Amoeboids Movements

Amoebae exhibit this form of locomotion (e.g., Amoeba proteus). Their cytoplasm is made up of plasmasol (central fluid) and a viscous plasmagel. Plasmagel is converted to plasmasol, which causes the cytoplasm to slide forward and form a pseudopodium in front of the cell, propelling it forward.

Amoeboids are cells that migrate in this manner. Apart from amoeba, other examples include cellular slime moulds (e.g., Dictyostelium discoideum) and human cells, including liver Kupffer cells, monocytes, neutrophils, macrophages, and malignant cells. 

When the cytoplasm glides forward and produces a pseudopodium in front, the cell advances. Amoebae (such as Amoeba proteus and Naegleria gruberi), slime moulds, and some human cells such as leukocytes are all examples of creatures that demonstrate this sort of movement. Sarcomas, or tumours of connective tissue cells, are very effective in amoeboid mobility, which contributes to their high rate of metastasis.

This movement pattern has been associated with changes in action potential. While various suggestions have been advanced to explain amoeboid movement, its precise mechanics remain unknown. Actin filament formation and deconstruction in cells may be critical for the biochemical and biophysical mechanisms behind many types of cellular movement in striated muscle structures and nonmuscle cells. Polarity establishes distinct leading and lagging edges in cells by selectively moving proteins to the poles, and may play a role in eukaryotic chemotaxis.

Types of amoeboid motion

Crawling

Crawling is a type of amoeboid movement that begins when an extension of the moving cell (pseudopod) forms a strong attachment to the surface. The cell’s primary bulk gravitates toward the bound patch. The cell can continue this process until the initial bound patch reaches the ultimate end of the cell, at which point it detaches. Although the speed at which cells crawl varies significantly, crawling is generally faster than swimming but slower than gliding on a flat surface. However, crawling is not significantly slower over uneven and irregular terrain, although gliding is significantly slower. Crawling appears to be either bleb- or action-driven (see sections below), depending on the surface’s composition.

Gliding

When gliding, it is comparable to crawling, but it is characterised by significantly less adherence to the surface, allowing it to be faster on smoother surfaces that require less traction while being slower on more difficult and complex terrain. A similar technique to crawling is used by certain cells to glide, but with larger pseudopods and less surface adherence than crawling. Other cells glide in a different way: a small patch of the cell that is already touching the surface bonds to the surface, after which the cytoskeleton pushes or pulls on an anchored patch to move the cell forward in the direction of the surface. Since the cell does not extend a pseudopod in this method, the cell deforms relatively little as growth develops, in contrast to the previously discussed technique.

Swimming

Many distinct prokaryotic and eukaryotic cells are capable of swimming, and many of these include either flagella or cilia to aid them in their endeavours. Swimming, however, is not necessitated by the presence of flagella and cilia, as amoeba and other eukaryotic cells can swim despite the absence of these structures, albeit at a slower rate than crawling or gliding. There have been two separate hypothesised processes for amoeboid swimming put forward by scientists. In the first, the cell extends little pseudopods that slide down the sides of the cell, resembling paddles in their movement. When a cell develops an internal flow cycle, the cytoplasm flows backward along the membrane border and forward through the centre, creating a force on the membrane that propels it forward.

Molecular mechanism of cell motion

Amoeboid movement modalities

Actin-driven motility

Recent studies hypothesise a novel biological model for collective biomechanical and molecular mechanisms of cellular motion based on mathematical models. Microdomains are thought to weave the cytoskeleton’s texture and their interactions serve as a marker for the development of new adhesion sites. Microdomain signalling dynamics, according to this hypothesis, organise the cytoskeleton and its interaction with the substratum. 

Because microdomains initiate and maintain active polymerization of actin filaments, their propagation and zigzagging motion across the membrane result in a dense network of curved or linear filaments orientated at a broad variety of angles to the cell border. Additionally, microdomain interaction has been postulated to be involved in the development of new focal adhesion sites at the cell periphery.

 Myosin’s interaction with the actin network then results in membrane retraction/ruffling, retrograde flow, and forward contractile forces. Finally, repeated stress on the old focal adhesion sites may result in calcium-induced activation of calpain and, consequently, focal adhesion detachment, completing the cycle. Apart from actin polymerization, microtubules may also be involved in cell migration via the creation of lamellipodia. Although microtubules are not required for actin polymerization to form lamellipodial extensions, they are required for cellular mobility, as demonstrated in one experiment.

Bleb-driven motility

Another hypothesised mechanism, dubbed ‘bleb-driven amoeboid movement,’ posits that actomyosin in the cell cortex contracts to raise intracellular hydrostatic pressure. Blebbing occurs in amoeboid cells when the cell membrane develops a roughly spherical protrusion that detaches from the actomyosin cortex. Myosin II is required for this kind of amoeboid motility because it generates the hydrostatic pressure that enables the bleb to extend. This is in contrast to actin-driven motility, in which the actin polymerizes while remaining linked to the actomyosin cortex and pushing against the cell’s barrier. The cytoplasmic sol-gel state is controlled during amoeboid movement mediated by blebs.

Additionally, blebbing might be a sign that a cell is undergoing apoptosis.

Additionally, it has been shown that the blebs generated by motile cells have a somewhat regular life cycle of about one minute. This involves an initial phase of outward expansion during which the membrane separates from the membranous cytoskeleton. This is followed by a brief static phase during which the bleb’s size is maintained by the hydrostatic pressure that has built up. This is followed by the last phase, during which the bleb gradually retracts and the membrane is reintroduced to the cytoskeleton infrastructure.

As a mechanism of migration, cells may rapidly switch between blebbing and lamellipodium-based movement. The rate at which these transformations occur, however, is uncertain. Tumor cells may also switch rapidly between amoebic and mesenchymal motility, another type of cell movement.

Related movement mechanisms

Dictyostelium cells and neutrophils can also swim by a mechanism similar to that of crawling.

Metaboly is another unicellular mode of movement demonstrated in Euglena.

Conclusion

Amoebae exhibit this form of locomotion (e.g., Amoeba proteus). Their cytoplasm is made up of plasmasol (central fluid) and a viscous plasmagel. Plasmagel is converted to plasmasol, which causes the cytoplasm to slide forward and form a pseudopodium in front of the cell, propelling it forward. Amoeboids are cells that migrate in this manner. Crawling is a type of amoeboid movement that begins when an extension of the moving cell (pseudopod) forms a strong attachment to the surface. The cell’s primary bulk gravitates toward the bound patch.