Mini Review

Calcium ions (Ca⁺²) in eukaryotic cells have to; cell cycle, transport, mobility, gene expression and metabolism. Cells respond to various stimuli with transient changes in intracellular free Ca⁺² concentrations. Indirect evidence indicates that Ca⁺² also influence and such as spore formation, chemotaxis, heterosist differentiation, transport, and virulence. Many studies have shown that bacteria can maintain intracellular Ca⁺² homeostasis. In addition, Ca⁺²; nitrogen starvation, environmental stress and metabolites of carbohydrate metabolism. According to studies with Escherichia coli, Bacillus subtilis and Pseudomonas aeruginosa, it has been shown that expression of hundreds of genes is regulated by extracellular Ca⁺² changes. Processes affected by these changes include, for example, swarming, type III secretion, polysaccharide production, iron uptake, quinolone signaling, and general stress responses. Many studies demonstrate that Ca⁺² play a regulatory role in the physiology of prokaryotes. The mutation analysis of EF-el protein (EfhP) from P. aeruginosa appears to be necessary for the maintenance of intracellular Ca⁺² homeostasis. Specifically, adenylate kinase and fructose- bisphosphate-aldolase have also been detected in association with Ca⁺² regulations in eukaryotic organisms.

Bacteria Ca⁺² are; membrane-bound structures. Agrobacterium tumefaciens and Rhodospiriullum rubrum are very similar to the acidoccalcisomas first described in eukaryotic organisms. Asidocalcisom on; other elements such as Ca⁺², Na+, K+, Mg⁺², Zn⁺² and phosphorus (P) are acidic organelles that serve as the main storage for Ca⁺² in pyrophosphate (PPi) and polyphosphate (poly P) form. In eukaryotic microbes, acidocalcisomes function in P metabolism, Ca⁺² homeostasis, maintenance of intracellular pH and osmo regulation. Prokaryotic acidocalcisomes are very similar to eukaryotic structures that contain H+-ATPase carriers and vacuum proton translocated pyrophosphatase responsible for their acidification. The ability of R. rubrum acidocalcisomes to store Ca⁺² could be demonstrated by X-ray microanalysis when bacterial cells were grown at 100 mM CaCl₂. As a result, it has been suggested that acidocalcisomes may be involved in Ca⁺² homeostasis in some bacteria. In Gram (-) bacteria, this region includes the region between the periplasmic space, the outer membrane and the cytoplasmic membrane.

The presence of this compartment was also detected in Gram (+) bacteria. X-ray mapping and electron loss spectroscopy showed that high concentrations of Ca⁺² were related to the cellular structure of E. coli. The periplasma contains oligosaccharides and anionic proteins that may play a role in the storage of Ca⁺² in this compartment. According to a study, the outer membrane and periplasm first serve as a barrier to Ca⁺² entries. Secondly, it is thought to play a very important role by buffering and storing Ca⁺². By targeting the photoprotein aequorin using the N-terminal OmpT signal sequence, the periplasma has been shown to store Ca⁺² in the periplasm of living E. coli cells ranging from 3-6-fold relative to the external environment. These results show us that bacterial cells; it supports our idea that it may have the ability to regulate Ca⁺² concentrations by using different mechanisms within cellular separate compartments. However, the answer to this question is unknown today; to what extent do micro-regions in bacteria contribute to Ca⁺² homeostasis? [1] this is one of the pending questions.

Ca⁺² are a well-known signal molecule that regulates a number of basic processes in eukaryotes. Abnormalities in cellular Ca⁺² regulations have been associated with bacterial infections such as cystic fibrosis (CF) and endocarditic. All evidence; shows that intracellular and extracellular Ca⁺² balances in a host can be a clue to opportunistic pathogenic bacteria and trigger their virulence. In addition, Ca⁺² in prokaryotes; spore formation, mobility, cell differentiation, transport and virulence. It has also been shown that Ca⁺² regulate bacterial gene expression and its regulatory role in prokaryotes. There is also increasing evidence that Ca⁺² play a signaling role in the regulation of cellular Ca⁺² in prokaryotes. The intracellular Ca⁺² of various bacteria such as E. coli, Propionibacterium acnes, Streptococcus pneumoniae, B. subtilis and Cyanobacteria were maintained at μM levels and the Ca⁺² effect was shown in response to environmental and physiological conditions. Such responses; Ca⁺² regulated bacteria may play a key role in physiology and virulence. Some studies show that bacteria control [Ca⁺²] using various mechanisms to transport or chelate Ca⁺². Some types of Ca⁺² transport systems have been described in prokaryotes:

a) Gradient driven Ca⁺² heat exchangers,

b) ATPase

c) Non-protein polyhydroxybutyratepolyphosphate (PHBPP) channels.

It is also thought that Ca⁺² modifiers are identified in some bacterial strains and serve as a main mechanism for Ca⁺² transports in prokaryotes. These are low affinity Ca⁺² carriers that used the stored energy of the electrochemical gradient of ions. They can work in both directions depending on the gradient. P. aeruginosa is an opportunistic human pathogen and is known to be one of the main causes of nosocomial infections and severe chronic infections in endocarditis and CF patients. Previously, growth in high Ca⁺² has been shown to increase the formation of P. aeruginosa biofilm and induce biosynthesis of many secreted virulence factors including alginate, extracellular proteases and pyocyanin [2]. Ca⁺² levels include hydrolytic modulation of the hydrolytic enzyme in Pectobacterium carotovorum produced in V. cholerae. In addition, Ca⁺² in animal and plant hosts; as a secondary messenger, it regulates defense responses based on regulatory systems. Calcium, magnesium and iron are known to be involved in the process of X. fastidiosa infection.

However, it has also been suggested that in some cases (e.g. Ca⁺² and Mg⁺²), these elements are non-specific and act as bridges of adhesion between negatively charged bacterial cells and xylem vessels. The presence of Ca⁺²; increases biofilm formation, cell binding and mobility under in vitro conditions. Ca⁺² levels also affect biofilm production. Bivalent cations containing Ca⁺² and Mg⁺² have previously been shown to play a role in the formation of biofilm by different bacteria. In Erwinia carotovora, high Ca⁺² levels suppress the expression of PehA, an endopoliglaklacronase, one of the major virulence determinants. The opposite effect, ie increase in virulence, was observed in P. aeruginosa. Here, with the addition of Ca⁺², increased production of extracellular proteases and increased expression of alginate biosynthetic genes, which are the main components of extracellular matrix, also affected the increase of biofilm thickness. X. fastidiosa has been shown to play a role in the regulation of biofilm formation, its effect on the cell surface and twitch mobility. Some studies; it also shows that the addition of Ca⁺² significantly increases the surface binding strength of the cells. In addition to the “bridging” effect that may occur with Ca⁺², it has been shown that in addition to the effect of Ca⁺² on biofilm and movement, a metabolic dependent effect may be responsible [3].

In addition to their role in biofilm matrix stability, Ca⁺² can also affect bacterial gene expression. In eukaryotic cells, Ca⁺² is an important signaling molecule and can play a regulatory role in bacteria. Many bacteria; P. aeruginosa PA4107 also includes genes for calmodulin-like proteins with characteristic EF hand motifs, including PlcR, possibly shown to bind Ca⁺². The secretion and stability of some extracellular proteins in P. aeruginos are influenced by Ca⁺². The toxins secreted by the Type III secretion system are suppressed by Ca⁺². The amounts of extracellular elastase (LasB) and LasA secreted by Type II secretion increase in the presence of additional Ca⁺². It is also known that Ca⁺² affect the biofilm structure. Interestingly, added Ca⁺² has been shown to cause biofilms of mucoid P. aeruginosa FRD1, which is 10 to 20-fold thicker than non-Ca⁺² added biofilms. The amounts of extracellular proteases were increased in Ca⁺² modified biofilms and it was also found that the proteases were housed in the Ca⁺² enhanced alginate matrix [4]. To date, salt and glucose have always been studied and studied in health-related diets. As a result of this information, it should be remembered that Ca⁺² diets may also be effective in understanding and reducing the effects of microorganisms.

Acknowledgement

None.

Conflict of Interest

No conflict of interest.

References

• DC Domíngueza, M Guragain, M Patrauchan (2015) Calcium binding proteins and calcium signaling in prokaryotes. Cell Calcium 57(3): 151-165.
• M Guragain, DL Lenaburg, FS Moore, I Reutlinger, MA Patrauchan (2013) Calcium homeostasis in Pseudomonas aeruginosa requires multiple transporters and modulates swarming motility. Cell Calcium 54(5): 350- 361.
• LF Cruz, PA Cobine, L De La Fuente (2012) Calcium increases Xylella fastidiosa surface attachment, biofilm formation, and twitching motility. Applied and Environmental Microbiology 78 (5): 1321-1331.
• S Sarkisova, MA Patrauchan, D Berglund, DE Nivens, MJ Franklin (2005) Calcium-induced virulence factors associated with the extracellular matrix of mucoid Pseudomonas aeruginosa Journal of Bacteriology 187(13): 4327-4337.

Abstract

Calcium ions (Ca⁺²) in eukaryotic cells have to; cell cycle, transport, mobility, gene expression and metabolism. Cells respond to various stimuli with transient changes in intracellular free Ca⁺² concentrations. Indirect evidence indicates that Ca⁺² also influence and such as spore formation, chemotaxis, heterosist differentiation, transport, and virulence. Many studies have shown that bacteria can maintain intracellular Ca⁺² homeostasis. In addition, Ca⁺²; nitrogen starvation, environmental stress and metabolites of carbohydrate metabolism. According to studies with Escherichia coli, Bacillus subtilis and Pseudomonas aeruginosa, it has been shown that expression of hundreds of genes is regulated by extracellular Ca⁺² changes. Processes affected by these changes include, for example, swarming, type III secretion, polysaccharide production, iron uptake, quinolone signaling, and general stress responses. Many studies demonstrate that Ca⁺² play a regulatory role in the physiology of prokaryotes.