell Dormancy or Suicide -Abortive Infection (Abi) And Toxin-antitoxin (Ta) Systemsmentioning

confidence: 83%

Microbial Arsenal of Antiviral Defenses. Part II

Musharova

Severinov

2021

Biochemistry Moscow

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Bacteriophages or phages are viruses that infect bacterial cells (for the scope of this review we will also consider viruses that infect Archaea). The constant threat of phage infection is a major force that shapes evolution of microbial genomes. To withstand infection, bacteria had evolved numerous strategies to avoid recognition by phages or to directly interfere with phage propagation inside the cell. Classical molecular biology and genetic engineering had been deeply intertwined with the study of phages and host defenses. Nowadays, owing to the rise of phage therapy, broad application of CRISPR-Cas technologies, and development of bioinformatics approaches that facilitate discovery of new systems, phage biology experiences a revival. This review describes variety of strategies employed by microbes to counter phage infection. In the first part defense associated with cell surface, roles of small molecules, and innate immunity systems relying on DNA modification were discussed. The second part focuses on adaptive immunity systems, abortive infection mechanisms, defenses associated with mobile genetic elements, and novel systems discovered in recent years through metagenomic mining.

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“…ATCC39006 strain LacA (hereafter Serratia ) ( 24 , 25 ). This Serratia strain is an environmental isolate that encodes type I-E, I-F and III-A CRISPR-Cas systems, in addition to multiple toxin-antitoxin and other defence systems ( 22 , 26 ). Using SorTn-seq, we identified and characterised an Rcs stress response pathway that inversely controls CRISPR-Cas and surface immunity.…”

Section: Introductionmentioning

confidence: 99%

CRISPR-Cas immunity is repressed by the LysR-type transcriptional regulator PigU

Smith,

Hampton,

Yevstigneyeva

et al. 2023

Nucleic Acids Research

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Bacteria protect themselves from infection by bacteriophages (phages) using different defence systems, such as CRISPR-Cas. Although CRISPR-Cas provides phage resistance, fitness costs are incurred, such as through autoimmunity. CRISPR-Cas regulation can optimise defence and minimise these costs. We recently developed a genome-wide functional genomics approach (SorTn-seq) for high-throughput discovery of regulators of bacterial gene expression. Here, we applied SorTn-seq to identify loci influencing expression of the two type III-A Serratia CRISPR arrays. Multiple genes affected CRISPR expression, including those involved in outer membrane and lipopolysaccharide synthesis. By comparing loci affecting type III CRISPR arrays and cas operon expression, we identified PigU (LrhA) as a repressor that co-ordinately controls both arrays and cas genes. By repressing type III-A CRISPR-Cas expression, PigU shuts off CRISPR-Cas interference against plasmids and phages. PigU also represses interference and CRISPR adaptation by the type I-F system, which is also present in Serratia. RNA sequencing demonstrated that PigU is a global regulator that controls secondary metabolite production and motility, in addition to CRISPR-Cas immunity. Increased PigU also resulted in elevated expression of three Serratia prophages, indicating their likely induction upon sensing PigU-induced cellular changes. In summary, PigU is a major regulator of CRISPR-Cas immunity in Serratia.

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Functional genomics reveals the toxin–antitoxin repertoire and AbiE activity in Serratia

Cited by 9 publications

References 80 publications

Cell wall deficiency as an escape mechanism from phage infection

Cell wall deficiency as an escape mechanism from phage infection

Microbial Arsenal of Antiviral Defenses. Part II

CRISPR-Cas immunity is repressed by the LysR-type transcriptional regulator PigU

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