Editing Pseudopodia

{{Short description|False leg found on slime molds, archaea, protozoans, leukocytes and certain bacteria}}
{{About|eukaryotic cells|the band|Pseudopod (band)|the podcast|Pseudopod (podcast) |the structure in insect anatomy|Proleg}}
{{More citations needed|article|date=October 2007}}
[[File:Amoeba proteus with many pseudopodia.jpg|thumb|''Amoeba proteus'' extending lobose pseudopodia|300x300px]]

A '''pseudopod''' or '''pseudopodium''' ({{plural form}}: '''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 [[microtubule]]s and [[intermediate filament]]s.<ref name="Etienne-Manneville2004">{{cite journal |author=Etienne-Manneville S |title=Actin and Microtubules in Cell Motility: Which One is in Control? |journal=[[Traffic (journal)|Traffic]] |volume=5 |year=2004 |issue=7 |pages=470–77 |doi=10.1111/j.1600-0854.2004.00196.x|pmid=15180824 |s2cid=23083215 |doi-access=free }}</ref><ref name="Tang2017">{{cite journal |author=Tang DD |title=The roles and regulation of the actin cytoskeleton, intermediate filaments and microtubules in smooth muscle cell migration |journal=[[Respiratory Research]] |volume=18 |year=2017 |issue=1 |pages=54 |doi=10.1186/s12931-017-0544-7 |pmc=5385055 |pmid=28390425 |doi-access=free }}</ref> Pseudopods are used for [[motility]] and [[ingestion]]. They are often found in [[amoeba]]s.

Different types of pseudopodia can be classified by their distinct appearances.<ref>{{cite web |url=http://tolweb.org/notes/?note_id=51 |first=David J. |last=Patterson |title=Amoebae: Protists Which Move and Feed Using Pseudopodia |website= tolweb.org| publisher=[[Tree of Life Web Project]] |access-date=2017-11-12}}</ref> [[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|Axopodia]] are the [[phagocytosis]] type with long, thin pseudopods supported by complex microtubule arrays enveloped with cytoplasm; they respond rapidly to physical contact.<ref name=":0">{{cite web |url= https://www.arcella.nl/pseudopodia |title=Pseudopodia |website= Arcella.nl |date= May 23, 2017|access-date=2018-12-16 |archive-url= https://web.archive.org/web/20181216120714/https://www.arcella.nl/pseudopodia |archive-date=2018-12-16 |url-status= unfit}}</ref>

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]]'').<ref>{{cite book |doi=10.1016/B978-0-12-415915-0.00003-0 |chapter=General Characteristics of the Euprotista (Protozoa) |title= Human Parasitology |pages=37–51 |year=2013 |last1=Bogitsh |first1= Burton J. |last2=Carter |first2=Clint E. |last3=Oeltmann |first3=Thomas N. |isbn=978-0-12-415915-0|s2cid=83272826 }}</ref>

==Formation==
Cells which make pseudopods are generally referred to as ''[[amoeboids]]''.<ref>{{cite encyclopedia |title=Pseudopodia |encyclopedia=[[Encyclopedia.com]] |url=https://www.encyclopedia.com/history/latin-america-and-caribbean/mesoamerican-indigenous-peoples/pseudopodia |access-date=2018-12-16}}</ref>

===Via extracellular cue===
To move towards a target, the cell uses [[chemotaxis]]. It senses extracellular signalling molecules, chemoattractants (e.g. cAMP for ''[[Dictyostelium]]'' cells),<ref name="Bosgraaf2009">{{Cite journal | author=Bosgraaf L & Van Haastert PJM | title=The Ordered Extension of Pseudopodia by Amoeboid Cells in the Absence of External Cues | journal=PLOS ONE | volume=4 |issue= 4 | year=2009 | pages=626–634 | doi=10.1371/journal.pone.0005253 | pmc=2668753 | pmid=19384419| bibcode=2009PLoSO...4.5253B | doi-access=free }}</ref> to extend pseudopodia at the membrane area facing the source of these molecules.

The chemoattractants bind to [[G&nbsp;protein-coupled receptor]]s, which activate [[Rho family of GTPases|GTPases of the Rho family]] (e.g. Cdc42, Rac) via [[G&nbsp;protein]]s.

Rho GTPases are able to activate [[Wiskott–Aldrich syndrome protein|WASp]] which in turn activate [[Arp2/3 complex]] which serve as nucleation sites for [[Actin#Nucleation and polymerization|actin polymerization]].<ref name="Haastert2004">{{Cite journal | author=Van Haastert PJM & Devreotes PN | title=Chemotaxis: signalling the way forward | journal=Nature Reviews Molecular Cell Biology | volume=5 | year=2004 | issue=8 | pages=626–634 | doi=10.1038/nrm1435 | pmid=15366706 | s2cid=5687127 }}</ref> 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|adhesion proteins]] (e.g. [[integrin]]s), and then pull the cell's body forward via contraction of an actin-myosin complex in the pseudopod.<ref name="Campbell2017">{{Cite journal | author=Campbell EJ | title=A computational model of amoeboid cell swimming| journal=Physics of Fluids | volume=29 | year=2017 | issue=10| doi=10.1063/1.4990543 | page=101902| bibcode=2017PhFl...29j1902C}}</ref><ref name="Conti2008">{{Cite journal | author=Conti MA | title=Nonmuscle myosin II moves in new directions| journal=Journal of Cell Science | volume=121 | year=2008 | issue=Pt 1| pages=11–18 | doi=10.1242/jcs.007112 | pmid=18096687 | s2cid=16367236| doi-access= }}</ref> This type of locomotion is called ''[[amoeboid movement]]''.

Rho GTPases can also activate [[phosphatidylinositol 3-kinase]] (PI3K) which recruit [[Phosphatidylinositol (3,4,5)-trisphosphate|PIP<sub>3</sub>]] to the membrane at the leading edge and detach the PIP<sub>3</sub>-degrading enzyme [[PTEN (gene)|PTEN]] from the same area of the membrane. PIP<sub>3</sub> then activate GTPases back via [[Guanine nucleotide exchange factor|GEF]] stimulation. This serves as a feedback loop to amplify and maintain the presence of local GTPase at the leading edge.<ref name="Haastert2004" />

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 guanosine monophosphate|cyclic GMP]] in ''[[Dictyostelium discoideum|D. discoideum]]'' or [[Rho kinase]] in [[neutrophil]]s for example.<ref name="Haastert2004" />

Different physical parameters were shown to regulate the length and time-scale of pseudopodia formation. For example, an increase in membrane [[Tension (physics)|tension]] inhibits actin assembly and protrusion formation.<ref>{{Cite journal |last1=Houk |first1=Andrew R. |last2=Jilkine |first2=Alexandra |last3=Mejean |first3=Cecile O. |last4=Boltyanskiy |first4=Rostislav |last5=Dufresne |first5=Eric R. |last6=Angenent |first6=Sigurd B. |last7=Altschuler |first7=Steven J. |last8=Wu |first8=Lani F. |last9=Weiner |first9=Orion D. |date=2012-01-20 |title=Membrane tension maintains cell polarity by confining signals to the leading edge during neutrophil migration |journal=Cell |volume=148 |issue=1–2 |pages=175–188 |doi=10.1016/j.cell.2011.10.050 |issn=0092-8674 |pmc=3308728 |pmid=22265410}}</ref> It was demonstrated that the lowered negative [[surface charge]] on the inner surface of the [[Cell membrane|plasma membrane]] generates protrusions via activation of the Ras-[[PI3K/AKT/mTOR pathway|PI3K/AKT/mTOR]] signalling pathway.<ref>{{Cite journal |last1=Banerjee |first1=Tatsat |last2=Biswas |first2=Debojyoti |last3=Pal |first3=Dhiman Sankar |last4=Miao |first4=Yuchuan |last5=Iglesias |first5=Pablo A. |last6=Devreotes |first6=Peter N. |date=2022-10-06 |title=Spatiotemporal dynamics of membrane surface charge regulates cell polarity and migration |journal=[[Nature Cell Biology]] |volume=24 |issue=10 |pages=1499–1515 |doi=10.1038/s41556-022-00997-7 |issn=1476-4679 |pmid=36202973|s2cid=248990694 |pmc=10029748 }}</ref>

===Without extracellular cue===
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.

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 [[Phospholipase A2|PLA2]] and cGMP signalling pathways.<ref name="Bosgraaf2009" />

==Functions==
The functions of pseudopodia include locomotion and ingestion:
* Pseudopodia are critical in sensing targets which can then be engulfed; the engulfing pseudopodia are called [[phagocytosis]] pseudopodia. A common example of this type of amoeboid cell is the [[macrophage]].
* They are also essential to amoeboid-like locomotion. Human [[mesenchymal stem cell]]s are a good example of this function: these migratory cells are responsible for in-utero remodeling; for example, in the formation of the [[trilaminar germ disc]] during [[gastrulation]].<ref>{{cite book |last1=Schoenwolf|first1=Gary |title=Larsen's Human Embryology |edition=4th |date=2009 |publisher=Churchill Livingstone Elsevier}}</ref>

==Morphology==
[[File:PseudopodiaFormsDavidPatterson.jpg|thumb|upright=1.3|The forms of pseudopodia, from left: polypodial and lobose; monopodial and lobose; filose; conical; reticulose; tapering actinopods; non-tapering actinopods]]

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 of [[lamellipodia]] and [[filopodia]] to migrate<ref name="Xue2010">{{cite journal |author=Xue F |display-authors=etal |year=2010 |title=Contribution of Filopodia to Cell Migration: A Mechanical Link between Protrusion and Contraction |journal=[[International Journal of Cell Biology]] |volume=2010 |pages=1–13 |doi=10.1155/2010/507821 |pmc=2910478 |pmid=20671957 |doi-access=free}}</ref> (e.g. metastatic cancer cells).<ref name="Machesky2012">{{cite journal |author=Machesky LM |display-authors=etal |year=2008 |title=Lamellipodia and filopodia in metastasis and invasion |journal=[[FEBS Letters]] |volume=582 |issue=14 |pages=2102–11 |doi=10.1016/j.febslet.2008.03.039 |pmid=18396168 |s2cid=46438967 |doi-access=}}</ref> Human [[foreskin]] fibroblasts can either use lamellipodia- or lobopodia-based migration in a 3D matrix depending on the matrix elasticity.<ref name="Petrie2012">{{cite journal |author=Petrie RJ |display-authors=etal |year=2012 |title=Nonpolarized signaling reveals two distinct modes of 3D cell migration |journal=[[Journal of Cell Biology]] |volume=197 |issue=3 |pages=439–455 |doi=10.1083/jcb.201201124 |pmc=3341168 |pmid=22547408}}</ref>

===Lamellipodia===
Lamellipodia are broad and flat pseudopodia used in locomotion.<ref name=":0" /> They are supported by microfilaments which form at the leading edge, creating a mesh-like internal network.<ref name="Bray2001">{{cite book |last=Bray |first=Dennis |author-link=Dennis Bray |date=2001 |title=Cell Movements: From molecules to motility second edition}}</ref>

===Filopodia===
Filopodia (or filose pseudopods) are slender and filiform with pointed ends, consisting mainly of [[ectoplasm (cell biology)|ectoplasm]]. These formations are supported by [[microfilament]]s which, unlike the filaments of lamellipodia with their net-like actin, form loose bundles by [[cross-link]]ing. This formation is partly due to bundling proteins such as [[fimbrin]]s and [[fascin]]s.<ref name="Bray2001" /><ref name="Vignjevic2006">{{Cite journal | author=Danijela Vignjevic|display-authors=etal| title=Role of fascin in filopodial protrusion| journal=Journal of Cell Biology | volume=174 | issue = 6  | year=2006 | pages=863–875 | doi=10.1083/jcb.200603013 | pmc=2064340 | pmid=16966425}}</ref>
Filopodia are observed in some animal cells: in part of [[Filosa]] ([[Rhizaria]]), in "[[Testaceafilosia]]", in [[Vampyrellidae]] and [[Pseudosporida]] ([[Rhizaria]]) and in [[Nucleariida]] ([[Opisthokonta]]).<ref name=":0" />

===Lobopodia===
Lobopodia (or lobose pseudopods) are bulbous, short, and blunt in form.<ref>{{Cite web|url=https://www.britannica.com/science/pseudopodium|title=Pseudopodium {{!}} cytoplasm|website=Encyclopedia Britannica|language=en|access-date=2018-12-16}}</ref> These finger-like, tubular pseudopodia contain both [[ectoplasm (cell biology)|ectoplasm]] and [[endoplasm]]. They can be found in different kind of cells, notably in [[Lobosa]] and other [[Amoebozoa]] and in some [[Heterolobosea]] ([[Excavata]]).

High-pressure lobopodia can also be found in human [[fibroblast]]s travelling through a complex network of 3D [[Extracellular matrix|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|nesprin 3]], [[integrin]]s, [[RHOA|RhoA]], [[Rho-associated protein kinase|ROCK]] and [[Myosin#Myosin II|myosin II]].
Otherwise, lobopods are often accompanied with small lateral [[Bleb (cell biology)|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.<ref name="Chengappa2018">{{Cite journal | author=Chengappa P |display-authors=etal | title=Chapter Seven - Intracellular Pressure: A Driver of Cell Morphology and Movement | journal=International Review of Cell and Molecular Biology | volume=337 | year=2018 | pages=185–211 | doi=10.1016/bs.ircmb.2017.12.005 |pmid=29551161 }}</ref><ref name="Petrie2012" /><ref name="Petrie2017">{{Cite journal | author=Petrie RJ |display-authors=etal | title=Activating the nuclear piston mechanism of 3D migration in tumor cells | journal=Journal of Cell Biology | volume=216 | issue = 1  | year=2017 | pages=93–100 | doi=10.1083/jcb.201605097 |pmid=27998990 |pmc=5223602 | doi-access=free }}</ref>

===Reticulopodia===
Reticulopodia (or reticulose pseudopods),<ref>{{cite web |url=http://www.eforams.icsr.agh.edu.pl/index.php/Reticulopodia |title=Reticulopodia |website=eForams |access-date=2005-12-30 |url-status=dead |archive-url=https://web.archive.org/web/20070717192718/http://www.eforams.icsr.agh.edu.pl/index.php/Reticulopodia |archive-date=2007-07-17 }}</ref> 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 of [[Foraminifera]], [[Chlorarachnea]], ''[[Gromia]]'' and ''[[Filoreta]]'' (Rhizaria).<ref name=":0" />

===Axopodia===
Axopodia (also known as actinopodia) are narrow pseudopodia containing complex arrays of [[microtubule]]s 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]]".<ref name=":0" />

==References==
{{reflist}}

{{Protist structures}}
{{Authority control}}

[[Category:Actin-based structures]]
[[Category:Cell anatomy]]
[[Category:Cell movement]]