Amoeboid movement

The protoplasm of an amoeba is made up of an outer layer termed the ectoplasm which surrounds an inner portion called the endoplasm. The ectoplasm consists of a gelatinous semisolid called plasma gel whereas the endoplasm is made up of a less viscous fluid called plasma sol. The ectoplasm owes its highly viscous state, in part, to the cross-linking actomyosin complex. Locomotion of an amoeba is thought to occur due to the sol-gel conversion of the protoplasm within its cell. 'Sol-gel conversion describes the contraction and relaxation events which are enforced by osmotic pressure and other ionic charges.'[4]

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 proteins. Actin binding proteins are in turn regulated by calcium ions; hence, calcium ions are very important in the sol-gel conversion process.[1][4]

Based on some mathematical models, recent studies hypothesize a novel biological model for collective biomechanical and molecular mechanisms of cellular motion.[5] 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.[6]

Two common modes of amoeboid motility

Another such proposed mechanism, the 'bleb-driven amoeboid locomotion' mechanism, suggests that the cell cortex actomyosin contracts to increase hydrostatic pressure inside the cell. Blebbing occurs in amoeboid cells when there is a roughly spherical protrusion in the cell membrane characterized by detachment from the actomyosin cortex. This mode of amoeboid movement requires that myosin II play a role in generating the hydrostatic pressure that causes the bleb to extend.[7]  This is different from actin-driven locomotion where the protrusion created is by the actin polymerizing while remaining attached to the actomyosin cortex and physically pushing against the cell's barrier. During the bleb-driven amoeboid movement, the cytoplasmic sol-gel state is regulated.[1]

Blebbing can also be a sign of when a cell is undergoing apoptosis.[8]

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.[9]

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.[10]

Dictyostelium cells and neutrophils can also swim, using a similar mechanism as for crawling.[11][12]

Another unicellular form of movement shown in Euglena is known as metaboly. The basis of sol gel theory is interconversion of sol and gel.