Numbers of theories have been put forth to explain the movements of the Amoeba. The theories are: 1.Adhesion Theory 2. Contraction Theory 3. Rolling Movement Theory 4. Walking Movement Theory 5. Surface-Tension Theory 6. Sol-Gel Theory 7. Formation Zone Theory 8. Molecular Folding Unfolding Theory.
1. Adhesion Theory:
This theory explains that locomotion in Amoeba is performed by adhesion similar to drop of water which spreads irregularly on uneven glass plate. The protoplasm flows like the fluid of the drop in the path of greater adhesion. Due to adhesive properties, pseudopodia generally grow in the paths of adhesion. However, this explanation does not seem to hold good as the pseudopodia may be formed independently without contact with any surface.
2. Contraction Theory:
In early 19th century, a pseudopodium was regarded a hernia-like protrusion bulged out at a weak point, probably due to contraction of body. In 1835, scientists believed that Amoeba contains contractile strands of gel which pull the whole body mass in the direction of advancing pseudopodium.
Later, when Heitzmann suggested that the body of amoeba was a 3-dimensional network (Reticular Theory of cytoplasmic structure) of live contractile fibres embedded in a non-living and non-contractile fluid, Schultze pointed out that contraction at the uroid end, pushes the formation pseudopodia at the forwarding end.
3. Rolling Movement Theory:
This theory was put forth by Jennings while working on Amoeba verrucosa which does not have pseudopodia. He explained that the movement in Amoeba takes place due to rolling movement of the body surface.
He noticed that if a particle of carmine is placed on the upper surface of a moving A. verrucosa, the particle flow forwards, rolls over the anterior edge, then it stops on the substratum until the entire animal has passed over it, then the particle moves upwards at the posterior end and comes on the upper surface and moves upwards. This is due to streaming movements of protoplasm of the animal accompanied by a rolling action of the body and these two processes bringing the locomotion of the animal.
4. Walking Movement Theory:
According to Dellinger (1906), when viewed, the amoebae from side and it can be noted that, during locomotion, the main part of body remains lifted from the substratum and supported on tips of pseudopodia. Thus, amoebae virtually “walk on pseudopodia”, just as higher animals move on their legs.
He explained that amoeba extends a pseudopodium free in water and swings it about. As the pseudopodium strikes an object, it sticks to it. This causes contraction of an endoplasmic fibrous network of contractile elements, pulling the whole body mass close to the pseudopodium. Thus the animal gradually walks about on the pseudopodia formed in the direction of locomotion.
5. Surface-Tension Theory:
It was put forward by Butschli and was widely accepted for long time. According to this theory locomotion in Amoeba is essentially like the movement of a globule of mercury or other liquid produced by local reduction of surface tension. As a matter of fact there exists a tension at the surface of the fluid protoplasm that makes the mass spherical.
From such a sphere an outflow will occur wherever the surface tension is locally lowered, either by internal or external changes. In such a projection the fluid will flow forward in the centre and backward along the sides. Such streaming movement can be seen in active pseudopods of some amoeboid forms.
Further, drops of certain chemical mixtures have been shown to move in amoeboid fashion because of local decrease in surface tension. It is very simple and attractive theory which has been extended in its application to various types of activity in Amoeba (by Rhumbler).
A number of fully established facts show conclusively. There are, however, that surface tension as applied in this theory plays but a very insignificant role in the process of movement and locomotion in Amoeba.
6. Sol-Gel Theory:
The sol-gel theory was first advocated by Hyman (1917) and has been adopted, among others, by Pantin (1923-1926) and Mast (1925).
This theory is based upon the fact that the plasmasol change into the plasmagel and vice versa. The plasmasol changes into rigid plasma-gel (gelates) at the anterior end and at the posterior end the plasmagel changes into plasmasol (solates) causine a forward streaming of the more fluid plasmasol.
That is why in actively progressing specimens the plasmasol is continuously rapidly streaming forward, while the plasmagel is practically everywhere at rest forming, so to say, a tube within which the plasmasol flows. If the course of a granule or crystal in the streaming plasmasol is pursued it will be noticed to take first a fairly straight course either until it reaches or nearly reaches the inner surface of the plasmagel at the tip of an advancing pseudopod, then it deflects to the right or to the left, upward or downward and sooner or later, directly or indirectly comes into contact with plasmagel into which it finally changes.
Other granules are similarly coming and changing into plasmagel after attaching to it behind the crystal under observation as more of these are coming in the same way the position of the first amoeba. When it reaches this end in gradually moves inward and enters in the plasmasol, after which it moves forward and the whole process is again repeated.
This gives an idea about the movement of liquefies or solates at any one place resulting in a local decrease in thickness and in elastic strength. The result is that the plasmagel bulges in this region, due to the elasticity of the plasmagel and turgidity of amoeba, and the plasmasol moves to this region. The principle involved in the formation is the same as the formation of a bulge on the surface of an inflated cycle tyre in which the wall has been locally weakened.
The bulge thus formed is the beginning of the pseudopod. The plasmagel is continuously stretched at the tip of pseudopod, due to the pressure of the plasmasol against it, and becomes a very thin sheet. The liquid from the plasmasol passes through it and forms a hyaline cap around the tip under the plasmalemma.
The plasmasol gelates on the side forming the tube forward as rapidly as the pseudopod extends. At the inner surface of the posterior end the plasmagel solates as rapidly as it gelates at the anterior end and the process becomes continuous.
The plasmalemma adheres to the substratum and to the adjoining plasmagel, the pressure of the plasmasol against the sheet of plasmagel under the hyaline cap pushes it forward, and as it pushes forward it draws the plasmalemma on the upper surface forward over the plasmagel, while it remains stationary below, producing locomotion with rolling movement of the surface.
7. Formation Zone Theory:
Allen (1962) has suggested that the amoeboid movement is caused as the endoplasmic molecules near the front end start moving before those at the posterior end. The endoplasm is believed to contain long protein chains which undergo contraction at the anterior end of the body so that the Amoeba is pulled forward.
8. Molecular Folding Unfolding Theory:
Goldacre and Lorch (1950, 52) provided a firmer footing to it by explaining the biophysical and biochemical processes involved in reversible “sol-gel” changes and contraction of plasmagel.
They reported that the long-chain protein molecules contract, become tightly folded and scatter in the temporary hind region, representing solation, but become unfolded, regularly arranged and tightly bonded together at the tip of advancing pseudopodium, representing gelation.
According to Huxley (1954), the proteins participating in solation and gelation are similar to actin and myosin of muscle fibres, and their folding-unfolding also involves formation of actomyosin rachets with great expenditure of ATP.