Bacterial morphological plasticity
Bacterial morphological plasticity refers to changes in the
Bacterial shape and size under selective forces
Normally, bacteria have different shapes and sizes which include coccus, rod and helical/spiral (among others less common) and that allow for their classification. For instance, rod shapes may allow bacteria to attach more readily in environments with shear stress (e.g., in flowing water). Cocci may have access to small pores, creating more attachment sites per cell and hiding themselves from external shear forces. Spiral bacteria combine some of the characteristics cocci (small footprints) and of filaments (more surface area on which shear forces can act) and the ability to form an unbroken set of cells to build biofilms. Several bacteria alter their morphology in response to the types and concentrations of external compounds. Bacterial morphology changes help to optimize interactions with cells and the surfaces to which they attach. This mechanism has been described in bacteria such as Escherichia coli and Helicobacter pylori.[2]
Bacterial shape | Example | Changes under selective forces |
---|---|---|
Filamentation Filamentation allows bacteria to have more surface area for long-term attachments and can interlink themselves with porous surfaces. | Caulobacter crescentus: in their niche (freshwater), filament is the regular shape that contributes to their resistance to heat and survival. |
|
Prosthecate Prosthecate bacteria are more easily attached by placing adhesins on the tips of thin appendages or may insinuate these into pores or crevices in solid substrates. | Prosthecomicrobium pneumaticum |
|
Bifid Y-shaped cell occurs most often in Gram positive, but also in Gram-negative bacteria. It is part of the normal cycle of several microorganisms, but could be induced by specific cues.[2] | Bifidobacterium longum |
|
Pleomorphic Pleomorphic bacteria grow adopting different forms under explicit genetic control and are associated with important physiological phenotypes (for example due to nutrient limitation).[2] | Legionella pneumophila This bacteria have 3 shapes in vitro and 5 in vivo, including rods, cocci, filaments, and a form created by "fragmented" cell septation. |
|
Helical/spiral | Leptospira spp |
|
Bacterial filamentation
Physiological mechanisms
Oxidative stress, nutrient limitation, DNA damage and antibiotic exposure are examples of
- Base Excision Repair (BER) mechanism
- This is a strategy to repair DNA damage observed in E. coli. This involves two types of enzymes:
- Bifunctional glycosylases: the endonuclease III (encoded by nth gene)
- Apurinic/Apirimidinic (AP)-endonucleases: endonuclease IV (encoded by nfo gene) and exonuclease III (encoded by xth gene).
- Under this mechanism, daughter cells are protected from receiving damaged copies of the bacterial chromosome, and at the same time promoting bacterial survival. A mutant for these genes lack BER activity and a strong formation of filamentous structures is observed.[6]
- SulA/FtsZ mediated filamentation
- This is a mechanism to halt cell division and repair DNA. In the presence of single-stranded DNA regions, due to the action of different external cues (that induce mutations), the major bacterial recombinase (RecA) binds to this DNA regions and is activated by the presence of free nucleotide triphosphates. This activated RecA stimulates the autoproteolysis of the SOS transcriptional repressor LexA. The LexA regulon includes a cell division inhibitor, SulA, that prevent the transmission of mutant DNA to the daughter cells. SulA is a dimer that binds FtsZ (a tubulin-like GTPase) in a 1:1 ratio and acts specifically on its polymerization which results in the formation of non-septated bacteria filaments.[7] A similar mechanism may occur in Mycobacterium tuberculosis,which also elongates after being phagocytized.[2]
- M. tuberculosis
- Septum site determining protein (Ssd) encoded by rv3660c promotes filamentation in response to the stressful intracellular environment. SSD inhibits septum and is also found in Mycobacterium smegmatis. The bacterial filament ultrastructure is consistent with inhibition of FtsZ polymerization (previously described). Ssd is believed to be part of a global regulatory mechanism in this bacteria that promotes a shift into an altered metabolic state.[8]
- Helicobacter pylori
- In this spriral-shaped Gram-negative bacterium, the filamentation mechanism are regulated by two mechanisms: the peptidases that cause peptidoglycan relaxation and the coiled-coil-rich proteins (Ccrp) that are responsible for the helical cell shape in vitro as well as in vivo. A rod shape could have probably an advantage for motility than the regular helical shape. In this model, there is another protein Mre, which is not exactly involved in the maintenance of cell shape but in the cell cycle. It has been demotrated that mutant cells were highly elongated due to a delay in cell division and contained non-segregated chromosomes.[9]
Environmental cues
Immune response
Some of the strategies for bacteria to bypass host defenses include the generation of filamentous structures. As it has been observed in other organisms (such as fungi), filamentous forms are resistant to phagocytosis. As an example of this, during urinary tract infection, filamentous structures of uropathogenic E. coli (UPEC) start to develop in response to host innate immune response (more exactly in response to Toll-like receptor 4-
Predator protist
Bacteria exhibit a high degree of "morphological plasticity" that protects them from predation. Bacterial capture by protozoa is affected by size and irregularities in shape of bacteria. Oversized, filamentous, or prosthecate bacteria may be too large to be ingested. On the other hand, other factors such as extremely tiny cells, high-speed motility, tenacious attachment to surfaces, formation of biofilms and multicellular conglomerates may also reduce predation. Several phenotypic features of bacteria are adapted to escape protistan-grazing pressure.[10][11]
Protistan grazing or bacterivory is a protozoan feeding on bacteria. It affects prokaryotic size and the distribution of microbial groups. There are several feeding mechanisms used to seek and capture prey, because the bacteria have to avoid being consumed from these factors. There are six feeding mechanisms listed by Kevin D. Young.[2]
- Filter feeding: transport water through a filter or sieve
- Sedimentation: allows prey to settle into a capture device
- Interception: capture by predator-induced current or motility and phagocytosis
- Raptorial: predator craws and ingests prey through pharynx or by pseudopods
- Pallium: prey engulfed e.g. by extrusion of feeding membrane
- Myzocytosis: punctures prey and suck out cytoplasm and content
Bacterial responses are elicited depending on the predator and prey combinations because feeding mechanisms differ among the protists. Moreover, the grazing protists also produce the by-products, which directly lead to the morphological plasticity of prey bacteria. For example, the morphological phenotypes of Flectobacillus spp. were evaluated in the presence and absence of the flagellate grazer Orchromonas spp. in a laboratory that has environmental control within a chemostat. Without grazer and with adequate nutrient supply, the Flectobacillus spp. grew mainly in medium-sized rod (4-7 μm), remaining a typical 6.2 μm in length. With the predator, the Flectobacillus spp. size was altered to an average 18.6 μm and it is resistant to grazing. If the bacteria are exposed to the soluble by-products produced by grazing Orchromonas spp. and pass through a dialysis membrane, the bacterial length can increase to an average 11.4 μm.[12] Filamentation occurs as a direct response to these effectors that are produced by the predator and there is a size preference for grazing that varies for each species of protist.[1] The filamentous bacteria that are larger than 7 μm in length are generally inedible by marine protists. This morphological class is called grazing resistant.[13] Thus, filamentation leads to the prevention of phagocytosis and killing by predator.[1]
Bimodal effect
Bimodal effect is a situation that bacterial cell in an intermediate size range are consumed more rapidly than the very large or the very small. The bacteria, which are smaller than 0.5 μm in diameter, are grazed by protists four to six times less than larger cells. Moreover, the filamentous cells or cells with diameters greater than 3 μm are often too large to ingest by protists or are grazed at substantially lower rates than smaller bacteria. The specific effects vary with the size ratio between predator and prey. Pernthaler et al. classified susceptible bacteria into four groups by rough size.[14]
- Bacterial size < 0.4 μm were not grazed well
- Bacterial size between 0.4 μm and 1.6 μm were "grazing vulnerable"
- Bacterial size between 1.6 μm and 2.4 μm were "grazing suppressed"
- Bacterial size > 2.4 μm were "grazing resistant"
Filamentous preys are resistant to protist predation in a number of marine environments. In fact, there is no bacterium entirely safe. Some predators graze the larger filaments to some degree. Morphological plasticity of some bacterial strains is able to show at different growth conditions. For instance, at enhanced growth rates, some strains can form large thread-like morphotypes. While filament formation in subpopulations can occur during starvation or at suboptimal growth conditions. These morphological shifts could be triggered by external chemical cues that might be released by the predator itself.[11]
Besides bacterial size, there are several factors affecting the predation of protists. Bacterial shape, the spiral morphology may play a defensive role towards predation feedings. For example, Arthrospira may reduce its susceptibility to predation by altering its spiral pitch. This alteration inhibits some natural geometric feature of the protist's ingestion apparatus. Multicellular complexes of bacterial cells also change the ability of protist's ingestion. Cells in
As for bacterial motility, the bacteria with high-speed motility sometimes avoid grazing better than their nonmotile or slower strains
Antibiotics
Antibiotics can induce a broad range of morphological changes in bacterial cells including
Antibiotics used to treat
In addition to the mechanism described above, some antibiotics induce filamentation via the
Nutritional stress
Nutritional stress can change bacterial morphology. A common shape alteration is filamentation which can be triggered by a limited availability of one or more substrates, nutrients or electron acceptors. Since the filament can increase a cell's uptake–surface area without significantly changing its volume appreciably. Moreover, the filamentation benefits bacterial cells attaching to a surface because it increases specific surface area in direct contact with the solid medium. In addition, the filamentation may allows bacterial cells to access nutrients by enhancing the possibility that part of the filament will contact a nutrient-rich zone and pass compounds to the rest of the cell's biomass.[2] For example, Actinomyces israelii grows as filamentous rods or branched in the absence of phosphate, cysteine, or glutathione. However, it returns to a regular rod-like morphology when adding back these nutrients.[25]
See also
References
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