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Apseudopod orpseudopodium (pl.:pseudopods orpseudopodia) is a temporary arm-like projection of aeukaryoticcell membrane that is emerged in the direction of movement. Filled withcytoplasm, pseudopodia primarily consist ofactin filaments and may also containmicrotubules andintermediate filaments.[1][2] Pseudopods are used formotility andingestion. They are often found inamoebas.
Different types of pseudopodia can be classified by their distinct appearances.[3]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 thephagocytosis type with long, thin pseudopods supported by complex microtubule arrays enveloped with cytoplasm; they respond rapidly to physical contact.[4]
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 asEntamoeba histolytica).[5]
Cells which make pseudopods are generally referred to asamoeboids.[6]
To move towards a target, the cell useschemotaxis. It senses extracellular signalling molecules, chemoattractants (e.g. cAMP forDictyostelium cells),[7] to extend pseudopodia at the membrane area facing the source of these molecules.
The chemoattractants bind toG protein-coupled receptors, which activateGTPases of the Rho family (e.g. Cdc42, Rac) viaG proteins.
Rho GTPases are able to activateWASp which in turn activateArp2/3 complex which serve as nucleation sites foractin polymerization.[8] The actin polymers then push the membrane as they grow, forming the pseudopod. The pseudopodium can then adhere to a surface via itsadhesion proteins (e.g.integrins), and then pull the cell's body forward via contraction of an actin-myosin complex in the pseudopod.[9][10] This type of locomotion is calledamoeboid movement.
Rho GTPases can also activatephosphatidylinositol 3-kinase (PI3K) which recruitPIP3 to the membrane at the leading edge and detach the PIP3-degrading enzymePTEN from the same area of the membrane. PIP3 then activate GTPases back viaGEF stimulation. This serves as a feedback loop to amplify and maintain the presence of local GTPase at the leading edge.[8]
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 bycyclic GMP inD. discoideum orRho kinase inneutrophils for example.[8]
Different physical parameters were shown to regulate the length and time-scale of pseudopodia formation. For example, an increase in membranetension inhibits actin assembly and protrusion formation.[11] It was demonstrated that the lowered negativesurface charge on the inner surface of theplasma membrane generates protrusions via activation of the Ras-PI3K/AKT/mTOR signalling pathway.[12]
In the case there is no extracellular cue, all moving cells navigate in random directions, but they can keep the same direction for some time before turning. This feature allows cells to explore large areas for colonization or searching for a new extracellular cue.
InDictyostelium cells, a pseudopodium can form eitherde novo as normal, or from an existing pseudopod, forming a Y-shaped pseudopodium.
The Y-shaped pseudopods are used byDictyostelium to advance relatively straight forward by alternating between retraction of the left or right branch of the pseudopod. Thede novo pseudopodia form at different sides than pre-existing ones, they are used by the cells to turn.
Y-shaped pseudopods are more frequent thande novo ones, which explain the preference of the cell to keep moving to the same direction. This persistence is modulated byPLA2 and cGMP signalling pathways.[7]
The functions of pseudopodia include locomotion and ingestion:
Pseudopods can be classified into several varieties according to the number of projections (monopodia and polypodia), and according to their appearance.
Some pseudopodial cells are able to use multiple types of pseudopodia depending on the situation. Most use a combination oflamellipodia andfilopodia to migrate[14] (e.g. metastatic cancer cells).[15] Humanforeskin fibroblasts can either use lamellipodia- or lobopodia-based migration in a 3D matrix depending on the matrix elasticity.[16]
Lamellipodia are broad and flat pseudopodia used in locomotion.[4] They are supported by microfilaments which form at the leading edge, creating a mesh-like internal network.[17]
Filopodia (or filose pseudopods) are slender and filiform with pointed ends, consisting mainly ofectoplasm. These formations are supported bymicrofilaments which, unlike the filaments of lamellipodia with their net-like actin, form loose bundles bycross-linking. This formation is partly due to bundling proteins such asfimbrins andfascins.[17][18]Filopodia are observed in some animal cells: in part ofFilosa (Rhizaria), in "Testaceafilosia", inVampyrellidae andPseudosporida (Rhizaria) and inNucleariida (Opisthokonta).[4]
Lobopodia (or lobose pseudopods) are bulbous, short, and blunt in form.[19] These finger-like, tubular pseudopodia contain bothectoplasm andendoplasm. They can be found in different kind of cells, notably inLobosa and otherAmoebozoa and in someHeterolobosea (Excavata).
High-pressure lobopodia can also be found in humanfibroblasts travelling through a complex network of 3Dmatrix (e.g. mammaliandermis, 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 thecytoplasm that in turn push the membrane, leading to pseudopod formation. To occur, this lobopodia-based fibroblast migration needsnesprin 3,integrins,RhoA,ROCK andmyosin II.Otherwise, lobopods are often accompanied with small lateralblebs 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.[20][16][21]
Reticulopodia (or reticulose pseudopods),[22] are complex formations in which individual pseudopods are merged and form irregular nets. The primary function of reticulopodia, also known as myxopodia, is food ingestion, with locomotion a secondary function. Reticulopods are typical ofForaminifera,Chlorarachnea,Gromia andFiloreta (Rhizaria).[4]
Axopodia (also known as actinopodia) are narrow pseudopodia containing complex arrays ofmicrotubules enveloped by cytoplasm. Axopodia are mostly responsible for phagocytosis by rapidly retracting in response to physical contact. These pseudopodia are primarily food-collecting structures, but also provide a means of hydrological transportation via the expansion of their surface areas. They are observed in "Radiolaria" and "Heliozoa".[4]
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