Ameboid Movement
Ameboid Movement
Ameboid movement is a form of movement especially characteristic of amebas and other unicellular forms; it is also found in many wandering cells of metazoans, such as white blood cells, embryonic mesenchyme, and numerous other mobile cells that move through the tissue spaces. Ameboid cells change their shape by sending out and withdrawing pseudopodia (false feet) from any point on the cell surface. Beneath the plasmalemma lies a nongranular layer, the gel-like ectoplasm, which encloses the more liquid endoplasm.
Research with a variety of ameboid cells, including the pathogen-fighting phagocytes present in blood, has produced a consensus model to explain pseudopodial extension and ameboid crawling. Optical studies of an ameba in movement suggest the outer layer of ectoplasm surrounds a rather fluid core of endoplasm. Movement depends on actin and other regulatory proteins. According to one hypothesis (Stossel, 1994), as the pseudopod extends, hydrostatic pressure forces actin subunits into the pseudopod where they assemble into a network to form a gel state. At the trailing edge of the gel, where the network disassembles, freed actin interacts with myosin to create a contractile force that pulls the cell along behind the extending pseudopod. Locomotion is assisted by membrane-adhesion proteins that attach temporarily to the substrate to provide traction, enabling the cell to crawl steadily forward.
Ameboid movement is a form of movement especially characteristic of amebas and other unicellular forms; it is also found in many wandering cells of metazoans, such as white blood cells, embryonic mesenchyme, and numerous other mobile cells that move through the tissue spaces. Ameboid cells change their shape by sending out and withdrawing pseudopodia (false feet) from any point on the cell surface. Beneath the plasmalemma lies a nongranular layer, the gel-like ectoplasm, which encloses the more liquid endoplasm.
Research with a variety of ameboid cells, including the pathogen-fighting phagocytes present in blood, has produced a consensus model to explain pseudopodial extension and ameboid crawling. Optical studies of an ameba in movement suggest the outer layer of ectoplasm surrounds a rather fluid core of endoplasm. Movement depends on actin and other regulatory proteins. According to one hypothesis (Stossel, 1994), as the pseudopod extends, hydrostatic pressure forces actin subunits into the pseudopod where they assemble into a network to form a gel state. At the trailing edge of the gel, where the network disassembles, freed actin interacts with myosin to create a contractile force that pulls the cell along behind the extending pseudopod. Locomotion is assisted by membrane-adhesion proteins that attach temporarily to the substrate to provide traction, enabling the cell to crawl steadily forward.
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