Contribution of N
            <sup>ε</sup>
            -lysine Acetylation towards Regulation of Bacterial Pathogenesis

Luu, Jackson; Carabetta, Valerie J.

doi:10.1128/msystems.00422-21

Cited by 15 publications

(15 citation statements)

References 91 publications

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“…S4). The accumulation of acetyl-CoA and succinyl-CoA in both phenylalanine metabolism and propanoate metabolism was related to bacterial physiology and virulence via lysine acetylation, which was a post-translational modification [42,43].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic analysis reveals the regulatory role of quorum sensing in the Acinetobacter baumannii ATCC 19606 via RNA-seq

Xiong

et al. 2022

BMC Microbiol

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Background Acinetobacter baumannii has emerged as the major opportunistic pathogen in healthcare-associated infections with high-level antibiotic resistance and high mortality. Quorum sensing (QS) system is a cell-to-cell bacterial communication mediated by the synthesis, secretion, and binding of auto-inducer signals. It is a global regulatory system to coordinate the behavior of individual bacteria in a population. The present study focused on the QS system, aiming to investigate the regulatory role of QS in bacterial virulence and antibiotic resistance. Method The auto-inducer synthase gene abaI was deleted using the A. baumannii ATCC 19606 strain to interrupt the QS process. The RNA-seq was performed to identify the differentially expressed genes (DEGs) and pathways in the mutant (△abaI) strain compared with the wild-type (WT) strain. Results A total of 380 DEGs [the adjusted P value < 0.05 and the absolute value of log2(fold change) > log21.5] were identified, including 256 upregulated genes and 124 downregulated genes in the △abaI strain. The enrichment analysis indicated that the DEGs involved in arginine biosynthesis, purine metabolism, biofilm formation, and type VI secretion system (T6SS) were downregulated, while the DEGs involved in pathways related to fatty acid metabolism and amino acid metabolism were upregulated. Consistent with the expression change of the DEGs, a decrease in biofilm formation was observed in the △abaI strain compared with the WT strain. On the contrary, no obvious changes were found in antimicrobial resistance following the deletion of abaI. Conclusions The present study demonstrated the transcriptomic profile of A. baumannii after the deletion of abaI, revealing an important regulatory role of the QS system in bacterial virulence. The deletion of abaI suppressed the biofilm formation in A. baumannii ATCC 19606, leading to decreased pathogenicity. Further studies on the role of abaR, encoding the receptor of auto-inducer in the QS circuit, are required for a better understanding of the regulation of bacterial virulence and pathogenicity in the QS network.

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Section: Discussionmentioning

confidence: 99%

Transcriptomic analysis reveals the regulatory role of quorum sensing in the Acinetobacter baumannii ATCC 19606 via RNA-seq

Xiong

et al. 2022

BMC Microbiol

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“…These metabolic pathways are essential for the continued growth and persistence of P. gingivalis in the microbial community as they produce ATP and promote the release of short fatty acids required for bacterial growth and survival [ 85 ]. Protein acetylation leads to the activation of proteases which aids pathogenesis in periodontitis through the degradation of host extracellular matrix components, degradation of antimicrobial peptides and cytokines [ 86 ]. Proteins such as Mfa1 fimbrilin, Haemagglutinin protein HagA and Methionine gamma-lyase related to P. gingivalis pigmentation were identified as targets of acetylation.…”

Section: Post-translational Mechanisms Of Pathogenicity In Periodonta...mentioning

confidence: 99%

Modulatory Mechanisms of Pathogenicity in Porphyromonas gingivalis and Other Periodontal Pathobionts

Sharaf

Hijazi

2022

Microorganisms

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The pathogenesis of periodontitis depends on a sustained feedback loop where bacterial virulence factors and immune responses both contribute to inflammation and tissue degradation. Periodontitis is a multifactorial disease that is associated with a pathogenic shift in the oral microbiome. Within this shift, low-abundance Gram-negative anaerobic pathobionts transition from harmless colonisers of the subgingival environment to a virulent state that drives evasion and subversion of innate and adaptive immune responses. This, in turn, drives the progression of inflammatory disease and the destruction of tooth-supporting structures. From an evolutionary perspective, bacteria have developed this phenotypic plasticity in order to respond and adapt to environmental stimuli or external stressors. This review summarises the available knowledge of genetic, transcriptional, and post-translational mechanisms which mediate the commensal-pathogen transition of periodontal bacteria. The review will focus primarily on Porphyromonas gingivalis.

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“…However, recent research has found that bacterial-derived effectors can directly modify host proteins PTMs. While some pathogens have acquired and incorporated host enzymes into their virulence factor repertoire, others have convergently evolved to mimic the activity of host enzymes (Bernal et al, 2014; Luu and Carabetta, 2021; Salomon and Orth, 2013). Importantly, bacterial effectors that are translocated and directly bind host proteins to differentially acetylate them remain to be identified.…”

Section: Mainmentioning

confidence: 99%

Battle for the histones: a secreted bacterial sirtuin from Campylobacter jejuni activates neutrophils and induces inflammation during infection

Callahan

Hancock

Doster

et al. 2022

Preprint

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Histone modifications alter numerous cornerstone processes in eukaryotes, including metabolism, physiology, and immunity. Numerous bacterial pathogens can alter expression of host-derived sirtuins to deacetylate histones in order to promote infection, yet, a bacterial-derived sirtuin has yet to be investigated to deacetylate host histones. Using Campylobacter jejuni, the leading cause of bacterial-derived gastroenteritis, we found a secreted sirtuin, SliP, which binds to and deacetylates neutrophil histones. We found neutrophil activation and extrusion of neutrophil extracellular traps was SliP dependent, whereby sliP mutants are unable to activate neutrophils or promote NETosis. Leveraging the mouse model of campylobacteriosis, we further demonstrate the sliP mutant can efficiently infect IL-10-/- mice, but induction of proinflammatory cytokine production and gastrointestinal pathology is SliP-dependent. In conclusion, we investigate a unique bacterial effector which targets host histones and is responsible for the inflammatory response and tissue pathology observed during campylobacteriosis.HighlightsC. jejuni encodes a secreted effector, SliP, which functions as a canonical sirtuinSliP binds to and deacetylates neutrophil histone H3 during bacterial infectionC. jejuni-induced neutrophil activation and NETosis are SliP-dependentInflammation and tissue pathology during C. jejuni infection is SliP-dependent

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Contribution of N ^ε -lysine Acetylation towards Regulation of Bacterial Pathogenesis

Cited by 15 publications

References 91 publications

Transcriptomic analysis reveals the regulatory role of quorum sensing in the Acinetobacter baumannii ATCC 19606 via RNA-seq

Transcriptomic analysis reveals the regulatory role of quorum sensing in the Acinetobacter baumannii ATCC 19606 via RNA-seq

Modulatory Mechanisms of Pathogenicity in Porphyromonas gingivalis and Other Periodontal Pathobionts

Battle for the histones: a secreted bacterial sirtuin from Campylobacter jejuni activates neutrophils and induces inflammation during infection

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Contribution of N ε -lysine Acetylation towards Regulation of Bacterial Pathogenesis

Cited by 15 publications

References 91 publications

Transcriptomic analysis reveals the regulatory role of quorum sensing in the Acinetobacter baumannii ATCC 19606 via RNA-seq

Transcriptomic analysis reveals the regulatory role of quorum sensing in the Acinetobacter baumannii ATCC 19606 via RNA-seq

Modulatory Mechanisms of Pathogenicity in Porphyromonas gingivalis and Other Periodontal Pathobionts

Battle for the histones: a secreted bacterial sirtuin from Campylobacter jejuni activates neutrophils and induces inflammation during infection

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Contribution of N ^ε -lysine Acetylation towards Regulation of Bacterial Pathogenesis