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Bacterial morphological plasticity
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Bacterial morphological plasticity
Bacterial morphological plasticity refers to changes in the shape and size that bacterial cells undergo when they encounter stressful environments. Although bacteria have evolved complex molecular strategies to maintain their shape, many are able to alter their shape as a survival strategy in response to protist predators, antibiotics, the immune response, and other threats.
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.
Oxidative stress, nutrient limitation, DNA damage and antibiotic exposure are examples of stressors that cause bacteria to halt septum formation and cell division. Filamentous bacteria have been considered to be over-stressed, sick and dying members of the population. However, the filamentous members of some communities have vital roles in the population's continued existence, since the filamentous phenotype can confer protection against lethal environments. Filamentous bacteria can be over 90 μm in length and play an important role in the pathogenesis of human cystitis. Filamentous forms arise via several different mechanisms.
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-TLR4). TLR-4 is stimulated by the lipopolysaccharide (LPS) and recruits neutrophils (PMN) which are important leukocytes to eliminate these bacteria. Adopting filamentous structures, bacteria resist these phagocytic cells and their neutralizing activity (which include antimicrobial peptides, degradative enzyme and reactive oxygen species). It is believed that filamentation is induced as a response of DNA damage (by the mechanisms previously exposed), participating SulA mechanism and additional factors. Furthermore, the length of the filamentous bacteria could have a stronger attachment to the epithelial cells, with an increased number of adhesins participating in the interaction, making even harder the work for (PMN). The interaction between phagocyte cells and adopting filamentous-shape bacteria provide an advantage to their survival. In this relate, filamentation could be not only a virulence, but also a resistance factor in these bacteria.
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.
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.
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. 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. The filamentous bacteria that are larger than 7 μm in length are generally inedible by marine protists. This morphological class is called grazing resistant. Thus, filamentation leads to the prevention of phagocytosis and killing by predator.
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.
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Bacterial morphological plasticity
Bacterial morphological plasticity refers to changes in the shape and size that bacterial cells undergo when they encounter stressful environments. Although bacteria have evolved complex molecular strategies to maintain their shape, many are able to alter their shape as a survival strategy in response to protist predators, antibiotics, the immune response, and other threats.
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.
Oxidative stress, nutrient limitation, DNA damage and antibiotic exposure are examples of stressors that cause bacteria to halt septum formation and cell division. Filamentous bacteria have been considered to be over-stressed, sick and dying members of the population. However, the filamentous members of some communities have vital roles in the population's continued existence, since the filamentous phenotype can confer protection against lethal environments. Filamentous bacteria can be over 90 μm in length and play an important role in the pathogenesis of human cystitis. Filamentous forms arise via several different mechanisms.
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-TLR4). TLR-4 is stimulated by the lipopolysaccharide (LPS) and recruits neutrophils (PMN) which are important leukocytes to eliminate these bacteria. Adopting filamentous structures, bacteria resist these phagocytic cells and their neutralizing activity (which include antimicrobial peptides, degradative enzyme and reactive oxygen species). It is believed that filamentation is induced as a response of DNA damage (by the mechanisms previously exposed), participating SulA mechanism and additional factors. Furthermore, the length of the filamentous bacteria could have a stronger attachment to the epithelial cells, with an increased number of adhesins participating in the interaction, making even harder the work for (PMN). The interaction between phagocyte cells and adopting filamentous-shape bacteria provide an advantage to their survival. In this relate, filamentation could be not only a virulence, but also a resistance factor in these bacteria.
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.
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.
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. 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. The filamentous bacteria that are larger than 7 μm in length are generally inedible by marine protists. This morphological class is called grazing resistant. Thus, filamentation leads to the prevention of phagocytosis and killing by predator.
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.