View source for Cilium

{{Short description|Organelle found on eukaryotic cells}}
{{About|organelles|fine hairs on insect wings|Cilium (entomology)}}{{Distinguish|Cilium (computing)}}{{Distinguish|Psyllium}}
{{Use dmy dates|date=November 2018}}
{{Infobox microanatomy
| Name        = Cilium
| Latin       = cilium
| Image       = Bronchiolar epithelium 3 - SEM.jpg
| Caption     = [[Scanning electron microscope|SEM]] micrograph of motile cilia projecting from [[respiratory epithelium]] in the [[trachea]] 
| Width       = 
| Image2      = 
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{{wikt | cilium}}

The '''cilium''' ({{plural form}}: '''cilia'''; {{ety|la|cilium|[[eyelid]]}}; in Medieval Latin and in anatomy, ''cilium'') is a short hair-like [[membrane protrusion]] from many types of [[eukaryotic cell]].<ref name="MW1">{{cite web | title=Definition of CILIUM |url=https://www.merriam-webster.com/dictionary/cilium | website=www.merriam-webster.com | access-date=15 April 2022 | language=en}}</ref><ref name="HHMIB2005"/> (Cilia are absent in [[bacteria]] and [[archaea]].) The cilium has the shape of a slender threadlike projection that extends from the surface of the much larger cell body.<ref name="HHMIB2005"/> Eukaryotic [[flagella]] found on [[sperm cell]]s and many [[protozoan]]s have a similar structure to motile cilia that enables swimming through liquids; they are longer than cilia and have a different undulating motion.<ref name="Haimo_JCB198112">{{cite journal |vauthors=Haimo LT, Rosenbaum JL |date=December 1981 |title=Cilia, flagella, and microtubules |journal=The Journal of Cell Biology |volume=91 |issue=3 Pt 2 |pages=125s–130s |doi=10.1083/jcb.91.3.125s |pmc=2112827 |pmid=6459327}}</ref><ref name="Alberts1">{{cite book | last1=Alberts | first1=Bruce |title =Molecular biology of the cell | year=2015 | location=New York, NY | isbn=9780815344643 | pages=941–942 | edition=6}}</ref>

There are two major classes of cilia: ''motile'' and ''non-motile'' cilia, each with two subtypes, giving four types in all.<ref name="Falk">{{cite journal | last1=Falk | first1=N | last2=Lösl | first2=M | last3=Schröder | first3=N | last4=Gießl | first4=A | title=Specialized Cilia in Mammalian Sensory Systems | journal=Cells | date=11 September 2015 | volume=4 | issue=3 | pages=500–19 | doi=10.3390/cells4030500 | pmid=26378583| pmc=4588048 | doi-access=free }}</ref> A cell will typically have one primary cilium or many motile cilia.<ref name="Wheatley">{{cite journal | last1=Wheatley | first1=DN | title=Primary cilia: turning points in establishing their ubiquity, sensory role and the pathological consequences of dysfunction | journal=Journal of Cell Communication and Signaling | date=September 2021 | volume=15 | issue=3 | pages=291–297 | doi=10.1007/s12079-021-00615-5 | pmid=33970456 |pmc=8222448 }}</ref> The structure of the cilium core, called the [[axoneme]], determines the cilium class. Most motile cilia have a central pair of single [[microtubule]]s surrounded by nine pairs of double microtubules called a [[9+2 axoneme]]. Most non-motile cilia have a [[9+0 axoneme]] that lacks the central pair of microtubules. Also lacking are the associated components that enable motility including the outer and inner [[dynein]] arms, and radial spokes.<ref name="Fisch">{{cite journal | last1=Fisch | first1=C | last2=Dupuis-Williams | first2=P | title=Ultrastructure of cilia and flagella - back to the future! | journal=Biology of the Cell | date=June 2011 | volume=103 | issue=6 | pages=249–70 | doi=10.1042/BC20100139 | pmid=21728999 |s2cid=7636387 | doi-access=free }}</ref> Some motile cilia lack the central pair, and some non-motile cilia have the central pair, hence the four types.<ref name="Falk"/><ref name="Fisch"/>

Most non-motile cilia, termed ''primary cilia'' or ''sensory cilia'', serve solely as sensory organelles.<ref name="Prevo">{{cite journal | last1=Prevo | first1=B | last2=Scholey | first2=JM | last3=Peterman | first3=EJG | title=Intraflagellar transport: mechanisms of motor action, cooperation, and cargo delivery | journal=The FEBS Journal | date=September 2017 | volume=284 | issue=18 | pages=2905–2931 | doi=10.1111/febs.14068 | pmid=28342295| pmc=5603355 }}</ref><ref name ="Elliott">{{Cite journal |last1=Elliott |first1=Kelsey H. |last2=Brugmann |first2=Samantha A. |date=1 March 2019 |title=Sending mixed signals: Cilia-dependent signaling during development and disease |journal=Developmental Biology |volume=447 |issue=1 |pages=28–41 |doi=10.1016/j.ydbio.2018.03.007 |issn=1095-564X |pmc=6136992 |pmid=29548942}}</ref> Most vertebrate cell types possess a single non-motile primary cilium, which functions as a cellular antenna.<ref name="Singla 629–633">{{Cite journal |last1=Singla |first1=Veena |last2=Reiter |first2=Jeremy F. |date=2006-08-04 |title=The primary cilium as the cell's antenna: signaling at a sensory organelle |url=https://www.ncbi.nlm.nih.gov/pubmed/16888132 |journal=Science |volume=313 |issue=5787 |pages=629–633 |doi=10.1126/science.1124534 |issn=1095-9203 |pmid=16888132 |bibcode=2006Sci...313..629S |s2cid=29885142}}</ref><ref name="Patel">{{cite journal | last1=Patel | first1=MM | last2=Tsiokas | first2=L | title=Insights into the Regulation of Ciliary Disassembly | journal=Cells | date=1 November 2021 | volume=10 | issue=11 | page=2977 | doi=10.3390/cells10112977 | pmid=34831200 |pmc=8616418 | doi-access=free }}</ref> [[Olfactory neuron]]s possess a great many non-motile cilia. Non-motile cilia that have a central pair of microtubules are the [[Kinocilium|kinocilia]] present on [[hair cell]]s.<ref name="Falk"/>

Motile cilia are found in large numbers on [[Respiratory epithelium|respiratory epithelial cells]] – around 200 cilia per cell, where they function in [[mucociliary clearance]], and also have [[Mechanosensation|mechanosensory]] and [[Chemoreceptor|chemosensory]] functions.<ref name=Horani>{{Cite journal |last1=Horani |first1=A |last2=Ferkol |first2=T |date=May 2018 |title=Advances in the Genetics of Primary Ciliary Dyskinesia |journal=Chest |volume=154 |issue=3 |pages=645–652 |pmid=29800551 |pmc=6130327 |doi=10.1016/j.chest.2018.05.007}}</ref><ref name="2012-Enuka" /><ref name="Bloodgood">{{cite journal | last1=Bloodgood | first1=RA | title=Sensory reception is an attribute of both primary cilia and motile cilia | journal=Journal of Cell Science | date=15 February 2010 | volume=123 | issue=Pt 4 | pages=505–9 | doi=10.1242/jcs.066308 | pmid=20144998 |s2cid=207165576 }}</ref> Motile cilia on [[ependymal cells]] move the [[cerebrospinal fluid]] through the [[ventricular system]] of the [[brain]]. Motile cilia are also present in the [[oviduct]]s ([[fallopian tube]]s) of female ([[theria]]n) mammals, where they function in moving [[egg cell]]s from the [[ovary]] to the [[uterus]].<ref name="2012-Enuka" /><ref name="Panelli"/> Motile cilia that lack the central pair of microtubules are found in the cells of the embryonic [[primitive node]]; termed ''nodal cells'', these nodal cilia are responsible for the [[left-right asymmetry]] of [[bilaterians]].<ref name="Desgrange">{{cite journal | last1=Desgrange | first1=A | last2=Le Garrec | first2=JF | last3=Meilhac | first3=SM | title=Left-right asymmetry in heart development and disease: forming the right loop | journal=Development | date=22 November 2018 | volume=145 | issue=22 | doi=10.1242/dev.162776 | pmid=30467108 | s2cid=53719458 |url=https://hal.archives-ouvertes.fr/hal-03094768/file/dev162776.full.pdf |archive-url=https://ghostarchive.org/archive/20221009/https://hal.archives-ouvertes.fr/hal-03094768/file/dev162776.full.pdf | archive-date=2022-10-09 | url-status=live}}
</ref>

== Structure==
[[File:Eukaryotic cilium diagram en.svg|thumb|300px|Eukaryotic motile cilium]]
A cilium is assembled and built from a [[basal body]] on the cell surface. From the basal body, the ciliary rootlet forms ahead of the transition plate and transition zone where the earlier microtubule triplets change to the microtubule doublets of the axoneme.

===Basal body===
The foundation of the cilium is the basal body, a term applied to  the mother centriole when it is associated with a cilium. Mammalian basal bodies consist of a barrel of nine triplet microtubules, subdistal appendages and nine strut-like structures, known as distal appendages, which attach the basal body to the membrane at the base of the cilium. Two of each of the basal body's triplet microtubules extend during growth of the axoneme to become the doublet microtubules.

===Ciliary rootlet===
The ciliary rootlet is a cytoskeleton-like structure that originates from the basal body at the proximal end of a cilium. Rootlets are typically 80-100&nbsp;nm in diameter and contain cross striae distributed at regular intervals of approximately 55-70&nbsp;nm. A prominent component of the rootlet is [[rootletin]] a coiled coil rootlet protein coded for by the [[Rootletin|''CROCC'' gene]].<ref name="uniprot">{{cite web |title=Rootelin |url=https://www.uniprot.org/uniprot/Q5TZA2 |access-date=28 March 2022}}</ref>

===Transition zone===
To achieve its distinct composition, the proximal-most region of the cilium consists of a '''transition zone''', also known as the '''ciliary gate''', that controls the entry and exit of proteins to and from the cilium.<ref>{{Cite journal|last1=Garcia|first1=Galo|last2=Raleigh|first2=David R.|last3=Reiter|first3=Jeremy F.|date=23 April 2018|title=How the Ciliary Membrane Is Organized Inside-Out to Communicate Outside-In|journal=Current Biology|volume=28|issue=8|pages=R421–R434|doi=10.1016/j.cub.2018.03.010|issn=1879-0445|pmc=6434934|pmid=29689227|bibcode=2018CBio...28.R421G }}</ref><ref>{{Cite journal|last1=Garcia-Gonzalo|first1=Francesc R.|last2=Reiter|first2=Jeremy F.|date=2017-02-01|title=Open Sesame: How Transition Fibers and the Transition Zone Control Ciliary Composition|journal=Cold Spring Harbor Perspectives in Biology|volume=9|issue=2|pages=a028134|doi=10.1101/cshperspect.a028134|issn=1943-0264|pmc=5287074|pmid=27770015}}</ref><ref>{{Cite journal|last1=Gonçalves|first1=João|last2=Pelletier|first2=Laurence|date=April 2017|title=The Ciliary Transition Zone: Finding the Pieces and Assembling the Gate|journal=Molecules and Cells|volume=40|issue=4|pages=243–253|doi=10.14348/molcells.2017.0054|issn=0219-1032|pmc=5424270|pmid=28401750}}</ref> At the transition zone, Y-shaped structures connect the ciliary membrane to the underlying axoneme. Control of selective entry into cilia may involve a sieve-like function of transition zone. Inherited defects in components of the transition zone cause ciliopathies, such as Joubert syndrome. Transition zone structure and function is conserved across diverse organisms, including vertebrates, ''[[Caenorhabditis elegans]]'', ''[[Drosophila melanogaster]]'' and ''[[Chlamydomonas reinhardtii]]''. In mammals, disruption of the transition zone reduces the ciliary abundance of membrane-associated ciliary proteins, such as those involved in [[Hedgehog signaling pathway|Hedgehog signal transduction]], compromising Hedgehog-dependent embryonic development of digit number and central nervous system patterning.

===Axoneme===
Inside a cilium is a [[microtubule]]-based [[cytoskeleton|cytoskeletal core]] called the [[axoneme]].  The axoneme of a primary cilium typically has a ring of nine outer microtubule doublets (called a [[9+0 axoneme]]),  and the axoneme of a motile cilium has, in addition to the nine outer doublets,  two central microtubule singlets (called a [[9+2 axoneme]]). This is the same axoneme type of the [[flagellum]]. The axoneme in a motile cilium acts as a scaffold for the inner and outer [[dynein arm]]s that move the cilium, and provides tracks for the microtubule [[Motor protein|motor proteins]] of [[kinesin]] and dynein.<ref name="HHMIB2005"/><ref>{{cite journal | vauthors = Rosenbaum JL, Witman GB | title = Intraflagellar transport | journal = Nature Reviews. Molecular Cell Biology | volume = 3 | issue = 11 | pages = 813–25 | date = November 2002 | pmid = 12415299 | doi = 10.1038/nrm952 | s2cid = 12130216 }}</ref><ref>{{cite journal | vauthors = Scholey JM | title = Intraflagellar transport motors in cilia: moving along the cell's antenna | journal = The Journal of Cell Biology | volume = 180 | issue = 1 | pages = 23–29 | date = January 2008 | pmid = 18180368 | pmc = 2213603 | doi = 10.1083/jcb.200709133 }}</ref> The transport of ciliary components is carried out by [[intraflagellar transport]] (IFT) which is similar to the [[axonal transport]] in a [[axon|nerve fibre]]. Transport is bidirectional and [[Motor protein#Cytoskeletal motor proteins|cytoskeletal motor proteins]] kinesin and dynein transport ciliary components along the microtubule tracks; kinesin in an anterograde movement towards the ciliary tip and dynein in a retrograde movement towards the cell body. The cilium has its own ciliary membrane enclosed within the surrounding [[cell membrane]].<ref>{{cite journal | vauthors = Rohatgi R, Snell WJ | title = The ciliary membrane | journal = Current Opinion in Cell Biology | volume = 22 | issue = 4 | pages = 541–46 | date = August 2010 | pmid = 20399632 | pmc = 2910237 | doi = 10.1016/j.ceb.2010.03.010 }}</ref>

==Types==
===Non-motile cilia===
In animals, non-motile '''primary cilia''' are found on nearly every type of cell, blood cells being a prominent exception.<ref name="HHMIB2005"/> Most cells only possess one, in contrast to cells with motile cilia, an exception being [[Olfactory epithelium#Olfactory sensory neurons|olfactory sensory neurons]], where the [[odorant receptors]] are located, which each possess about ten cilia. Some cell types, such as retinal photoreceptor cells, possess highly specialized primary cilia.<ref name="Wolfrum">{{cite journal |last1=Wolfrum |first1=U |last2=Schmitt |first2=A |title=Rhodopsin transport in the membrane of the connecting cilium of mammalian photoreceptor cells. |journal=Cell Motility and the Cytoskeleton |date=June 2000 |volume=46 |issue=2 |pages=95–107 |doi=10.1002/1097-0169(200006)46:2<95::AID-CM2>3.0.CO;2-Q |pmid=10891855}}</ref>

Although the primary cilium was discovered in 1898, it was largely ignored for a century and considered a [[vestigial]] organelle without important function.<ref>{{Cite journal|last=Satir|first=Peter|date=2017|title=CILIA: before and after|journal=Cilia|volume=6|pages=1|doi=10.1186/s13630-017-0046-8|issn=2046-2530|pmc=5343305|pmid=28293419 |doi-access=free }}</ref><ref name="HHMIB2005" />  Recent findings regarding its physiological roles in chemosensation, signal transduction, and cell growth control, have revealed its importance in cell function. Its importance to human biology has been underscored by the discovery of its role in a diverse group of diseases caused by the [[Anterior segment dysgenesis|dysgenesis]] or dysfunction of cilia, such as [[polycystic kidney disease]],<ref name="pmid18264930">{{cite journal | vauthors = Wagner CA | title = News from the cyst: insights into polycystic kidney disease | journal = Journal of Nephrology | volume = 21 | issue = 1 | pages = 14–16 | year = 2008 | pmid = 18264930 | url = http://www.jnephrol.com/Article.action?cmd=navigate&urlkey=Public_Details&t=JN&uid=9A13E591-2E27-441B-8356-23BF86D9CFB0 }}{{Dead link|date=July 2019 |bot=InternetArchiveBot |fix-attempted=yes }}</ref> [[congenital heart disease]],<ref name="pmid17548739">{{cite journal | vauthors = Brueckner M | title = Heterotaxia, congenital heart disease, and primary ciliary dyskinesia | journal = Circulation | volume = 115 | issue = 22 | pages = 2793–95 | date = June 2007 | pmid = 17548739 | doi = 10.1161/CIRCULATIONAHA.107.699256 | s2cid = 14405881 | doi-access =  }}</ref> [[mitral valve prolapse]],<ref name="pmid 32380895">{{cite journal |vauthors=Toomer KA et al. | title = Primary cilia defects causing mitral valve prolapse | journal = Sci. Transl. Med. | volume = 11 | issue = 493| pages = eaax0290 | year = 2019 | pmid = 31118289 | doi = 10.1126/scitranslmed.aax0290| pmc = 7331025 | doi-access = free }}</ref>  and retinal degeneration,<ref>{{Cite journal|last1=Chen|first1=Holly Y.|last2=Kelley|first2=Ryan A.|last3=Li|first3=Tiansen|last4=Swaroop|first4=Anand|date=2020-07-31|title=Primary cilia biogenesis and associated retinal ciliopathies|journal=Seminars in Cell & Developmental Biology|volume=110|pages=70–88|doi=10.1016/j.semcdb.2020.07.013|issn=1096-3634|pmid=32747192|pmc=7855621|doi-access=free}}</ref> called [[ciliopathy|ciliopathies]].<ref name="badano2006">{{cite journal | vauthors = Badano JL, Mitsuma N, Beales PL, Katsanis N | title = The ciliopathies: an emerging class of human genetic disorders | journal = Annual Review of Genomics and Human Genetics | volume = 7 | pages = 125–48 | year = 2006 | pmid = 16722803 | doi = 10.1146/annurev.genom.7.080505.115610 }}</ref><ref name="Reiter 533–547">{{Cite journal|last1=Reiter|first1=Jeremy F.|last2=Leroux|first2=Michel R.|date=September 2017|title=Genes and molecular pathways underpinning ciliopathies|journal=Nature Reviews. Molecular Cell Biology|volume=18|issue=9|pages=533–547|doi=10.1038/nrm.2017.60|issn=1471-0080|pmc=5851292|pmid=28698599}}</ref> The primary cilium is now known to play an important role in the function of many human organs.<ref name="HHMIB2005">{{cite journal | last = Gardiner | first = Mary Beth | name-list-style = vanc | title = The Importance of Being Cilia | journal = HHMI Bulletin | volume = 18 | issue = 2 | date = September 2005 | url = http://www.hhmi.org/sites/default/files/Bulletin/2005/September/sept2005_fulltext.pdf | access-date = 26 July 2008 }}</ref><ref name="Singla 629–633"/> Primary cilia on pancreatic [[beta cell]]s regulate their function and energy metabolism. Cilia deletion can lead to islet dysfunction and [[type 2 diabetes]].<ref name="Hegyi">{{cite journal |last1=Hegyi |first1=P |last2=Petersen |first2=OH |title=The exocrine pancreas: the acinar-ductal tango in physiology and pathophysiology. |journal=Reviews of Physiology, Biochemistry and Pharmacology |date=2013 |volume=165 |pages=1–30 |doi=10.1007/112_2013_14 |pmid=23881310|isbn=978-3-319-00998-8 }}</ref>

Cilia are assembled during the [[G1 phase|G<sub>1</sub> phase]] and are disassembled before mitosis occurs.<ref>{{cite journal | vauthors = Pan J, Snell W | title = The primary cilium: keeper of the key to cell division | journal = Cell | volume = 129 | issue = 7 | pages = 1255–57 | date = June 2007 | pmid = 17604715 | doi = 10.1016/j.cell.2007.06.018 | s2cid = 17712155 | doi-access = free }}</ref><ref name="Patel"/> Disassembly of cilia requires the action of [[aurora kinase A]].<ref name="entrez">{{cite journal|vauthors=Pugacheva EN, Jablonski SA, Hartman TR, Henske EP, Golemis EA|date=June 2007|title=HEF1-dependent Aurora A activation induces disassembly of the primary cilium|journal=Cell|volume=129|issue=7|pages=1351–63|doi=10.1016/j.cell.2007.04.035|pmc=2504417|pmid=17604723}}</ref> 
The current scientific understanding of primary cilia views them as "sensory [[Cell (biology)|cellular]] antennae that coordinate many cellular signaling pathways, sometimes coupling the signaling to ciliary motility or alternatively to cell division and differentiation."<ref name="Satir2008">{{cite journal | vauthors = Satir P, Christensen ST | title = Structure and function of mammalian cilia | journal = Histochemistry and Cell Biology | volume = 129 | issue = 6 | pages = 687–93 | date = June 2008 | pmid = 18365235 | pmc = 2386530 | doi = 10.1007/s00418-008-0416-9 }}</ref>
The cilium is composed of subdomains{{clarify|date=October 2020}} and enclosed by a plasma membrane continuous with the plasma membrane of the cell. For many cilia, the [[basal body]], where the cilium originates, is located within a membrane invagination called the ciliary pocket. The cilium membrane and the basal body microtubules are connected by distal appendages (also called transition fibers). Vesicles carrying molecules for the cilia dock at the distal appendages. Distal to the transition fibers form a transition zone where entry and exit of molecules is regulated to and from the cilia.  Some of the signaling with these cilia occur through ligand binding such as [[Hedgehog signaling]].<ref>{{Cite journal|last1=Wong|first1=Sunny Y.|last2=Reiter|first2=Jeremy F.|date=2008|title=The primary cilium at the crossroads of mammalian hedgehog signaling|journal=Current Topics in Developmental Biology|volume=85|pages=225–260|doi=10.1016/S0070-2153(08)00809-0|issn=0070-2153|pmc=2653622|pmid=19147008}}</ref> Other forms of signaling include [[G protein-coupled receptor]]s including the [[somatostatin receptor 3]] in neurons.<ref>{{cite journal | vauthors = Wheway G, Nazlamova L, Hancock JT | title = Signaling through the Primary Cilium | journal = Frontiers in Cell and Developmental Biology | volume = 6 | pages = 8 | year = 2018 | pmid = 29473038 | pmc = 5809511 | doi = 10.3389/fcell.2018.00008 | doi-access = free }}</ref>
[[File:Blausen 0766 RespiratoryEpithelium.png|thumb|Illustration depicting motile cilia on [[respiratory epithelium]].]]

====Modified non-motile cilia====
[[Kinocilia]] that are found on hair cells in the inner ear are termed as specialized primary cilia, or modified non-motile cilia. They possess the 9+2 axoneme of the motile cilia but lack the inner dynein arms that give movement. They do move passively following the detection of sound, allowed by the outer dynein arms.<ref name="Wang">{{cite journal |last1=Wang |first1=D |last2=Zhou |first2=J |title=The Kinocilia of Cochlear Hair Cells: Structures, Functions, and Diseases. |journal=Frontiers in Cell and Developmental Biology |date=2021 |volume=9 |pages=715037 |doi=10.3389/fcell.2021.715037 |pmid=34422834|pmc=8374625 |doi-access=free }}</ref><ref name=Takeda>{{cite journal |last1=Takeda |first1=Sen |last2=Narita |first2=Keishi |title=Structure and function of vertebrate cilia, towards a new taxonomy |journal=Differentiation |date=February 2012 |volume=83 |issue=2 |pages=S4–S11 |doi=10.1016/j.diff.2011.11.002|pmid=22118931 }}</ref>

===Motile cilia===
[[File:Bronchiolar epithelium 4 - SEM.jpg|thumb|[[Trachea]]l respiratory epithelium showing cilia and much smaller [[microvilli]] on non-ciliated cells in [[Scanning electron microscope|scanning electron micrograph]].]]
[[Mammal]]s also have '''motile cilia''' or '''secondary cilia''' that are usually present on a cell's surface in large numbers (multiciliate), and beat in coordinated [[Metachronal rhythm|metachronal waves]].<ref name="Lewin2007">{{cite book|author=Benjamin Lewin|title=Cells|url=https://books.google.com/books?id=2VEGC8j9g9wC&pg=PA359|year=2007|publisher=Jones & Bartlett Learning|isbn=978-0-7637-3905-8|page=359}}</ref> Multiciliated cells are found [[respiratory epithelium|lining the respiratory tract]] where they function in [[mucociliary clearance]] sweeping mucus containing debris away from the [[lung]]s.<ref name="2012-Enuka">{{cite journal | vauthors = Enuka Y, Hanukoglu I, Edelheit O, Vaknine H, Hanukoglu A | title = Epithelial sodium channels (ENaC) are uniformly distributed on motile cilia in the oviduct and the respiratory airways | journal = Histochemistry and Cell Biology | volume = 137 | issue = 3 | pages = 339–53 | date = March 2012 | pmid = 22207244 | doi = 10.1007/s00418-011-0904-1 | s2cid = 15178940 }}</ref> Each cell in the respiratory epithelium has around 200 motile cilia.<ref name=Horani/>

In the [[reproductive tract]], [[smooth muscle]] contractions help the beating of the cilia in moving the [[egg cell]] from the ovary to the uterus.<ref name="2012-Enuka" /><ref name="Panelli"/>
In the [[ventricular system|ventricles of the brain]] ciliated [[ependymal cells]] circulate the [[cerebrospinal fluid]].

The functioning of motile cilia is strongly dependent on the maintenance of optimal levels of [[Periciliary liquid layer|periciliary fluid]] bathing the cilia. [[Epithelial sodium channel]]s (ENaCs) are specifically expressed along the entire length of cilia in the respiratory tract, and [[fallopian tube]] or ''[[oviduct]]'' that apparently serve as sensors to regulate the periciliary fluid.<ref name="2012-Enuka" /><ref name="2016-Hanukoglu" >{{cite journal | vauthors = Hanukoglu I, Hanukoglu A | title = Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases | journal = Gene | volume = 579 | issue = 2 | pages = 95–132 | date = April 2016 | pmid = 26772908 | pmc = 4756657 | doi = 10.1016/j.gene.2015.12.061 }}</ref>

====Modified motile cilia====
Motile cilia without the central pair of singlets (9+0) are found in early embryonic development. They are present as nodal cilia on the nodal cells of the [[primitive node]]. Nodal cells are responsible for the [[left-right asymmetry]] in [[bilaterians|bilateral animals]].<ref name="Desgrange"/> While lacking the central apparatus there are [[dynein arm]]s present that allow the nodal cilia to move in a spinning  fashion. The movement creates a current flow of the extraembryonic fluid across the [[primitive node|nodal surface]] in a leftward direction that initiates the left-right asymmetry in the developing embryo.
<ref name="Horani"/><ref name="Larsen"/>

Motile, multiple, 9+0 cilia are found on the epithelial cells of the [[choroid plexus]]. Cilia also can change structure when introduced to hot temperatures and become sharp. They are present in large numbers on each cell and move relatively slowly, making them intermediate between motile and primary cilia. In addition to 9+0 cilia that are mobile, there are also solitary 9+2 cilia that stay immobile found in hair cells.<ref name=Takeda/>

====Nodal cilia====
[[File:Nodal cilia.jpg|thumb|[[Scanning electron micrograph]] of nodal cilia on a [[mouse]] embryo]]
'''Nodal cells''' have a single cilium called a monocilium. They are present in the very early [[Embryonic development|development of the embryo]] on the [[primitive node]]. There are two areas of the node with different types of '''nodal cilia'''. On the central node are motile cilia, and on the peripheral area of the node the nodal cilia are modified motile.<ref name="Larsen">{{cite book |last1=Schoenwolf |first1=Gary C. |title=Larsen's human embryology |date=2015 |location=Philadelphia, PA |isbn=9781455706846 |page=64 |edition=Fifth}}</ref>

The motile cilia on the central cells rotate to generate the leftward flow of extracellular fluid needed to initiate the left-right asymmetry.<ref name="Larsen"/>

===Cilia versus flagella===
{{See also|Flagellum#Terminology}}
The motile cilia on [[sperm cell]]s and many [[protozoan]]s enables swimming through liquids and are traditionally referred to as "[[flagella]]".<ref name="Haimo_JCB198112"/> As these protrusions are structurally identical to motile cilia, attempts at preserving this terminology include making a distinction by morphology ("flagella" are typically longer than ordinary cilia and have a different undulating motion)<ref name="Alberts1"/> and by number.<ref name=pmid20145000>{{cite journal |last1=Lindemann |first1=CB |last2=Lesich |first2=KA |title=Flagellar and ciliary beating: the proven and the possible. |journal=Journal of Cell Science |date=15 February 2010 |volume=123 |issue=Pt 4 |pages=519–28 |doi=10.1242/jcs.051326 |pmid=20145000 |s2cid=18673550 |doi-access=}}</ref>

===Microorganisms===
[[Ciliate]]s are [[eukaryotic]] [[microorganism]]s that possess motile cilia exclusively and use them for either locomotion or to simply move liquid over their surface. A ''[[Paramecium]]'' for example is covered in thousands of cilia that enable its swimming. These motile cilia have been shown to be also sensory.<ref name="Valentine">{{cite journal |last1=Valentine |first1=M |last2=Van Houten |first2=J |title=Using ''Paramecium'' as a Model for Ciliopathies. |journal=Genes |date=24 September 2021 |volume=12 |issue=10 |page=1493 |doi=10.3390/genes12101493 |pmid=34680887|pmc=8535419 |doi-access=free }}</ref>

==Ciliogenesis==
{{Main|Ciliogenesis}}
Cilia are formed through the process of [[ciliogenesis]]. An early step is docking of the basal body to the growing ciliary membrane, after which the transition zone forms. The building blocks of the ciliary axoneme, such as [[tubulins]], are added at the ciliary tips through a process that depends partly on [[intraflagellar transport]] (IFT).<ref>{{cite journal | vauthors = Johnson KA, Rosenbaum JL | title = Polarity of flagellar assembly in Chlamydomonas | journal = The Journal of Cell Biology | volume = 119 | issue = 6 | pages = 1605–11 | date = December 1992 | pmid = 1281816 | pmc = 2289744 | doi = 10.1083/jcb.119.6.1605 }}</ref><ref>{{cite journal | vauthors = Hao L, Thein M, Brust-Mascher I, Civelekoglu-Scholey G, Lu Y, Acar S, Prevo B, Shaham S, Scholey JM | title = Intraflagellar transport delivers tubulin isotypes to sensory cilium middle and distal segments | journal = Nature Cell Biology | volume = 13 | issue = 7 | pages = 790–98 | date = June 2011 | pmid = 21642982 | pmc = 3129367 | doi = 10.1038/ncb2268 }}</ref> Exceptions include ''Drosophila'' sperm and ''[[Plasmodium falciparum]]'' flagella formation, in which cilia assemble in the cytoplasm.<ref>[http://www.pandasthumb.org/archives/2007/06/of_cilia_and_si.html Of cilia and silliness (more on Behe) – The Panda's Thumb] {{webarchive|url=https://web.archive.org/web/20071017161257/http://pandasthumb.org/archives/2007/06/of_cilia_and_si.html |date=17 October 2007 }}</ref>

At the base of the cilium where it attaches to the cell body is the [[microtubule organizing center]], the [[basal body]]. Some basal body proteins as [[CEP164]], [[ODF2]]<ref name="entrez2">{{cite journal | vauthors = Ishikawa H, Kubo A, Tsukita S, Tsukita S | title = Odf2-deficient mother centrioles lack distal/subdistal appendages and the ability to generate primary cilia | journal = Nature Cell Biology | volume = 7 | issue = 5 | pages = 517–24 | date = May 2005 | pmid = 15852003 | doi = 10.1038/ncb1251 | s2cid = 35443570 }}</ref>
and [[CEP170]],<ref name="edoc">{{cite thesis | last = Lamla | first = Stefan | name-list-style = vanc | title = Functional characterisation of the centrosomal protein Cep170| url = http://edoc.ub.uni-muenchen.de/9783/| date = 2009-01-22| publisher = Ludwig-Maximilians-Universität München| type = Ph.D. }}</ref> are required for the formation and the stability of the cilium.

In effect, the cilium is a [[Molecular machine|nanomachine]] composed of perhaps over 600 proteins in molecular complexes, many of which also function independently as nanomachines.  [[Flexible linker]]s allow the 
[[Protein domain#Domains and protein flexibility|mobile protein domains]]
connected by them to recruit their binding partners and induce 
long-range [[allostery]] via 
[[Protein dynamics#Global flexibility: multiple domains|protein domain dynamics]].<ref name="Satir2008"/>

== Function ==
The [[dynein]] in the axoneme – [[axonemal dynein]] forms bridges between neighbouring microtubule doublets. When [[Adenosine triphosphate|ATP]] activates the motor domain of dynein, it attempts to walk along the adjoining microtubule doublet. This would force the adjacent doublets to slide over one another if not for the presence of [[nexin]] between the microtubule doublets. And thus the force generated by dynein is instead converted into a bending motion.<ref>{{Cite book |url = https://www.ncbi.nlm.nih.gov/books/NBK26888/|title = Molecular Biology of the Cell|last = Alberts|first = Bruce| chapter=Molecular Motors |year = 2002| publisher=Garland Science }}{{ISBN?}}{{page needed|date=April 2020}}</ref><ref name="King">{{cite journal |last1=King |first1=SM |title=Axonemal Dynein Arms. |journal=Cold Spring Harbor Perspectives in Biology |date=1 November 2016 |volume=8 |issue=11 |pages=a028100 |doi=10.1101/cshperspect.a028100 |pmid=27527589|pmc=5088525 }}</ref>

===Sensing the extracellular environment===
Some primary cilia on [[epithelial]] cells in eukaryotes act as ''cellular antennae'', providing [[Molecular sensor|chemosensation]], [[thermosensation]] and [[mechanosensation]] of the extracellular environment.<ref name="Adams2008"/><ref name="Singla 629–633"/> These cilia then play a role in mediating specific signalling cues, including soluble factors in the external cell environment, a [[Secretion|secretory]] role in which a soluble protein is released to have an effect downstream of the fluid flow, and mediation of fluid flow if the cilia are [[Motility|motile]].<ref name=Adams2008>{{cite journal | vauthors = Adams M, Smith UM, Logan CV, Johnson CA | title = Recent advances in the molecular pathology, cell biology and genetics of ciliopathies | journal = Journal of Medical Genetics | volume = 45 | issue = 5 | pages = 257–67 | date = May 2008 | pmid = 18178628 | doi = 10.1136/jmg.2007.054999 | doi-access = free }}</ref>

Some [[epithelial]] cells are ciliated, and they commonly exist as a sheet of polarized cells forming a tube or tubule with cilia projecting into the [[Lumen (anatomy)|lumen]]. This sensory and signalling role puts cilia in a central role for maintaining the local cellular environment and may be why [[Ciliopathy|ciliary defects]] cause such a wide range of human diseases.<ref name="Reiter 533–547"/>

In the embryo, [[nodal cilia]] are used to direct the flow of extracellular fluid.  This leftward movement is to generate [[left-right asymmetry]] across the midline of the embryo.  Central cilia coordinate their rotational beating while the immotile cilia on the sides sense the direction of the flow.<ref name="Larsen"/><ref>{{cite book|last1=Wolpert|first1=Lewis|title=Principles of Development|last2=Tickle|first2=Cheryll|last3=Martinez Arias|first3=Alfonso|date=2015|publisher=Oxford University Press|edition=5th|page=227}}</ref><ref>[https://www.science.org/doi/10.1126/science.abq7317 Cilia function as calcium-mediated mechanosensors that instruct left-right asymmetry], Science, 5 January 2023, Vol 379, Issue 6627, pp. 71-78; DOI: 10.1126/science.abq7317</ref> Studies in mice suggest a biophysical mechanism by which the direction of flow is sensed.<ref name=science20230105>[https://www.science.org/doi/10.1126/science.abq8148 Immotile cilia mechanically sense the direction of fluid flow for left-right determination], Science, 5 January 2023, Vol 379, Issue 6627, pp. 66-71; DOI: 10.1126/science.abq8148</ref>

===Axo-ciliary synapse===
With axo-ciliary [[synapse]]s,<!-- first reported in 2022,--> there is communication between [[Serotonin|serotonergic]] [[axon]]s and <!--at least the -->primary cilia of [[Hippocampus anatomy#Basic hippocampal circuit|CA1]] [[Pyramidal cell|pyramidal]] [[neuron]]s that alters the neuron's [[epigenetic]] state in the [[Cell nucleus|nucleus]] – "a way to change what is being transcribed or made in the nucleus" via this signalling distinct from that at the [[plasma membrane]] which also is longer-term.<ref>{{cite news |last1=Tamim |first1=Baba |title=New discovery: Synapse hiding in the mice brain may advance our understanding of neuronal communication |url=https://interestingengineering.com/science/new-discovery-synapse-hiding-in-mice-brain |access-date=19 October 2022 |work=interestingengineering.com |date=4 September 2022}}</ref><ref>{{cite journal |last1=Sheu |first1=Shu-Hsien |last2=Upadhyayula |first2=Srigokul |last3=Dupuy |first3=Vincent |last4=Pang |first4=Song |last5=Deng |first5=Fei |last6=Wan |first6=Jinxia |last7=Walpita |first7=Deepika |last8=Pasolli |first8=H. Amalia |last9=Houser |first9=Justin |last10=Sanchez-Martinez |first10=Silvia |last11=Brauchi |first11=Sebastian E. |last12=Banala |first12=Sambashiva |last13=Freeman |first13=Melanie |last14=Xu |first14=C. Shan |last15=Kirchhausen |first15=Tom |last16=Hess |first16=Harald F. |last17=Lavis |first17=Luke |last18=Li |first18=Yulong |last19=Chaumont-Dubel |first19=Séverine |last20=Clapham |first20=David E. |title=A serotonergic axon-cilium synapse drives nuclear signaling to alter chromatin accessibility |journal=Cell |date=1 September 2022 |volume=185 |issue=18 |pages=3390–3407.e18 |doi=10.1016/j.cell.2022.07.026 |pmid=36055200 |pmc=9789380 |s2cid=251958800 |language=English |issn=0092-8674}}
* University press release: {{cite news |title=Scientists discover new kind of synapse in neurons' tiny hairs |url=https://phys.org/news/2022-09-scientists-kind-synapse-neurons-tiny.html |access-date=19 October 2022 |work=Howard Hughes Medical Institute via phys.org |language=en}}</ref>

==Clinical significance==
{{Main|Ciliopathy}}
Ciliary defects can lead to a number of human diseases.<ref name="Reiter 533–547"/><ref>{{Cite journal|last1=Braun|first1=Daniela A.|last2=Hildebrandt|first2=Friedhelm|date=2017-03-01|title=Ciliopathies|journal=Cold Spring Harbor Perspectives in Biology|volume=9|issue=3|pages=a028191|doi=10.1101/cshperspect.a028191|issn=1943-0264|pmc=5334254|pmid=27793968}}</ref> Defects in cilia adversely affect many critical signaling pathways essential to embryonic development and to adult physiology, and thus offer a plausible hypothesis for the often [[pleiotropic|multi-symptom]] nature of diverse ciliopathies.<ref name="badano2006"/><ref name="Reiter 533–547" /> Known ciliopathies include [[primary ciliary dyskinesia]], [[Bardet–Biedl syndrome]], [[polycystic kidney disease|polycystic kidney]] and [[polycystic liver disease|liver disease]], [[nephronophthisis]], [[Alström syndrome]], [[Meckel–Gruber syndrome]], [[Sensenbrenner syndrome]] and some forms of [[retinopathy|retinal degeneration]].<ref name="badano2006"/><ref name=Adams2008/> Genetic mutations compromising the proper functioning of cilia, [[ciliopathy|ciliopathies]], can cause chronic disorders such as [[primary ciliary dyskinesia]] (PCD), [[nephronophthisis]], and [[Senior–Løken syndrome]]. In addition, a defect of the primary cilium in the [[Nephron#Renal tubule|renal tubule]] cells can lead to [[polycystic kidney disease]] (PKD). In another genetic disorder called [[Bardet–Biedl syndrome]] (BBS), the mutant gene products are the components in the basal body and cilia.<ref name="badano2006"/>  Defects in cilia cells are linked to obesity and often pronounced in type 2 diabetes. Several studies already showed impaired glucose tolerance and reduction in the insulin secretion in the ciliopathy models. Moreover, the number and length of cilia was decreased in the [[type 2 diabetes]] models.<ref>{{cite journal| doi=10.1038/ncomms6308| title=Ciliary dysfunction impairs beta-cell insulin secretion and promotes development of type 2 diabetes in rodents| year=2014| last1=Gerdes| first1=Jantje M.| last2=Christou-Savina| first2=Sonia| last3=Xiong| first3=Yan| last4=Moede| first4=Tilo| last5=Moruzzi| first5=Noah| last6=Karlsson-Edlund| first6=Patrick| last7=Leibiger| first7=Barbara| last8=Leibiger| first8=Ingo B.| last9=Östenson| first9=Claes-Göran| last10=Beales| first10=Philip L.| last11=Berggren| first11=Per-Olof| journal=Nature Communications| volume=5| page=5308| pmid=25374274| bibcode=2014NatCo...5.5308G| s2cid=41645398| doi-access=free}}</ref>

[[Epithelial sodium channels]] (ENaCs) that are expressed along the length of cilia regulate [[Periciliary liquid layer|periciliary fluid]] level. Mutations that decrease the activity of ENaCs result in multisystem [[pseudohypoaldosteronism]], that is associated with fertility problems.<ref name="2012-Enuka" /> In [[cystic fibrosis]] that results from mutations in the chloride channel [[Cystic fibrosis transmembrane conductance regulator|CFTR]], ENaC activity is enhanced leading to a severe reduction of the fluid level that causes complications and infections in the respiratory airways.<ref name="2016-Hanukoglu" />

Since the flagellum of human sperm has the same internal structure of a cilium, ciliary dysfunction can also be responsible for male infertility.<ref name="pmid16850538">{{cite journal | vauthors = Ichioka K, Kohei N, Okubo K, Nishiyama H, Terai A | title = Obstructive azoospermia associated with chronic sinopulmonary infection and situs inversus totalis | journal = Urology | volume = 68 | issue = 1 | pages = 204.e5–7 | date = July 2006 | pmid = 16850538 | doi = 10.1016/j.urology.2006.01.072 }}</ref>

There is an association of primary ciliary dyskinesia with left-right anatomic abnormalities such as [[situs inversus]] (a combination of findings is known as [[Kartagener syndrome]]), and [[situs ambiguus]] (also known as ''Heterotaxy syndrome'').<ref name="Worsley">{{cite journal |last1=Worsley |first1=Calum |last2=Weerakkody |first2=Yuranga |title=Heterotaxy syndrome |url=https://radiopaedia.org/articles/heterotaxy-syndrome?lang=gb |website=Radiopaedia.org |access-date=10 June 2022 |doi=10.53347/rID-7420 |date=1 November 2009|doi-access=free }}</ref> These left-right anatomic abnormalities can also result in [[congenital heart disease]].<ref name="pmid17515466">{{cite journal | vauthors = Kennedy MP, Omran H, Leigh MW, Dell S, Morgan L, Molina PL, Robinson BV, Minnix SL, Olbrich H, Severin T, Ahrens P, Lange L, Morillas HN, Noone PG, Zariwala MA, Knowles MR | title = Congenital heart disease and other heterotaxic defects in a large cohort of patients with primary ciliary dyskinesia | journal = Circulation | volume = 115 | issue = 22 | pages = 2814–21 | date = June 2007 | pmid = 17515466 | doi = 10.1161/CIRCULATIONAHA.106.649038 | doi-access = free }}</ref> It has been shown that proper cilial function is responsible for the normal left-right asymmetry in mammals.<ref name="pmid12888012">{{cite journal | vauthors = McGrath J, Brueckner M | title = Cilia are at the heart of vertebrate left-right asymmetry | journal = Current Opinion in Genetics & Development | volume = 13 | issue = 4 | pages = 385–92 | date = August 2003 | pmid = 12888012 | doi = 10.1016/S0959-437X(03)00091-1 }}</ref>

The diverse outcomes caused by ciliary dysfunction may result from alleles of different strengths that compromise ciliary functions in different ways or to different extents. Many ciliopathies are inherited in a Mendelian manner, but specific genetic interactions between distinct functional ciliary complexes, such as transition zone and BBS complexes, can alter the phenotypic manifestations of recessive ciliopathies.<ref>{{Cite journal|last1=Leitch|first1=Carmen C.|last2=Zaghloul|first2=Norann A.|last3=Davis|first3=Erica E.|last4=Stoetzel|first4=Corinne|last5=Diaz-Font|first5=Anna|last6=Rix|first6=Suzanne|last7=Alfadhel|first7=Majid|last8=Al-Fadhel|first8=Majid|last9=Lewis|first9=Richard Alan|last10=Eyaid|first10=Wafaa|last11=Banin|first11=Eyal|date=April 2008|title=Hypomorphic mutations in syndromic encephalocele genes are associated with Bardet-Biedl syndrome|url=https://www.ncbi.nlm.nih.gov/pubmed/18327255|journal=Nature Genetics|volume=40|issue=4|pages=443–448|doi=10.1038/ng.97|issn=1546-1718|pmid=18327255|s2cid=5282929}}</ref><ref>{{Cite journal|last1=Yee|first1=Laura E.|last2=Garcia-Gonzalo|first2=Francesc R.|last3=Bowie|first3=Rachel V.|last4=Li|first4=Chunmei|last5=Kennedy|first5=Julie K.|last6=Ashrafi|first6=Kaveh|last7=Blacque|first7=Oliver E.|last8=Leroux|first8=Michel R.|last9=Reiter|first9=Jeremy F.|date=November 2015|title=Conserved Genetic Interactions between Ciliopathy Complexes Cooperatively Support Ciliogenesis and Ciliary Signaling|journal=PLOS Genetics|volume=11|issue=11|pages=e1005627|doi=10.1371/journal.pgen.1005627|issn=1553-7404|pmc=4635004|pmid=26540106 |doi-access=free }}</ref> Some mutations in transition zone proteins can cause specific serious ciliopathies.<ref name="Cavalier-Smith">{{cite journal |last1=Cavalier-Smith |first1=T |title=Ciliary transition zone evolution and the root of the eukaryote tree: implications for opisthokont origin and classification of kingdoms Protozoa, Plantae, and Fungi. |journal=Protoplasma |date=May 2022 |volume=259 |issue=3 |pages=487–593 |doi=10.1007/s00709-021-01665-7 |pmid=34940909 |pmc=9010356 |bibcode=2022Prpls.259..487C }}</ref>

===Extracellular changes===
Reduction of cilia function can also result from infection. Research into [[biofilm]]s has shown that bacteria can alter cilia. A biofilm is a community of bacteria of either the same or multiple species of bacteria. The cluster of cells secretes different factors which form an extracellular matrix. Cilia in the respiratory system is known to move mucus and pathogens out of the airways. It has been found that patients with biofilm positive infections have impaired cilia function. The impairment may present as decreased motion or reduction in the number of cilia. Though these changes result from an external source, they still effect the pathogenicity of the bacteria, progression of infection, and how it is treated.<ref>{{cite journal | vauthors = Fastenberg JH, Hsueh WD, Mustafa A, Akbar NA, Abuzeid WM | title = Biofilms in chronic rhinosinusitis: Pathophysiology and therapeutic strategies | journal = World Journal of Otorhinolaryngology – Head and Neck Surgery | volume = 2 | issue = 4 | pages = 219–29 | date = December 2016 | pmid = 29204570 | pmc = 5698538 | doi = 10.1016/j.wjorl.2016.03.002 }}</ref>

The transportation of the [[oocyte|immature egg cell]], and the embryo to the [[uterus]] for [[Implantation (human embryo)|implantation]] depends on the combination of regulated smooth muscle contractions, and ciliary beating. Dysfunction in this transportation can result in an [[ectopic pregnancy]] where the embryo is implanted (usually) in the [[fallopian tube]] before reaching its proper destination of the uterus. Many factors can affect this stage including infection and menstrual cycle hormones. Smoking (causing inflammation), and infection can reduce the numbers of cilia, and the ciliary beat can be affected by hormonal changes.<ref name="Panelli">{{cite journal |last1=Panelli |first1=DM |last2=Phillips |first2=CH |last3=Brady |first3=PC |title=Incidence, diagnosis and management of tubal and nontubal ectopic pregnancies: a review. |journal=Fertility Research and Practice |date=2015 |volume=1 |pages=15 |doi=10.1186/s40738-015-0008-z |pmid=28620520|pmc=5424401 |doi-access=free }}</ref><ref>{{cite journal | vauthors = Horne AW, Critchley HO | title = Mechanisms of disease: the endocrinology of ectopic pregnancy | journal = Expert Reviews in Molecular Medicine | volume = 14 | pages = e7 | date = March 2012 | pmid = 22380790 | doi = 10.1017/erm.2011.2 | s2cid = 10039212 }}</ref>

=== Primary cilia in pancreatic cells ===
The pancreas is a mixture of highly differentiated exocrine and endocrine cells. Primary cilia are present in exocrine cells, which are centroacinar duct cells.<ref>{{cite journal|vauthors=Cano DA, Murcia NS, Pazour GJ, Hebrok M|year=2004|title=''orpk'' mouse model of polycystic kidney disease reveals essential role of primary cilia in pancreatic tissue organization|journal=Development|volume=131|issue=14|pages=3457–3467|pmid=15226261|doi=10.1242/dev.01189|doi-access=free}}</ref><ref name="Hegyi"/> Endocrine tissue is composed of different hormone-secreting cells. Insulin-secreting beta cells and glucagon-secreting alpha cells are highly ciliated.<ref>{{cite journal|vauthors=Zhang Q, Davenport JR, Croyle MJ, Haycraft CJ, Yoder BK|year=2005|title=Disruption of IFT results in both exocrine and endocrine abnormalities in the pancreas of Tg737(orpk) mutant mice|journal=Laboratory Investigation|volume=85|issue=1|pages=45–64|doi=10.1038/labinvest.3700207|doi-access=free|pmid=15580285}}</ref><ref>{{cite journal|vauthors=Yamamoto M, Kataoka K|year=1986|title=Electron microscopic observation of the primary cilia in the pancreatic islets|journal=Archivum Histologicum Japonicum|volume=49|issue=4|pages=449–457|doi-access=free|doi=10.1679/aohc.49.449|pmid=3545133}}</ref>

== See also ==

* {{annotated link|Molecular machine#Biological molecular machines}}
* {{annotated link|Protein dynamics#Global flexibility: multiple domains}}
* {{annotated link|Protein domain#Domains and protein flexibility}}
* {{annotated link|Stereocilia}}

== References ==
{{Reflist}}

== External links ==
* [https://web.archive.org/web/20060710113703/http://www.hhmi.org/bulletin/sept2005/pdf/Cilia.pdf Brief summary of importance of cilia to many organs in human physiology]
* [http://www.ciliaproteome.org The Ciliary Proteome Web Page at Johns Hopkins]

{{Cellular structures}}
{{Epithelial proteins}}
{{Protist structures}}
{{Authority control}}

[[Category:Cell movement]]
[[Category:Eukaryotic cell anatomy]]
[[Category:Organelles]]