Characterization of Osmotically Induced Filaments of Salmonella enterica

Pratt, Zachary L.; Chen, Bingming; Czuprynski, Charles J.; Wong, Amy C. Lee; Kaspar, Charles W.

doi:10.1128/aem.01784-12

Cited by 23 publications

(13 citation statements)

References 64 publications

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“…The bacteria regained normal size after removal of stress. This type of phenomenon was also observed earlier (Pratt et al, 2012).…”

Section: Discussionsupporting

confidence: 85%

Elucidation of the role of the minC gene in filament formation by Listeria monocytogenes under stress conditions

2017

IJCRR

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Aim:The study was conducted to understand structural changes in cell morphology of stress tolerant Listeria monocytogenes strains after exposure to the different food related stresses and to investigate the involvement of the minC gene in filament formation under stress as a putative mechanism.Methods: Morphological changes in L. monocytogenes were studied under the stresses of high salt concentration (12.5%), extreme pH (4.5 and 9.0) and low temperature (4°C). The structural changes were recorded employing light and electron microscopy. The expression of the minC gene under stress was studied by qPCR.Results: Long filament formations were observed under salt stress, while, no structural changes could be observed for isolates grown in extreme pH and low temperature stresses. Scanning electron microscopic studies showed 3-10 times elongation of cells under stress which got reverted to normal size after removal of stress. Interestingly, it was noted that with the increase in stress, rod shaped cells became elongated. Six to 11 fold expression of the minC gene was observed under high salt stress. Conclusion:The results suggested that the filament formation could be one of the mechanisms by bacteria to tolerate high salt stress. It also supported the hypothesis that the minC gene over-expression could be the factor behind filamentous morphology.

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“…The bacteria regained normal size after removal of stress. This type of phenomenon was also observed earlier (Pratt et al, 2012).…”

Section: Discussionsupporting

confidence: 85%

Elucidation of the role of the minC gene in filament formation by Listeria monocytogenes under stress conditions

2017

IJCRR

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“…Unexpectedly, we discovered that ⌬glyA mutants formed elongated cells in vitro. Filament formation in Salmonella is well known as a response to osmotic and cold stress (42,43), but this phenotype of glyA mutation, to the best of our knowledge, has not previously been described for this genus or any of its close relatives. The phenotype could be reversed by genetic complementation in trans, ruling out the possibility that it was caused by secondary mutations in genes of relevance for Zring formation.…”

Section: Discussionmentioning

confidence: 99%

The In Vitro Redundant Enzymes PurN and PurT Are Both Essential for Systemic Infection of Mice in Salmonella enterica Serovar Typhimurium

et al. 2016

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Metabolic enzymes show a high degree of redundancy, and for that reason they are generally ignored in searches for novel targets for anti-infective substances. The enzymes PurN and PurT are redundant in vitro in Salmonella enterica serovar Typhimurium, in which they perform the third step of purine synthesis. Surprisingly, the results of the current study demonstrated that singlegene deletions of each of the genes encoding these enzymes caused attenuation (competitive infection indexes [CI] of <0.03) in mouse infections. While the ⌬purT mutant multiplied as fast as the wild-type strain in cultured J774A.1 macrophages, net multiplication of the ⌬purN mutant was reduced approximately 50% in 20 h. The attenuation of the ⌬purT mutant was abolished by simultaneous removal of the enzyme PurU, responsible for the formation of formate, indicating that the attenuation was related to formate accumulation or wasteful consumption of formyl tetrahydrofolate by PurU. In the process of further characterization, we disclosed that the glycine cleavage system (GCV) was the most important for formation of C 1 units in vivo (CI ‫؍‬ 0.03 ؎ 0.03). In contrast, GlyA was the only important enzyme for the formation of C 1 units in vitro. The results with the ⌬gcvT mutant further revealed that formation of serine by SerA and further conversion of serine into C 1 units and glycine by GlyA were not sufficient to ensure C 1 formation in S. Typhimurium in vivo. The results of the present study call for reinvestigations of the concept of metabolic redundancy in S. Typhimurium in vivo. Salmonella enterica is a common cause of foodborne disease worldwide. Annually, more than 93 million people have been estimated to suffer from nontyphoid salmonellosis, and more than 155,000 people succumb to the disease (1). Infection of mice with S. enterica serovar Typhimurium does not cause diarrhea but results in a systemic, life-threatening condition in which bacteria predominantly localize to cells of the immune system in the liver and spleen. For this reason, S. Typhimurium infection of mice is used as a model for systemic salmonellosis, including infection with the host-specific serovar S. Typhi (2).The diversity of intracellular and extracellular host niches occupied by S. Typhimurium is reflected in a high degree of metabolic flexibility (3). This flexibility is achieved through component and system-level redundancy in the metabolic network (4), and recent years have seen several studies of S. Typhimurium in order to understand the importance of metabolic redundancy for its pathogenic lifestyle (5-8). These studies have used genome-scale metabolic modeling to predict essential and combined lethal metabolic reactions; the latter group consists of two or more nonessential reactions which, when considered as one unit, are found to be essential. Such combinations are referred to as minimal cut sets in metabolic modeling (9).A list of 102 cut sets of metabolic reactions in S. Typhimurium was recently produced using a novel genome-scale metabolic model. Eac...

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“…For example, many bacteria, including B. subtilis, Listeria monocytogenes, Campylobacter jejuni, and S. enterica produce filaments in response to salt stress (Cameron, Frirdich, Huynh, Parker, & Gaynor, 2012;Liu, Miller, Basu, & McMullen, 2014;Pratt, Chen, Czuprynski, Wong, & Kaspar, 2012). In Bacillus cereus, salt stressinduced filamentation was proposed to depend on the general salt stress response, although the precise mechanism remains unknown (den Besten, Mols, Moezelaar, Zwietering, & Abee, 2009).…”

Section: Bacterial Filamentation As a Stress Responsementioning

confidence: 97%