scholarly journals Outer membrane-deprived cyanobacteria liberate periplasmic and thylakoid luminal components that support the growth of heterotrophs

2020 ◽  
Author(s):  
Seiji Kojima ◽  
Yasuaki Okumura
Keyword(s):  
Host Cell ◽  
Outer Membrane ◽  
Cell Function ◽  
Heterotrophic Bacteria ◽  
Photosynthetic Electron Transport ◽  
Physical Interaction ◽  
Free Living ◽  
Chloroplast Evolution ◽  
Photosynthetic Products ◽  
Host Metabolism

ABSTRACTChloroplasts originate from endosymbiosis of a cyanobacterium within a heterotrophic host cell. Establishing endosymbiosis requires the translocation across its envelope of photosynthetic products generated inside the once free-living cyanobacterium to be exploited by host metabolism. However, the nature of this translocation event is unknown. We previously found that most cyanobacterial outer membrane components were eliminated during the primitive stage of chloroplast evolution, suggesting the importance of evolutionary changes of the outer membrane. Here, we removed the outer membrane from Synechocystis sp. PCC 6803 by disrupting the physical interaction with peptidoglycan, and characterized the effects on cell function. Outer membrane-deprived cells liberated diverse substances into the environment without significantly compromising photoautotrophic growth. The amount of liberated proteins increased to ~0.35 g/L within five days of culture. Proteomic analysis showed that most liberated proteins were periplasmic and thylakoid luminal components. Connectivity between the thylakoid lumen-extracellular space was confirmed by findings that an exogenous hydrophilic oxidant was reduced by photosynthetic electron transport chain on the thylakoid membrane. Metabolomic analysis detected the release of nucleotide-related metabolites at concentrations around 1 μM. The liberated materials supported the proliferation of heterotrophic bacteria. These findings show that breaching the outer membrane, without any manipulations to the cytoplasmic membrane, converts a cyanobacterium to a chloroplast-like organism that conducts photosynthesis and releases its biogenic materials. This conversion not only represents a potential explanation why the outer membrane markedly changed during the earliest stage of chloroplast evolution, but also provides the opportunity to harness cyanobacterial photosynthesis for biomanufacturing processes.SIGNIFICANCE STATEMENTAlthough it is well accepted that chloroplasts stem from endosymbiosis of a cyanobacterium within a heterotrophic host cell, the issue of how photosynthetic products generated inside a formerly free-living cyanobacterium are translocated across its envelope and exploited by host metabolism has been little addressed. Here we show that breaching the cyanobacterial outer membrane barrier converts a cyanobacterium to a chloroplast-like organism that conducts photosynthesis and releases its diverse biogenic materials into its external environment, which sustains the growth of heterotrophic organisms. This conversion represents a possible example of metabolic exploitation of cyanobacterial photosynthesis. Further, this “quasi-chloroplast” provides a potential opportunity for industrial application such as producing feedstock for biomanufacturing processes that harnesses heterotrophic bacteria.

Enteropathogenic Escherichia coli adherence to intestinal epithelial monolayers diminishes barrier function

1995 ◽  
Vol 268 (2) ◽  
pp. G374-G379 ◽  
Author(s):  
J. Spitz ◽  
R. Yuhan ◽  
A. Koutsouris ◽  
C. Blatt ◽  
J. Alverdy ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Host Cell ◽  
Barrier Function ◽  
Cell Function ◽  
Cytoskeletal Proteins ◽  
Calcium Stores ◽  
Intestinal Epithelial ◽  
Enteropathogenic Escherichia Coli ◽  
Wild Type ◽  
Cell Monolayers

The mechanism by which enteropathogenic Escherichia coli (EPEC) causes diarrhea remains elusive. Several alterations within the host cell have been demonstrated to occur following EPEC attachment including increases in intracellular Ca2+ concentration and rearrangement and phosphorylation of several cytoskeletal proteins. The consequences of these intracellular perturbations on host cell function, however, have not been determined. The aim of this study was to examine the effect of EPEC adherence on intestinal epithelial barrier function. T84 cell monolayers were infected with either wild-type EPEC or a nonadherent isogenic derivative. Transepithelial electrical resistance, a measure of barrier function, decreased 33.5 +/- 6.4% after a 6-h incubation with the wild-type strain. Electron microscopy revealed ultrastructurally normal cells, and lactate dehydrogenase release assays failed to demonstrate cytotoxicity. Dual 22Na+ and [3H]mannitol flux studies localized the permeability defect to tight junctions. In addition, cumulative flux of the paracellular marker mannitol was four- to fivefold greater across monolayers infected with wild-type EPEC. Sequestration of intracellular calcium stores by dantrolene completely abrogated the resistance drop associated with EPEC attachment. These data demonstrate that adherence of EPEC to intestinal epithelial cell monolayers disrupts tight junction barrier function via a calcium-requiring event.

scholarly journals Brucella abortusinduces a Warburg shift in host metabolism that is linked to enhanced intracellular survival of the pathogen

2017 ◽  
Author(s):  
Daniel M. Czyż ◽  
Jonathan Willett ◽  
Sean Crosson
Keyword(s):  
Lactic Acid ◽  
Host Cell ◽  
Brucella Abortus ◽  
Cell Metabolism ◽  
Lactate Production ◽  
Human Macrophage ◽  
Metabolic Shift ◽  
Intracellular Infections ◽  
Host Metabolism

ABSTRACTIntracellular bacterial pathogens exploit host cell resources to replicate and survive inside the host. Targeting these host systems is one promising approach to developing novel antimicrobials to treat intracellular infections. We show that human macrophage-like cells infected withBrucella abortusundergo a metabolic shift characterized by attenuated tricarboxylic acid cycle metabolism, reduced amino acid consumption, altered mitochondrial localization, and increased lactate production. This shift to an aerobic glycolytic state resembles the Warburg effect, a change in energy production that is well-described in cancer cells, and also occurs in activated inflammatory cells.B. abortusefficiently uses lactic acid as its sole carbon and energy source and requires the ability to metabolize lactate for normal survival in human macrophage-like cells. We demonstrate that chemical inhibitors of host glycolysis and lactate production do not affectin vitrogrowth ofB. abortusin axenic culture, but decrease its survival in the intracellular niche. Our data support a model in which infection shifts host metabolism to a Warburg-like state, andB. abortususes this change in metabolism to promote intracellular survival. Pharmacological perturbation of these features of host cell metabolism may be a useful strategy to inhibit infection by intracellular pathogens.IMPORTANCEBrucellaspp. are intracellular bacterial pathogens that cause disease in a range of mammals, including livestock. Transmission from livestock to humans is common and can lead to chronic human disease. Human macrophage-like cells infected withBrucella abortusundergo a Warburg-like metabolic shift to an aerobic glycolytic state where the host cells produce lactic acid and have reduced amino acid catabolism. We provide evidence that the pathogen can exploit this change in host metabolism to support growth and survival in the intracellular niche. Drugs that inhibit this shift in host cell metabolism inhibit intracellular replication and decrease the survival ofB. abortusin anin vitroinfection model; these drugs may be broadly useful therapeutics for intracellular infections.

scholarly journals Global Transcriptional Responses of Pseudomonas aeruginosa to Phage PRR1 Infection

2007 ◽  
Vol 82 (5) ◽  
pp. 2324-2329 ◽  
Author(s):  
Janne J. Ravantti ◽  
Tanja M. Ruokoranta ◽  
A. Marika Alapuranen ◽  
Dennis H. Bamford
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Viral Infection ◽  
Host Cell ◽  
Cell Function ◽  
Growth Conditions ◽  
Growth Cycle ◽  
Global Changes ◽  
Mrna Levels ◽  
Transcriptional Responses ◽  
Number Of Genes

ABSTRACT The infectious cycles of viruses are known to cause dramatic changes to host cell function. The development of microarray technology has provided means to monitor host cell responses to viral infection at the level of global changes in mRNA levels. We have applied this methodology to investigate gene expression changes caused by a small, icosahedral, single-stranded-RNA phage, PRR1 (a member of the Leviviridae family), on its host, Pseudomonas aeruginosa, at different times during its growth cycle. Viral infection in this system resulted in changes in expression levels of <4% of P. aeruginosa genes. Interestingly, the number of genes affected by viral infection was significantly lower than the number of genes affected by changes in growth conditions during the experiment. Compared with a similar study that focused on the complex, double-stranded-DNA bacterial virus PRD1, it was evident that there were no universal responses to viral infection. However, in both cases, translation was affected in infected cells.

First report of developmental changes inside the eggs of the Chinese freshwater crab, Sinopotamon yangtsekiense Bott, 1967 (Potamoidea, Potamidae), with comments on its evolutionary significance

2010 ◽  
Vol 79 (2) ◽  
pp. 79-84 ◽  
Author(s):  
Junzeng Xue ◽  
Yan Liu ◽  
Neil Cumberlidge ◽  
Huixian Wu
Keyword(s):  
Outer Membrane ◽  
Morphological Changes ◽  
Zhejiang Province ◽  
Developmental Changes ◽  
Evolutionary Significance ◽  
Freshwater Crab ◽  
Yolk Mass ◽  
Free Living ◽  
Inner Membrane ◽  
Larval Stages

This paper focuses on the developmental changes that take place inside the eggs of the semi-terrestrial freshwater crab, Sinopotamon yangtsekiense, from Qiantang River in Zhejiang Province, China. The egg consists of two layers, a thick outer membrane and a thin inner membrane that encloses the fluidfilled embryonic sac. Development in this species took up to 77 days, after which the free-living juvenile hatchling crab emerged from the egg. During development the embryo underwent a series of morphological changes that corresponded to the free-living larval stages of marine crabs, and the yolk mass decreased in size and changed color (from creamy pale yellow, to orange, and finally grey). The eggs remained attached to the pleopods in the female’s abdominal brood pouch during development and showed a great deal of independence from water. Embryos developed normally whether they were immersed in water or in air. The implications of this adaptation for freshwater crab evolution are discussed.

The Phycobihproteids in Cyanophora paradoxa as Accessoric Pigments and Nitrogen Storage Proteins

1983 ◽  
Vol 38 (11-12) ◽  
pp. 972-977 ◽  
Author(s):  
Hainfried E. A. Schenk ◽  
Jürgen Hanf ◽  
Margarete Neu-Müller
Keyword(s):  
Electron Transport ◽  
Stress Proteins ◽  
Nitrogen Starvation ◽  
Storage Proteins ◽  
Photosynthetic Electron Transport ◽  
Lower Degree ◽  
Nitrogen Storage ◽  
Cyanophora Paradoxa ◽  
Free Living

The phycobiliproteids of cyanobacteria have two functions. They are accessoric pigments for the light-dependent photosynthetic electron transport, and, secondly, they are storage proteins. Cyanocyta korschikoffiana, the endocyanelle of Cyanophora paradoxa, a hardly adapted endocytobiotic cyanobacterium, is responsible for the photoautotrophy of the host flagellate. The biosynthesis of the phycobiliproteids takes place in the endocyanelles and is reversible. Under nitrogen starvation the phycobiliproteids were disintegrated again, in contrast to the carotenoids (and in a lower degree to chlorophyll), whose contents rem ain more constant in the cells, as shown by in vivo measurements. Therefore, it is concluded that sim ilar to the function in free living cyanobacteria the phycobiliproteids of C. paradoxa also serve as storage substances (“stress proteins”). This opinion is supported by experiments with chloramphenicol

scholarly journals Outer Membrane Vesicle-Host Cell Interactions

2019 ◽  
pp. 201-214 ◽  
Author(s):  
Jessica D. Cecil ◽  
Natalie Sirisaengtaksin ◽  
Neil M. O’Brien-Simpson ◽  
Anne Marie Krachler
Keyword(s):  
Host Cell ◽  
Outer Membrane ◽  
Membrane Vesicle ◽  
Cell Interactions ◽  
Outer Membrane Vesicle ◽  
Host Cell Interactions
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