Bacterial Amyloids

Marcoleta, Andrés E.; Wien, Frank; Arluison, Véronique; Lagos, Rosalba; Giraldo, Rafael

doi:10.1002/9780470015902.a0028401

Cited by 7 publications

(3 citation statements)

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“…Nevertheless, functional amyloids also exist in nature [ 25 ]. Among them, functional amyloids form in bacteria [ 26 ]. They can form in either the cytoplasm, as in the case of Hfq, or on the cell surface, for instance with proteins constituting curli [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Apomorphine Targets the Pleiotropic Bacterial Regulator Hfq

et al. 2021

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Hfq is a bacterial regulator with key roles in gene expression. The protein notably regulates translation efficiency and RNA decay in Gram-negative bacteria, thanks to its binding to small regulatory noncoding RNAs. This property is of primary importance for bacterial adaptation and survival in hosts. Small RNAs and Hfq are, for instance, involved in the response to antibiotics. Previous work has shown that the E. coli Hfq C-terminal region (Hfq-CTR) self-assembles into an amyloid structure. It was also demonstrated that the green tea compound EpiGallo Catechin Gallate (EGCG) binds to Hfq-CTR amyloid fibrils and remodels them into nonamyloid structures. Thus, compounds that target the amyloid region of Hfq may be used as antibacterial agents. Here, we show that another compound that inhibits amyloid formation, apomorphine, may also serve as a new antibacterial. Our results provide an alternative in order to repurpose apomorphine, commonly used in the treatment of Parkinson’s disease, as an antibiotic to block bacterial adaptation to treat infections.

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Section: Introductionmentioning

confidence: 99%

Apomorphine Targets the Pleiotropic Bacterial Regulator Hfq

et al. 2021

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“…In E. coli , these amyloid fibers are formed from polymerisation of the amyloidogenic protein subunit of curli fibers CsgA in a membrane-anchored nucleator protein CsgB subunit induced process. Many other proteins and transcriptional regulators are also required for amyloid production, including molecular channels that allow the curli subunits secretion and molecular chaperones, which prohibits uncontrolled aggregation ( 26 ). The principal subunit of curli amyloid fibers CsgA is encoded by the csgA gene under the regulation of the master regulator of adhesive curli fimbriae expression CsgD.…”

Section: Resultsmentioning

confidence: 99%

CRISPRi-mediated suppression of E. coli Nissle 1917 virulence factors: A strategy for creating an engineered probiotic using csgD gene suppression

Azam

Khan

2022

Front. Nutr.

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BackgroundBiofilm formation is a complex phenomenon, and it is the causative agent of several human infections. Bacterial amyloids are involved in biofilm formation leading to infection persistence. Due to antibiotic resistance, their treatment is a great challenge for physicians. Probiotics, especially E. coli Nissle 1917 (EcN), are used to treat human intestinal disorders and ulcerative colitis. It also expresses virulence factors associated with biofilm and amyloid formation. EcN produces biofilm equivalent to the pathogenic UPEC strains.MethodsCRISPRi was used to create the knockdown mutants of the csgD gene (csgD-KD). The qRT-PCR was performed to assess the expression of the csgD gene in csgD-KD cells. The csgD-KD cells were also evaluated for the expression of csgA, csgB, fimA, fimH, ompR, luxS, and bolA genes. The gene expression data obtained was further confirmed by spectroscopic, microscopic, and other assays to validate our study.ResultsCRISPRi-mediated knockdown of csgD gene shows reduction in curli amyloid formation, biofilm formation, and suppression of genes (csgA, csgB, fimA, fimH, ompR, bolA, and luxS) involved in virulence factors production.ConclusionCurli amyloid fibers and fimbriae fibers play a critical role in biofilm formation leading to pathogenicity. CsgD protein is the master regulator of curli synthesis in E. coli. Hence, curli amyloid inhibition through the csgD gene may be used to improve the EcN and different probiotic strains by suppressing virulence factors.

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“…These latter processes damage proteins in a covalent way and thereby make the proteins irreversibly misfolded (Schramm et al, 2019). When inclusion bodies consist of, and are induced by, overexpression of proteins (e.g., amyloidogenic CsgA protein; Marcoleta et al, 2019), these inclusion bodies are mostly cordial to the host cell, and a fraction of the overexpressed proteins can maintain their activity in the aggregated state (De Marco et al, 2019). Such differences in decomposition properties and harmfulness can help to understand what role inclusion bodies play for senescence-to date, differentiation among inclusion body types has rarely been considered in aging studies, and the potential positive effects of the types of inclusion bodies are little explored.…”

Section: Loss Of Proteostasismentioning

confidence: 99%

Senescence in Bacteria and Its Underlying Mechanisms

Steiner

2021

Front. Cell Dev. Biol.

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Bacteria have been thought to flee senescence by dividing into two identical daughter cells, but this notion of immortality has changed over the last two decades. Asymmetry between the resulting daughter cells after binary fission is revealed in physiological function, cell growth, and survival probabilities and is expected from theoretical understanding. Since the discovery of senescence in morphologically identical but physiologically asymmetric dividing bacteria, the mechanisms of bacteria aging have been explored across levels of biological organization. Quantitative investigations are heavily biased toward Escherichia coli and on the role of inclusion bodies—clusters of misfolded proteins. Despite intensive efforts to date, it is not evident if and how inclusion bodies, a phenotype linked to the loss of proteostasis and one of the consequences of a chain of reactions triggered by reactive oxygen species, contribute to senescence in bacteria. Recent findings in bacteria question that inclusion bodies are only deleterious, illustrated by fitness advantages of cells holding inclusion bodies under varying environmental conditions. The contributions of other hallmarks of aging, identified for metazoans, remain elusive. For instance, genomic instability appears to be age independent, epigenetic alterations might be little age specific, and other hallmarks do not play a major role in bacteria systems. What is surprising is that, on the one hand, classical senescence patterns, such as an early exponential increase in mortality followed by late age mortality plateaus, are found, but, on the other hand, identifying mechanisms that link to these patterns is challenging. Senescence patterns are sensitive to environmental conditions and to genetic background, even within species, which suggests diverse evolutionary selective forces on senescence that go beyond generalized expectations of classical evolutionary theories of aging. Given the molecular tool kits available in bacteria, the high control of experimental conditions, the high-throughput data collection using microfluidic systems, and the ease of life cell imaging of fluorescently marked transcription, translation, and proteomic dynamics, in combination with the simple demographics of growth, division, and mortality of bacteria, make the challenges surprising. The diversity of mechanisms and patterns revealed and their environmental dependencies not only present challenges but also open exciting opportunities for the discovery and deeper understanding of aging and its mechanisms, maybe beyond bacteria and aging.

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Bacterial Amyloids

Cited by 7 publications

References 73 publications

Apomorphine Targets the Pleiotropic Bacterial Regulator Hfq

Apomorphine Targets the Pleiotropic Bacterial Regulator Hfq

CRISPRi-mediated suppression of E. coli Nissle 1917 virulence factors: A strategy for creating an engineered probiotic using csgD gene suppression

Senescence in Bacteria and Its Underlying Mechanisms

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