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Magnetotactic Bacteria (MTB) Adaptations

Magnetotactic bacteria (MTB) are a polyphyletic group of motile bacteria that has been observed in freshwater and marine aquatic environments. Discovered in 1975 by Richard Blakemore, these microorganisms are able to passively navigate along the earth’s magnetic field toward the bottom of their aquatic habitats, to efficiently find low oxygen environments. The MTB passive navigation is enabled by the biomineralization of crystals of the iron oxide magnetite (Fe3O4) or, in some cases, the iron sulfide greigite (Fe3S4). These crystals are enveloped in a specialized, bilayer membrane organelle named the magnetosome (Komeili, 2012).
MTB are not pulled northward or southward by the magnetic field, they are only aligned and swim parallel to it. North seeking MTB are found in the northern hemisphere; whereas, south-seeking MTB are found in the southern hemisphere (Blakemore, 1982).
Surveys describing the ecology of MTB show that they are found in the highest numbers close to the oxic anoxic transition zone (OATZ), an habitat where opposing horizontal gradients of reduced compounds (usually sulfide from the bottom of sediments) and oxidized compounds (oxygen, diffusing from the surface of the aquatic environment) are present. (Komeili, 2012).
When coupling these observations, it is clear to see how the magnetosome organelle is advantageous to the MTB – By using the earth’s magnetic field as a vertical guide through the horizontal opposing gradients, these bacteria use a one-dimensional, simpler route to finding the OATZ, rather than the labyrinthine, three dimensional chemotactic or aerotactic search mechanisms (Komeili, 2012).
Synthesized through an invagination process from the cell’s inner membrane, the magnetosomes are intracellular, bilayer membrane organelle that provides both spatial and physicochemical control over the magnetic crystals biomineralization (Komeili, 2012). Through strict genetic control mechanisms, the magnetosomes are organized into highly ordered intracellular chains (one to several), which is essential for the ability of the cell to align with the earth’s magnetic field. The biomineralization process in magnetosomes is also genetically controlled, leading to a similarity of crystal’s size, shape and number within a single bacterial strain (Komeili, 2012).
Since Blakemore’s serendipitous discovery of the MTB, these unique bacteria are of considerable research interest and the magnetosome formation and biomineralization has evolved into an interdisciplinary field of research. In recent years, great effort to find the molecular basis of the magnetosome synthesis and biomineralization has resulted in a fuller understanding of this process. To answer the question just how well adapted are these organisms to align with the earth’s magnetic field, I will present the possible molecular mechanisms of cytoskeletal organization and biomineralization that allows for the formation of a functional magnetosome organelle.
The efficiency of the MTB magnetic response largely depends on the total magnetic dipole moment that the cell exhibits. To maximize the magnetic moment dipole, first, they must precisely control the biomineralization of a magnetite crystal within the single magnetic domain size range, meaning that the crystals enveloped by the magnetosome should be characterized by a stable and uniform magnetization, in a way that the magnetic moment of the particle attains a maximum value. Therefore, these crystals exhibit narrow size distributions where mature crystals typically fall within the range of about 35–120 nm (Komeili, 2012). Smaller superparamagnetic particles would not efficiently contribute to the cellular magnetic moment at ambient temperature, whereas larger crystals tend to reduce their total magnetic moment because they naturally form multiple magnetic domains (Komeili, 2012).
Second, to truly function as a compass needle, the magnetosomes needs to be arranged in a linear fashion into chains to achieve the maximum possible magnetic moment. Without this chain structure, magnetosomes have the tendency to agglomerate in order to reduce the system’s energy (Scheffel, 2006). The magnetosome chains are built on a filament cytoskeletal structures that run along the length of the MTB and orient the magnetic dipole moments of the particles parallel to each other along the chain. The total magnetic dipole moment is then the sum of the moments of the individual particles, thus constructing a permanent magnetic dipole large enough to align the MTB with earth’s magnetic field (Scheffel, 2006).
Recent genetic studies of MTB have led to the identification of a large area named the magnetosome gene island (MAI). This island contains many of the genes that encode most of the magnetosome membrane proteins, which in turn, are responsible for forming a functioning organelle (Scheffel, 2006). Genetic studies of two MAI genes, mamJ and mamK, have revealed that they play a key role in the formation and stability of the magnetosome chain (Komeili, 2012).
mamK, is predicted to code a bacterial actin-like protein that form the cytoskeletal chains filament. To test this assumption, a mutant MTB was generated using an inframe deletion mutation of the mamK gene (Komeili, 2005).
The deletion of the mamK gene did not affect the biomineralization or the magnetosomes formation and the mutant continued to form magnetite crystals. However, the magnetosomes were dispersed in the cell cytoplasm and did not organize as one coherent chain (Komeili, 2005). To ensure that this phenotype is due to the deletion of mamK, a plasmid carrying the mamK gene was introduced to the mutants, and some of the cells showed full reversal of the mutant phenotype (Komeili, 2005). These results could indicate that MamK codes for the long filament that organizes and maintains the magnetosomes in a coherent chain structure.
mamK and mamJ genes are located consecutively on the MTB genome and are co-transcribed (Scheffel, 2006). To test the role of the mamJ gene in the biomineralization process of MTB, a mutant was generated in which the mamJ gene was removed through an inframe deletion mutation. Magnetite biomineralization was not affected and the mutant continued to form magnetite crystals (Scheffel, 2006). The magnetosome associated cytoskeletal filament that forms the chain was still present in the mamJ mutant strain, but the magnetosomes were not attached to the chain and were dispersed in the cell’s cytoplasm (Scheffel, 2006). Thus, when combining the results from both experiments described above, it appears that that mamJ, while not responsible for the formation of the cytoskeletal filaments, works in cooperation with mamK and mediates the interaction between the magnetosome and the cytoskeletal filaments (Komeili, 2012).
These results demonstrate that in order to achieve a high structural level that allows for functional magnetotactic ability, the magnetosome chain assembly is strictly genetically controlled. In terms of cellular organization, the MTB magnetotactic ability is among the most elaborated prokaryotic traits (Komeili, 2012). Understanding this cellular organization and its genetic control mechanisms in a model organism such as the MTB, could lead to innovative treatments for diseases in which magnetite is linked to a pathological conditions. For example, defects in the protein ferritin causes patients who suffer from the genetic neurodegenerative disorder, neuroferritinopathy, to accumulate magnetite in the brain (Komeili, 2012). A clearer understanding of the genetic control that governs the MTB magnetotactic ability could lead to insights into the molecular biology of this disorder.
References
Blakemore, R. P. 1982. Magnetotactic bacteria. Annu. Rev. Microbiol. 36:217-238.
Komeili, A., Z. Li, D. K. Newman, and G. J. Jensen.2005. Magnetosomes are cell membrane invaginations organized by the actin-like protein MamK.Science311:242-245
Komeili, A. “Molecular Mechanisms of Compartmentalization and Biomineralization in Magnetotactic Bacteria.”FEMS microbiology reviews36.1 (2012): 232–255.PMC. Web. 23 June 2015.
Scheffel, M. Gruska, D. Faivre, A. Linaroudis, J.M. Plitzko, D. Schuler An acidic protein aligns magnetosomes along a filamentous structure in magnetotactic bacteria Nature, 440 (2006), pp. 110–114

Regulating Extracellular Fluid Volume

About 60% of an adult human body is fluid, mainly a water solution of ions and other substances. Most of this fluid is inside the cells and in known as the intracellular fluid, but about one third is in the spaces outside the cells. This is the extracellular fluid (ECF). The ECF is divided into several smaller compartments, mainly blood plasma fluid and interstitial fluid which constitute 20% and 80% of the ECF respectively. (Guyton and Hall 2006) The distribution of fluid between these two compartments is determined by the balance between two opposing forces, hydrostatic pressure which is the pressure in the circulatory system that exerted by the volume of blood and osmotic pressure which is the pressure required to maintain an equilibrium in movement of particles between the fluid compartments. The concentration of these particles dissolved in a fluid its called osmolality. The blood plasma fluid communicates with the interstitial fluid across the walls of small capillary vessels within the organs. (Mohrman and Heller 2006)
The extracellular fluid contains large amounts of electrolytes that are dissolved in body fluids, such as sodium, calcium and potassium, but and nutrients and other substances that required by the cells to maintain cell life. All body systems, principally the cardiovascular, nervous and endocrine systems contribute to maintaining fluid and electrolyte balance something that is necessary for the proper functioning of the cells. (Guyton and Hall 2006)
The hypothalamus helps in regulation of these electrolytes, nutrients and water as monitors the composition of the blood, maintaining homeostasis. That makes it an important center for information concerning the internal environment. This information is then used to control the release of hormones from the pituitary.
Sodium is the major electrolyte that regulates the extracellular fluid levels in the body. Because of its osmotic effects, changes in sodium content in the body can influence the extracellular fluid volume, including plasma volume which must be closely regulated to help maintain blood pressure. Excess sodium leads to the retention of water and an increase to plasma volume which leads to an increase in arterial blood pressure, while sodium deficit leads to water loss and decreased plasma volume which leads to a decrease in blood pressure.
Therefore sodium balance is very important in the long term regulation of extracellular fluid volume and is achieved when sodium intake is equal to sodium output. (Kelly 2005)
The kidneys adjust salt and water excretion to maintain a constant extracellular fluid volume and osmolality regulating the sodium chloride balance. Around 8-15 g of NaCl are absorbed every day and the kidneys have to excrete the same amount over time to maintain sodium ECF homeostasis. Changes in sodium content leads to changes in extracellular fluid volume and that is regulated mainly by Renin-angiotensin system (RAS), atrial natriuretic hormone (ANT), aldosterone and andidiuretic hormone (ADH) which stimulates water conservation and the thirst center. (Despopoulos and Silbernagl 2003)
ADH is the most important regulator of blood osmolality. It is released into the bloodstream from the posterior pituitary, which is an extension of the brain when its receptors detect an increase in sodium concentration and is mediated through cells in the hypothalamus.
Antidiuretic hormone reduces renal excretion of water by acting on the collecting ducts of the kidney and influence urinary output rate. An increase in sodium concentration which can be brought about by increased salt intake, dehydration or hemorrhage which is loss of blood cause an increase in ADH secretion which has as effect an increase of water reabsorption in the kidney and the production of small volume of concentrated urine which has as a result a decrease of blood osmolality as reabsorbed water dilutes the blood. On the other hand a decrease in sodium concentration cause a decrease in ADH secretion which has as effect a decrease of water reabsorption in the kidney and the production of large volume of dilute urine and that result in an increase of blood osmolality as water is lost from the blood into the urine.
ADH can also be affected by blood volume and cardiac output and is activated by significant decreases in blood pressure. A decrease in arterial blood pressure can cause an increase in ADH secretion from the posterior pituitary mediated through baroreceptors. This has as affect an increase of water reabsorption in the kidney and the production of a small volume of concentrated urine which results in an increase of blood pressure because of increased blood volume and in a decrease of blood osmolality. An increase of blood pressure causes a decrease in ADH secretion which in turn causes a decrease of water reabsorption in the kidney and the production of a large volume of dilute urine which results in a decrease of blood pressure and in an increase of blood osmolality. (Rushton 2004)
Because the kidneys receive extensive sympathetic innervations, changes in sympathetic activity can alter renal sodium and water excretion as well as regulation of ECF volume. A reduction of blood volume in case of a hemorrhage causes a reduction in blood pressure which can result in reflex activation of the sympathetic nervous system. This in turn increases renal sympathetic nerve activity, which has several effects including the stimulation of renin release. (Guyton and Hall 2006)
Renin is an enzyme that is produced in the kidneys and catalyzes the formation of angiotensin I from angiotensinogen, a serum glycoprotein. Angiotensin I is then converted to angiotensin II by the action of angiotensin-converting enzyme that is located on the surface of endothelial cells. This sequence of events is known as Renin angiotensin-aldosterone system. Angiotensin II stimulates the release of aldosterone by adrenal cortex which increases blood volume and therefore blood pressure. (Mohrman and Heller 2006) An increase in aldosterone secretion results on the increase of sodium reabsorption in the kidney, an increase of water reabsorption as water follows the sodium and a decrease in urine volume, which in turn cause an increase of blood pressure while blood osmolality is maintained because both sodium and water are reabsorbed. On the other hand a decrease in aldosterone secretion decreases sodium reabsorption in the kidney and water reabsorption as less sodium is reabsorbed and increases urine volume. This result in a decrease of blood pressure as blood volume decreases while blood osmolality is maintained as both water and sodium lost in the urine. (Rushton 2004) Angiotensin II also acts on the brain to induce drinking behavior and is a very potent vasoconstrictor agent. (Mohrman and Heller 2006)
Another important factor that regulates ECF volume is atrial natriuretic hormone (ANH). This is a hormone that causes blood vessels to dilate and the kidneys to produce more urine. That results in a decrease of blood pressure and a reduction of blood volume by excreting more water. (Rushton 2004) Atrial natriuretic hormone is release by specific cells of atria the upper chambers of the heart and acts on several parts of the body. (Despopoulos and Silbernagl 2003)
A reduction of ANH causes an increase of water and sodium reabsorption in the kidney as water follows the sodium and a decrease in urinary volume. That results in an increase of blood pressure. An increase of ANH causes water and sodium reabsorption reduction as water is lost with sodium in the urine and that results in an increase of blood pressure and a reduction of cardiac output. Either ANH excretion is increase or decreased, blood osmolality is maintained as both water and sodium are either reabsorbed or lost in the urine. The central nervous system is affected by ANH by the inhibition of ADH release and a decrease in water and salt appetite. (Rushton 2004)
Thus when there is an increase of sodium in the extracellular fluid, the osmolality of the fluid increases and this in turn stimulates the thirst center in the brain making a person to reduce the amount of water in his body returning the extracellular sodium concentration back to normal, and that increases the extacellular fluid volume. On the other hand an increase of water in the body reduces the osmolality of extracellular fluid. (Guyton and Hall 2006)

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