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A pseudopod or pseudopodium (: pseudopods or pseudopodia) is a temporary arm-like projection of a eukaryotic cell membrane that is emerged in the direction of movement. Filled with cytoplasm, pseudopodia primarily consist of actin filaments and may also contain and intermediate filaments. Pseudopods are used for motility and ingestion. They are often found in .
Different types of pseudopodia can be classified by their distinct appearances. Lamellipodia are broad and thin. Filopodia are slender, thread-like, and are supported largely by microfilaments. Lobopodia are bulbous and amoebic. Reticulopodia are complex structures bearing individual pseudopodia which form irregular nets. Axopodia are the phagocytosis type with long, thin pseudopods supported by complex microtubule arrays enveloped with cytoplasm; they respond rapidly to physical contact.
Generally, several pseudopodia arise from the surface of the body, ( polypodial, for example, Amoeba proteus), or a single pseudopod may form on the surface of the body ( monopodial, such as Entamoeba histolytica). (2025). 9780124159150 ISBN 9780124159150
The chemoattractants bind to G protein-coupled receptors, which activate GTPases of the Rho family (e.g. Cdc42, Rac) via G proteins.
Rho GTPases are able to activate WASp which in turn activate Arp2/3 complex which serve as nucleation sites for actin polymerization. The actin polymers then push the membrane as they grow, forming the pseudopod. The pseudopodium can then adhere to a surface via its Cell adhesion (e.g. ), and then pull the cell's body forward via contraction of an actin-myosin complex in the pseudopod. This type of locomotion is called amoeboid movement.
Rho GTPases can also activate phosphatidylinositol 3-kinase (PI3K) which recruit PIP3 to the membrane at the leading edge and detach the PIP3-degrading enzyme PTEN from the same area of the membrane. PIP3 then activate GTPases back via GEF stimulation. This serves as a feedback loop to amplify and maintain the presence of local GTPase at the leading edge.
Otherwise, pseudopodia cannot grow on other sides of the membrane than the leading edge because myosin filaments prevent them to extend. These myosin filaments are induced by cyclic GMP in D. discoideum or Rho kinase in for example.
Different physical parameters were shown to regulate the length and time-scale of pseudopodia formation. For example, an increase in membrane tension inhibits actin assembly and protrusion formation. It was demonstrated that the lowered negative surface charge on the inner surface of the Cell membrane generates protrusions via activation of the Ras-PI3K/AKT/mTOR signalling pathway.
In Dictyostelium cells, a pseudopodium can form either de novo as normal, or from an existing pseudopod, forming a Y-shaped pseudopodium.
The Y-shaped pseudopods are used by Dictyostelium to advance relatively straight forward by alternating between retraction of the left or right branch of the pseudopod. The de novo pseudopodia form at different sides than pre-existing ones, they are used by the cells to turn.
Y-shaped pseudopods are more frequent than de novo ones, which explain the preference of the cell to keep moving to the same direction. This persistence is modulated by PLA2 and cGMP signalling pathways.
Some pseudopodial cells are able to use multiple types of pseudopodia depending on the situation. Most use a combination of lamellipodia and filopodia to migrate (e.g. metastatic cancer cells). Human foreskin fibroblasts can either use lamellipodia- or lobopodia-based migration in a 3D matrix depending on the matrix elasticity.
High-pressure lobopodia can also be found in human travelling through a complex network of 3D matrix (e.g. mammalian dermis, cell-derived matrix). Contrarily to other pseudopodia using the pressure exerted by actin polymerization on the membrane to extend, fibroblast lobopods use the nuclear piston mechanism consisting in pulling the nucleus via actomyosin contractility to push the cytoplasm that in turn push the membrane, leading to pseudopod formation. To occur, this lobopodia-based fibroblast migration needs Nesprin, , RHOA, ROCK and myosin II. Otherwise, lobopods are often accompanied with small lateral blebs forming along the side of the cell, probably due to the high intracellular pressure during lobopodia formation increasing the frequency of plasma membrane-cortex rupture.
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