E. M. Mrak und George F. Stewart: Fortschritte in der Lebensmittelforschung

Lindner, Willy

doi:10.1007/bf01098555

Cited by 2 publications

(3 citation statements)

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“…We suspected that these dark foci would be protein aggresomes-a collection of protein aggregates formed when intracellular proteostasis is disrupted. To test this hypothesis, we labeled IbpA, a small molecular chaperone that tightly associates with bacterial protein aggregates (Lindner et al, 2008; , persister-SR (middle), and VBNC (lower) cells during antibiotic killing and subsequent resuscitation of survival cells (replacing the killing medium with fresh growth medium, Video S1). Persister-FR cells resuscitate very soon after removal of antibiotic, whereas persister-SR cells resuscitate slowly.…”

Section: Aggresome Correlates With Bacterial Dormancy Depthmentioning

confidence: 99%

“…In contrast, when heat shock temperature was below 48 C, the persister ratio of the population increased with temperature, but above this temperature, the persister ratio decreased gradually ( Figures 3D and S3B), again suggesting that survival cells with deeper dormancy depth are more difficult to resuscitate. Furthermore, we tried to induce protein aggresome formation by adding streptomycin (Lindner et al, 2008) or hydrogen peroxide (Mirzaei and Regnier, 2008) ( Figure S3C). The dormant cell ratio increased similarly when protein aggregation occurred ( Figure S3D).…”

Section: Formation Of Aggresomes Facilitates Bacterial Cell Dormancymentioning

confidence: 99%

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ATP-Dependent Dynamic Protein Aggregation Regulates Bacterial Dormancy Depth Critical for Antibiotic Tolerance

et al. 2019

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Graphical Abstract Highlights d The degree of drug-tolerant cells being dormant can be measured by ''dormancy depth'' d Cellular dark foci, proved to be protein aggresomes, indicate dormancy depth d Depletion of intracellular ATP is the major force driving aggresomes formation d DnaK is vital in the disaggregation of aggresomes when a dormant cell resuscitates In this work, Pu et al. introduced a concept of ''dormancy depth'' that provides a unifying framework for understanding both persisters and viable but non-culturable cells. Subsequent mechanistic investigations revealed how ATP-dependent dynamic protein aggregation regulates cellular dormancy and resuscitation, the fine control of which facilitates bacterial drug tolerance. SUMMARYCell dormancy is a widespread mechanism used by bacteria to evade environmental threats, including antibiotics. Here we monitored bacterial antibiotic tolerance and regrowth at the single-cell level and found that each individual survival cell shows different ''dormancy depth,'' which in return regulates the lag time for cell resuscitation after removal of antibiotic. We further established that protein aggresome-a collection of endogenous protein aggregates-is an important indicator of bacterial dormancy depth, whose formation is promoted by decreased cellular ATP level. For cells to leave the dormant state and resuscitate, clearance of protein aggresome and recovery of proteostasis are required. We revealed that the ability to recruit functional DnaK-ClpB machineries, which facilitate protein disaggregation in an ATP-dependent manner, determines the lag time for bacterial regrowth. Better understanding of the key factors regulating bacterial regrowth after surviving antibiotic attack could lead to new therapeutic strategies for combating bacterial antibiotic tolerance.

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Section: Aggresome Correlates With Bacterial Dormancy Depthmentioning

confidence: 99%

Section: Formation Of Aggresomes Facilitates Bacterial Cell Dormancymentioning

confidence: 99%

ATP-Dependent Dynamic Protein Aggregation Regulates Bacterial Dormancy Depth Critical for Antibiotic Tolerance

et al. 2019

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“…Aggregates of misfolded proteins have been reported to exist at the poles in E. coli 168 cells, but only under heat shock conditions (Lindner et al, 2008;Winkler et al, 2010). 169…”

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Regrowth-delay Body as a Bacterial Subcellular Structure marking multidrug tolerant Persisters

Chang

Jia-yu

Liu

et al. 2018

Preprint

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11Bacteria have long been recognized to be capable of entering a phenotypically non-12 growing persister state, in which the cells exhibit an extended regrowth lag and a 13 multidrug tolerance, thus posing a great challenge in treating infectious diseases. 14 Owing to their non-inheritability, low abundance of existence, lack of metabolic 15 activities, and high heterogeneity, properties of persisters remain poorly 16 understood. Here, we report our accidental discovery of a hitherto unreported 17 subcellular structure that we term the regrowth-delay body, which is formed only 18 in non-growing bacterial cells and sequesters multiple key proteins. As of now, 19 this structure, that dissolves when the cell resumes growth, is the most 20 distinguishable subcellular structure marking persisters. Our studies also indicate 21 2 that persisters exhibit different depth of persistence, as determined by the status 22 of their regrowth-delay bodies. Our findings imply that suppressing the formation 23 and/or promoting the dissolution of regrowth-delay bodies could be viable 24 strategies for eradicating persisters. 25 26

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E. M. Mrak und George F. Stewart: Fortschritte in der Lebensmittelforschung

Cited by 2 publications

References 0 publications

ATP-Dependent Dynamic Protein Aggregation Regulates Bacterial Dormancy Depth Critical for Antibiotic Tolerance

ATP-Dependent Dynamic Protein Aggregation Regulates Bacterial Dormancy Depth Critical for Antibiotic Tolerance

Regrowth-delay Body as a Bacterial Subcellular Structure marking multidrug tolerant Persisters

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