Amoeboid movement is a basic form of cellular crawling used by many eukaryotic cells. It is characterized by a cell extending a temporary projection and flowing its cytoplasm into that extension. This process allows the cell to change its shape continually and navigate complex environments. While most famously associated with single-celled organisms like the Amoeba, this ancient mechanism is also utilized by numerous cell types within complex multicellular organisms for migration in processes like defense against infection and tissue repair.
Cellular Components Required for Movement
The physical act of amoeboid movement relies on a specialized internal scaffold, the cytoskeleton, and its associated motor proteins. The temporary projection that forms at the cell’s leading edge is called a pseudopod, and its formation is powered by the protein actin. Actin filaments assemble into a dense, dynamic network directly beneath the cell membrane, creating a support structure known as the cortical cytoskeleton. This cortical cytoskeleton provides the mechanical framework for the cell and is responsible for transmitting the forces needed for crawling.
Actin rapidly assembles into filaments at the front of the cell to push the membrane forward. Conversely, the protein myosin functions as the molecular motor, concentrated mainly at the cell’s rear.
Myosin, specifically Myosin II, interacts with the actin filaments to generate the contractile force necessary for movement. This motor activity creates tension that pulls the cell body toward the newly formed pseudopod. The separation of function—actin for protrusion at the front and myosin for contraction at the back—is fundamental to establishing the cell’s necessary polarity for directed motion.
The Dynamic Process of Cytoskeletal Rearrangement
Amoeboid movement is a continuous, cyclic process that can be broken down into three coordinated phases: protrusion, adhesion, and contraction. The cycle begins with protrusion, where the cell extends its membrane in the direction of travel through the rapid polymerization of globular actin subunits into filamentous chains.
The Arp2/3 complex acts as a nucleator that generates new actin filaments as branches off existing ones. This branching mechanism creates a mesh-like network that physically pushes against the inner surface of the plasma membrane, driving the pseudopod forward. Chemical signals from the environment dictate where this polymerization occurs, establishing the cell’s direction.
Following protrusion, the cell must anchor the newly extended pseudopod to the underlying substrate or extracellular matrix through the phase of adhesion. Amoeboid cells typically form weak, transient adhesions rather than the strong, stable focal adhesions seen in other migration types. These temporary contacts provide traction, allowing the cell to gain purchase on the surface without slowing its rapid movement. The transient nature of these contacts is essential for maintaining a high speed of migration.
The final phase is the contraction and retraction of the cell body, which pulls the entire cell mass forward. Myosin II motors, concentrated in the cortical cytoskeleton at the cell’s trailing edge, interact with the local actin network to generate a powerful squeezing force. This actomyosin contraction effectively detaches the weak adhesive contacts at the rear while simultaneously driving the bulk of the cytoplasm forward to fill the advancing pseudopod. The entire process is orchestrated by internal signaling pathways, such as the Rho-ROCK-myosin II axis, which precisely regulates the timing and location of actin assembly and myosin contraction to ensure continuous, directed locomotion.
Essential Functions in Living Systems
Amoeboid movement is a fundamental process in vertebrate biology, particularly in the immune system. Macrophages and neutrophils, types of white blood cells, rely heavily on this motility to execute their protective functions. These immune cells use chemotaxis to rapidly migrate through tissues toward sites of infection or inflammation, guided by chemical gradients.
Once at the target site, they use their pseudopods to perform phagocytosis, a process of engulfing and destroying foreign particles or pathogens. The same mechanical principles are also employed by fibroblasts to facilitate wound healing and tissue repair. Fibroblasts migrate into damaged areas to lay down the new extracellular matrix that closes the wound.
Unfortunately, this highly effective migratory mechanism is also hijacked by pathological cells, most notably in cancer metastasis. Highly aggressive tumor cells can adopt an amoeboid migration mode, characterized by a rounded shape and low adhesion. This mode, driven by the Rho-ROCK-myosin II contractile axis, allows cancer cells to move quickly through the confined spaces of dense tissue. Their ability to switch from a slow, high-adhesion migration to this rapid, low-adhesion amoeboid mode contributes significantly to the spread of cancer throughout the body.