Motility mechanisms

Komnick, H., Stockem, W., Wohlfarth-Botterman, K.E. (1973). Cell motility Mechanisms in protoplasmic streaming and amoeboid movement. Int. Rev. Cytol. 34, 169-249. 

Myosins, kinesins, and dyneins move by cycling between states with different affinities for the long, polymeric macromolecules that serve as their tracks. For myosin, the molecular track is a polymeric form of actin, a 42-kd protein that is one of the most abundant proteins in eukaryotic cells, typically accounting for as much as 10% of the total protein. Actin polymers are continually being assembled and disassembled in cells in a highly dynamic manner, accompanied by the hydrolysis of ATP. On the microscopic scale, actin filaments participate in the dynamic reshaping of the cytoskeleton and the cell itself and in other motility mechanisms that do not include myosin. In muscle, myosin and actin together are the key components responsible for muscle contraction. 

This publication is aimed to serve as both a textbook for beginners and a reference book for professionals. For easier reading, each chapter that reviews a certain chemotaxis system follows a standard scheme it starts with a description of the motility mechanism specific to the system (motility is a prerequisite for chemotaxis) and ends with a description of how this motility is modulated by chemotaxis. 

SLIDING. Shear forces between filaments were suggested as a possible mitotic motile mechanism by BHaf (1929) even before the advent of the highly successful sUding filament model of force production in muscle. Since then such speculations have increased (Mazia, 1961 Bajer, 1968a,c Subirana, 1968 McIntosh et al., 1969). The commendably specific and testable model of McIntosh et al. will be considered first, followed by a more general discussion. 

The muscular contraction implies the most important, most versatile as performances motility mechanism in the living life, and practically the only one able of evolutionary perfecting. Its support, the skeletal muscle, presents a complex structure, having at list six levels of hierarchy, Figure 4.2. 

McBride, M., Bacterial gliding motility mechanisms and mysteries. Am. Soc. Microbiol. News, 2000, 66 203210. 

Huxley, H.E. A personal view of muscle and motility mechanisms. Annu. Rev. Physiol. 1996, 58, 1-19. 

Phosphorylation is the reversible process of introducing a phosphate group onto a protein. Phosphorylation occurs on the hydroxyamino acids serine and threonine or on tyrosine residues targeted by Ser/Thr kinases and tyrosine kinases respectively. Dephosphorylation is catalyzed by phosphatases. Phosphorylation is a key mechanism for rapid posttranslational modulation of protein function. It is widely exploited in cellular processes to control various aspects of cell signaling, cell proliferation, cell differentiation, cell survival, cell metabolism, cell motility, and gene transcription. 

Studies on muscle contraction carried out between 1930 and 1960 heralded the modem era of research on cytoskeletal stmctures. Actin and myosin were identified as the major contractile proteins of muscle, and detailed electron microscopic studies on sarcomeres by H.E. Huxley and associates in the 1950s produced the concept of the sliding filament model, which remains the keystone to an understanding of the molecular mechanisms responsible for cytoskeletal motility. 

Adams, R.J., Pollard, T.D. (1989). Membrane bound myosin-I provides new mechanism in cell motility. Cell Mot. Cytoskel. 14, 178-182. 

The process of activation of neutrophils is essentially similar. They are activated, via specific receptors, by interaction with bacteria, binding of chemotactic factors, or antibody-antigen complexes. The resultant rise in intracellular Ca affects many processes in neutrophils, such as assembly of micrombules and the actin-myosin system. These processes are respectively involved in secretion of contents of granules and in motility, which enables neutrophils to seek out the invaders. The activated neutrophils are now ready to destroy the invaders by mechanisms that include production of active derivatives of oxygen. 

Increased motility results in decreased contact between ingested food and drink and the intestinal mucosa, leading to reduced reabsorption and increased fluid in the stool. Diarrhea resulting from altered motility is often established after other mechanisms have been excluded. IBS-related diarrhea is due to altered motility. 

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