Amoeboid movement

Amoeboid movement is the most typical mode of locomotion in adherent
Movement occurs when the cytoplasm slides and forms a pseudopodium in front to pull the cell forward. Some examples of organisms that exhibit this type of locomotion are
This type of movement has been linked to changes in action potential. While several hypotheses have been proposed to explain the mechanism of amoeboid movement, its exact mechanisms are not yet well understood.[3][4] Assembly and disassembly of
Types of amoeboid motion

Crawling
Crawling is one form of amoeboid movement which starts when an extension of the moving cell (pseudopod) binds tightly to the surface.[9][10] The main bulk of the cell pulls itself toward the bound patch. By repeating this process the cell can move until the first bound patch is at the very end of the cell, at which point it detaches.[9][10] The speed at which cells crawl can vary greatly, but generally crawling is faster than swimming, but slower than gliding on a smooth surface.[9] However, crawling does not become notably slower on uneven and irregular surfaces, while gliding becomes much slower under such conditions.[9] It seems that crawling can be either bleb-driven or actin-driven (see sections below), depending on the nature of the surface.[10]
Gliding
Gliding is similar to crawling, but is characterized by much less adhesion to the surface, making it faster on smoother surfaces which require less traction but slower on more difficult and complicated surfaces.[9] Some cells glide with the same mechanism as crawling, but with larger pseudopods and less surface adhesion.[9] Other cells use a different method to glide: a small patch of the cell already touching the surface binds to the surface, after which the cytoskeleton pushes or pulls on the anchored patch to slide the cell forward.[11] This differs from the aforementioned mechanism in that the cell does not extend a pseudopod, so there is relatively little deformation of the cell as it progresses.[11]
Swimming
Many different prokaryotic and eukaryotic cells can swim and many of these have either flagella or cilia for that purpose. These dedicated structures are not necessary for swimming, though, as there are amoeba and other eukaryotic cells which lack flagella and cilia but can still swim, although it is slower than crawling or gliding.[9][10][12] There are two different proposed mechanisms for amoeboid swimming. In the first the cell extends small pseudopods which then move down the sides of the cell, acting like paddles.[9][10][12] In the second the cell generates an internal flow cycle, with the cytoplasm flowing backward along the membrane edge and forward through the middle, generating a force on the membrane which moves the cell forward.[10][12]
Molecular mechanism of cell motion
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Sol-gel theory
The
For example, when an amoeba moves, it extends a gelatinous, cytosolic pseudopodium, which then results in the more fluid cytosol (plasma sol) flowing after the gelatinous portion (plasma gel) where it congeals at the end of the pseudopodium. This results in the extension of this appendage. On the opposite (posterior) end of the cell, plasma gel is then converted to plasma sol and streamed toward the advancing pseudopodium. As long as the cell has a way to grapple the substratum, repetition of this process guides the cell forward. Inside the amoeba, there are proteins that can be activated to convert the gel into the more liquid sol state.
Cytoplasm consist largely of actin and actin is regulated by actin-binding protein. Actin binding proteins are in turn regulated by calcium ions; hence, calcium ions are very important in the sol-gel conversion process.[1][13]
Amoeboid movement modalities
Actin-driven motility
Based on some mathematical models, recent studies hypothesize a novel biological model for collective biomechanical and molecular mechanisms of cellular motion.[14] It is proposed that microdomains weave the texture of cytoskeleton and their interactions mark the location for formation of new adhesion sites. According to this model, microdomain signaling dynamics organize the cytoskeleton and its interaction with the substratum. As microdomains trigger and maintain active polymerization of actin filaments, their propagation and zigzagging motion on the membrane generate a highly interlinked network of curved or linear filaments oriented at a wide spectrum of angles to the cell boundary. It has also been proposed that microdomain interaction marks the formation of new focal adhesion sites at the cell periphery. The interaction of myosin with the actin network then generates membrane retraction/ruffling, retrograde flow, and contractile forces for forward motion. Finally, continuous application of stress on the old focal adhesion sites could result in the calcium-induced activation of calpain, and consequently the detachment of focal adhesions which completes the cycle.
In addition to actin polymerization, microtubules may also play an important role in cell migration where the formation of lamellipodia is involved. One experiment showed that although microtubules are not required for actin polymerization to create lamellipodial extensions, they are needed in order to afford cellular movement.[15]
Bleb-driven motility
Another such proposed mechanism, the 'bleb-driven amoeboid locomotion' mechanism, suggests that the cell cortex actomyosin contracts to increase
Blebbing can also be a sign of when a cell is undergoing apoptosis.[17]
It has also been observed that the blebs formed by motile cells undergo a roughly uniform life cycle that lasts approximately one minute. This includes a phase involving the initial outward expansion where the membrane breaks away from the membranous cytoskeleton. This is then followed by a short static phase where the hydrostatic pressure that has built up is just enough to maintain the size of the bleb. Following this is the last phase characterized by the bleb slowly retracting and the membrane being reintroduced to the cytoskeleton infrastructure.[18]
Cells may undergo fast transitions between blebbing and lamellipodium-based motility as a means of migration. However, the rate at which these transitions are made is still unknown. Tumor cells may also exhibit rapid transitions between amoeboid motility and mesenchymal motility, another form of cellular movement.[19]
Related movement mechanisms
Dictyostelium cells and neutrophils can also swim, using a similar mechanism as for crawling.[9][20]
Another unicellular form of movement shown in
See also
References
- ^ PMID 23940560.
- ^ PMID 2258833.
- PMID 352246.
- PMID 19262145.
- PMID 17477841.
- PMID 8280467.
- PMID 20192768.
- ISBN 978-0-12-656970-4.
- ^ PMID 22096590.
- ^ PMID 30854030.
- ^ PMID 16939778.
- ^ PMID 20534502.
- ^ ISBN 9788122430790. Retrieved 29 October 2014.
- S2CID 37036941.
- PMID 10982396.
- PMID 16926192.
- S2CID 2537726.
- PMID 18541702.
- PMID 22786929.
- PMID 20921382.