2021
DOI: 10.1371/journal.pgen.1009261
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Activation of a bacterial killing machine

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Cited by 6 publications
(4 citation statements)
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“…The IreK-mediated response to phage- or daptomycin-induced membrane damage in E. faecalis is highly specific, since the T7SS was not activated by treatment with membrane-destabilising bile salts, nor by the cell wall-inhibiting antibiotic ceftriaxone, which also activates an IreK-dependent stress response [ 71 ]. Interestingly the DNA-damaging antibiotic mitomycin C also activated T7SSb transcription leading to speculation that T7 upregulation might be activated in response to T7 attack from both membrane-permeabilising and nuclease toxins, activities frequently associated with LXG domains [ 108 ]. Collectively, data suggest that stressors stimulating T7 activity are specific, and pathways can vary between strains, perhaps reflecting the specific environmental challenges faced by different strains.…”
Section: The T7ssb As a Bacterial Weaponmentioning
confidence: 99%
“…The IreK-mediated response to phage- or daptomycin-induced membrane damage in E. faecalis is highly specific, since the T7SS was not activated by treatment with membrane-destabilising bile salts, nor by the cell wall-inhibiting antibiotic ceftriaxone, which also activates an IreK-dependent stress response [ 71 ]. Interestingly the DNA-damaging antibiotic mitomycin C also activated T7SSb transcription leading to speculation that T7 upregulation might be activated in response to T7 attack from both membrane-permeabilising and nuclease toxins, activities frequently associated with LXG domains [ 108 ]. Collectively, data suggest that stressors stimulating T7 activity are specific, and pathways can vary between strains, perhaps reflecting the specific environmental challenges faced by different strains.…”
Section: The T7ssb As a Bacterial Weaponmentioning
confidence: 99%
“…The 3′ region of rhs encodes a recombination of a C-terminal toxin tRNase domain and its downstream gene, while the 5′ end of rhs encodes a T5SS contact-dependent inhibition (CDI) passenger domain, which enables cell surface expression and transfer of the C-terminal toxic effector domain to inhibit the growth of E. coli prey cells [ 102 , 103 ]. In Gram-negative bacteria, both T5SS and T6SS secrete toxins to the extracellular space, which antagonize other microorganisms and thus seize the living environment [ 104 ].…”
Section: The Love and Hate Relationshipmentioning
confidence: 99%
“…The biofilm matrix shields bacteria from phage attack by trapping phage particles and preventing diffusion (Sutherland et al, A biofilm can protect phages from the eukaryotic immune system, and these trapped viruses may in turn limit biofilm growth (Simmons et al, 2018;Hansen et al, 2019;Bond et al, 2021) so that in a stabilized biofilm, bacteria and phages may coexist in dynamic equilibrium (Fern andez et al, 2018;Hansen et al, 2019;Pires et al, 2021). Bacteria may produce matrix-degrading substances when challenged with phages (Alcock & Palmer, 2021;de C assia Oliveira et al, 2021) and can also secrete phage-inactivating substances (Pires et al, 2021). E. coli can halt phage invasion of mature biofilms through expression of curli fibres that affect biofilm architecture, hinder phage diffusion and physically protect the bacterial cell surface (Price & Chapman, 2018;Vidakovic et al, 2018;Bond et al, 2021).…”
Section: Special States: Biofilmsmentioning
confidence: 99%