The single-celled organism Amoeba proteus navigates its environment through a fascinating process known as amoeboid movement. This method of locomotion is shared by various eukaryotic cells, including certain cells within the human body like white blood cells. As a protist, the amoeba lacks fixed structures like cilia or flagella, relying instead on the dramatic restructuring of its internal components to achieve movement. Understanding how this organism moves involves examining the temporary extensions it forms and the underlying cytoplasmic changes that drive them.
The Role of Pseudopods
The outward sign of amoeboid movement is the formation of a structure called a pseudopod, a term that translates literally to “false foot”. These are temporary, arm-like projections of the cell membrane and cytoplasm that extend in the direction of travel. To initiate movement, the amoeba anchors the tip of a developing pseudopod to the surface it is crawling upon.
The rest of the cell body then flows toward this anchor point, effectively pulling the organism forward. Amoeba proteus can form one or more projections simultaneously, allowing it to explore its surroundings with an ever-changing, amorphous shape.
Cytoplasmic Flow and the Sol-Gel Conversion
The physical extension of the pseudopod is powered by a continuous internal transformation of the cell’s cytoplasm. The cytoplasm is differentiated into two main states: the fluid, inner endoplasm (or plasmasol), and the more rigid, outer ectoplasm (or plasmagel). The core of the movement mechanism is the precise conversion between these two states, known as the sol-gel conversion.
At the trailing, posterior end of the cell, the rigid ectoplasm is converted back into the fluid endoplasm. This fluid streams forward, creating a current of cytoplasm that pushes toward the advancing front of the cell. As this fluid reaches the leading edge of the pseudopod, it undergoes a transformation back into ectoplasm. This change solidifies the new extension, forming a temporary tube through which the remaining endoplasm flows.
This conversion is controlled at a molecular level by the cytoskeleton, specifically the protein actin. In the fluid endoplasm, actin exists as individual, globular proteins. At the tip of the pseudopod, these individual units rapidly link together, or polymerize, to form a cross-linked network of filaments that creates the rigid, gel-like structure of the ectoplasm. Conversely, at the rear of the cell, the existing actin network is broken down, or depolymerized, returning the cytoplasm to its fluid state.
The interaction of actin with the motor protein myosin generates the contractile force needed to propel the cell. Myosin acts on the actin filaments to create the necessary pressure gradient and contraction that drives the forward flow of the endoplasm. Calcium ions play an important regulatory role by influencing the activity of the proteins that control the assembly and disassembly of the actin network. This dynamic cycle provides the continuous force necessary for amoeboid movement.
Sensing the Environment: How Movement is Directed
The movement of Amoeba proteus is not a random drifting but a directed response to external cues, a behavior categorized as taxis. The cell is capable of sensing environmental gradients and adjusting its direction of locomotion accordingly. One well-studied example is chemotaxis, which is the response to chemical signals in the environment, such as those released by potential food sources like bacteria.
The amoeba detects higher concentrations of an attractant chemical and biases pseudopod formation toward that source, triggering the sol-gel conversion preferentially on the side facing the chemical gradient. The cell also exhibits responses to other stimuli, such as galvanotaxis, which is directed movement in response to an electric field. These sensory inputs allow the amoeba to efficiently navigate its surroundings, moving toward nutrients and away from harmful conditions.