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Centriole
Centriole
Centriole
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3D rendering of centrioles showing the triplets

In cell biology a centriole is a cylindrical organelle composed mainly of a protein called tubulin.[1] Centrioles are found in most eukaryotic cells, but are not present in conifers (Pinophyta), flowering plants (angiosperms) and most fungi, and are only present in the male gametes of charophytes, bryophytes, seedless vascular plants, cycads, and Ginkgo.[2][3] A bound pair of centrioles, surrounded by a highly ordered mass of dense material, called the pericentriolar material (PCM),[4] makes up a structure called a centrosome.[1]

Centrioles are typically made up of nine sets of short microtubule triplets, arranged in a cylinder. Deviations from this structure include crabs and Drosophila melanogaster embryos, with nine doublets, and Caenorhabditis elegans sperm cells and early embryos, with nine singlets.[5][6] Additional proteins include centrin, cenexin and tektin.[7]

The main function of centrioles is to produce cilia during interphase and the aster and the spindle during cell division.

History

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The centrosome was discovered jointly by Walther Flemming in 1875[8][9] and Edouard Van Beneden in 1876.[10][9] Edouard Van Beneden made the first observation of centrosomes as composed of two orthogonal centrioles in 1883.[11] Theodor Boveri introduced the term "centrosome" in 1888[12][9][13][14] and the term "centriole" in 1895.[15][9] The basal body was named by Theodor Wilhelm Engelmann in 1880.[16][9] The pattern of centriole duplication was first worked out independently by Étienne de Harven and Joseph G. Gall c. 1950.[17][18]

Role in cell division

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A mother and daughter centriole, attached orthogonally

Centrioles are involved in the organization of the mitotic spindle and in the completion of cytokinesis.[19] Centrioles were previously thought to be required for the formation of a mitotic spindle in animal cells. However, more recent experiments have demonstrated that cells whose centrioles have been removed via laser ablation can still progress through the G1 stage of interphase before centrioles can be synthesized later in a de novo fashion.[20] Additionally, mutant flies lacking centrioles develop normally, although the adult flies' cells lack flagella and cilia and as a result, they die shortly after birth.[21] The centrioles can self replicate during cell division.

Cellular organization

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Centrioles are a very important part of centrosomes, which are involved in organizing microtubules in the cytoplasm.[22][23] The position of the centriole determines the position of the nucleus and plays a crucial role in the spatial arrangement of the cell.

Fertility

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Sperm centrioles are important for 2 functions:[24] (1) to form the sperm flagellum and sperm movement and (2) for the development of the embryo after fertilization. The sperm supplies the centriole that creates the centrosome and microtubule system of the zygote.[25]

Ciliogenesis

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In flagellates and ciliates, the position of the flagellum or cilium is determined by the mother centriole, which becomes the basal body. An inability of cells to use centrioles to make functional flagella and cilia has been linked to a number of genetic and developmental diseases. In particular, the inability of centrioles to properly migrate prior to ciliary assembly has recently been linked to Meckel–Gruber syndrome.[26]

Animal development

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Electron micrograph of a centriole from a mouse embryo.

Proper orientation of cilia via centriole positioning toward the posterior of embryonic node cells is critical for establishing left-right asymmetry, during mammalian development.[27]

Centriole duplication

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Before DNA replication, cells contain two centrioles, an older mother centriole, and a younger daughter centriole. During cell division, a new centriole grows at the proximal end of both mother and daughter centrioles. After duplication, the two centriole pairs (the freshly assembled centriole is now a daughter centriole in each pair) will remain attached to each other orthogonally until mitosis. At that point the mother and daughter centrioles separate dependently on an enzyme called separase.[28]

The two centrioles in the centrosome are tied to one another. The mother centriole has radiating appendages at the distal end of its long axis and is attached to its daughter at the proximal end. Each daughter cell formed after cell division will inherit one of these pairs. Centrioles start duplicating when DNA replicates.[19]

Origin

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LECA, the last common ancestor of all eukaryotes was a ciliated cell with centrioles.[citation needed] Some lineages of eukaryotes, such as land plants, do not have centrioles except in their motile male gametes. Centrioles are completely absent from all cells of conifers and flowering plants, which do not have ciliate or flagellate gametes.[29] It is unclear if the last common ancestor had one[30] or two cilia.[31] Important genes such as those coding for centrins, required for centriole growth, are only found in eukaryotes, and not in bacteria or archaea.[30]

Etymology and pronunciation

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The word centriole (/ˈsɛntrioʊl/) uses combining forms of centri- and -ole, yielding "little central part", which describes a centriole's typical location near the center of the cell.

Atypical centrioles

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Typical centrioles are made of 9 triplets of microtubules organized with radial symmetry.[32] Centrioles can vary the number of microtubules and can be made of 9 doublets of microtubules (as in Drosophila melanogaster) or 9 singlets of microtubules as in C. elegans. Atypical centrioles are centrioles that do not have microtubules, such as the Proximal Centriole-Like found in D. melanogaster sperm,[33] or that have microtubules with no radial symmetry, such as in the distal centriole of human spermatozoon.[34] Atypical centrioles may have evolved at least eight times independently during vertebrate evolution and may evolve in the sperm after internal fertilization evolves.[35]

It wasn't clear why the centriole became atypical until recently. The atypical distal centriole forms a dynamic basal complex (DBC) that, together with other structures in the sperm neck, facilitates a cascade of internal sliding that couples tail beating with head kinking. The atypical distal centriole's properties suggest that it evolved into a transmission system that couples the sperm tail motors to the whole sperm, thereby enhancing sperm function.[36]

References

[edit]
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Centriole

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from Grokipedia
Centrioles are cylindrical microtubule-based organelles present in the of most animal cells and many other eukaryotes, serving as the structural core of the centrosome—the primary microtubule-organizing center—and as basal bodies that nucleate the assembly of cilia and flagella. They typically measure approximately 250 nanometers in diameter and 500 nanometers in length, exhibiting a conserved barrel-shaped with ninefold radial symmetry that is essential for their organizational roles in and motility. The defining structure of the centriole consists of nine triplet arranged peripherally around a central cartwheel, where each triplet comprises a complete A-tubule (13 protofilaments) and incomplete B- and C-tubules (10 protofilaments each) that share walls and are interconnected by intertriplet linkages. The cartwheel, located at the proximal end, is assembled from SAS-6 proteins forming a hub and nine spokes that establish the symmetrical array during biogenesis, while the distal end often transitions to doublet in basal bodies. Mature "mother" centrioles are distinguished by distal appendages (e.g., involving CEP164) for ciliary docking and subdistal appendages (e.g., involving ninein) for anchoring, whereas newly formed "daughter" centrioles lack these until maturation in the next . Centrioles play critical roles in by organizing pericentriolar material (PCM) into functional centrosomes that nucleate astral and spindle , ensuring bipolar spindle formation and accurate segregation. In , they contribute to cytoplasmic arrays that support , intracellular transport, and migration, with PCM recruitment regulated by kinases like to adapt to cellular demands. As basal bodies, centrioles dock to the plasma membrane via distal appendages to template the nine-doublet of cilia and flagella, enabling sensory in primary cilia or motile beating in multiciliated epithelia. Beyond these core functions, centrioles influence broader cellular processes, including cytoskeleton regulation, protein degradation, and signaling pathways such as and Wnt, with structural variations (e.g., length from 150 nm in Drosophila to 500 nm in somatic cells) tailored to cell-type-specific needs like tissue differentiation or . Centriole duplication is a tightly controlled semiconservative process occurring once per at the G1/S transition, initiated by a preexisting mother centriole that licenses procentriole formation through PLK4 activity, followed by cartwheel assembly via SAS-6 and microtubule elongation regulated by CPAP and capped by CP110/Cep97 to prevent overduplication and maintain genomic stability.

Structure and Composition

Ultrastructure

The centriole exhibits a cylindrical barrel , measuring approximately 0.25 μm in and 0.4–0.5 μm in . This architecture forms the core of the in animal cells, consisting of a -based scaffold that provides . At its foundation, the centriole features a nine-fold symmetric array of triplet , each comprising an A tubule, a complete 13-protofilament , with a B tubule partially overlapping the A tubule and a C tubule attached to the B tubule. These triplets are arranged circumferentially around a central axis, forming a barrel-like wall that maintains the organelle's cylindrical integrity. The proximal end of the centriole contains a cartwheel structure, characterized by a central hub connected to nine radial spokes that extend to the bases of the microtubule triplets. This cartwheel is assembled from oligomers of the protein SAS-6, which self-organize into stacked rings to establish the nine-fold symmetry early in centriole formation. In mature mother centrioles, the distal end is adorned with distal centriole appendages (DCAs), which appear as nine radially arrayed, pinwheel-like projections that facilitate ciliogenesis and docking. These appendages form a ring approximately 350 nm in diameter, with each cluster measuring about 60 nm. Within the centriole lumen, bridges connect adjacent triplets, while A-C linkers span between the A and C tubules of each triplet to preserve their structural cohesion. Recent cryo-electron studies in 2025 have revealed that these A-C linkers, composed of multiple proteins including β-propeller domains, are essential for maintaining triplet integrity and overall centriole stability under mechanical stress. Structural variations occur along the centriole length, particularly at the distal end, where triplets may transition to doublets (lacking the C tubule) or, in nascent centrioles, singlets, reflecting maturation stages. The centriole associates with pericentriolar material (PCM) externally, which surrounds the structure to support centrosomal functions.

Key Proteins and Assemblies

The centriole's proximal region is defined by the cartwheel structure, a ninefold symmetrical scaffold essential for establishing radial organization. SAS-6 forms the central hub and spokes of this cartwheel through homo-oligomerization of its C-terminal domain, templating the ninefold symmetry observed across eukaryotes. In human cells, SAS-6 is recruited to the proximal lumen of the mother centriole during early , where it self-assembles into cartwheel-like configurations independent of pre-existing cartwheels. SAS-4/CPAP, a conserved , facilitates cartwheel integrity by recruiting additional components and stabilizing the structure during procentriole elongation. The microtubule wall of the centriole comprises nine triplet , primarily composed of α- and β-tubulin isoforms that form the A- and B-tubules, with the C-tubule contributed by specialized tubulins in some contexts. BLD10/CEP135 acts as a pinhead-like stabilizer at the microtubule plus ends, binding directly to and linking them to the cartwheel to promote triplet formation and structural rigidity. Recent studies have highlighted POC1A/B heterodimers as key organizers of the inner lumenal network, where they form crosslinks that seal triplet and maintain centriolar integrity; loss of these heterodimers leads to lumenal disintegration and microtubule splaying. Distal and subdistal appendages extend from the mother centriole's distal end, serving as docking sites for membranes and . CEP164 is a core component of distal appendages (DCAs), localizing to the distal ends via interactions with other appendage proteins and enabling primary formation through vesicular docking. ODF2 primarily assembles subdistal appendages (SDAs), recruiting ninein and other proteins to anchor astral during ; its deletion disrupts SDA formation while sparing DCAs. Lumenal and linker proteins reside within the centriole's interior, contributing to self-assembly and overall stability. FAM161A integrates into a helical scaffold alongside POC1B and centrin-2, providing radial links that reinforce the triplets against mechanical stress. SSNA1, identified as a distal lumenal organizer, bundles without direct association and interacts with SAS-1 to promote network integrity and ciliogenesis; its depletion results in fragmented lumenal structures. Centriole assembly proceeds through distinct temporal modules: the proximal module initiates with cartwheel formation via SAS-6 and SAS-4, the intermediate module extends the wall using CEP135 and POC1 proteins, and the distal module adds appendages like those involving CEP164 and ODF2. A 2024 study using time-series cryo-electron tomography reconstructed this 4D process in human cells, revealing sequential recruitment that ensures structural maturation over the . Molecular chaperones such as support centriole assembly by folding and stabilizing client proteins like Polo kinase, which is required for SAS-6 recruitment and cartwheel initiation; inhibition of HSP90 disrupts these interactions and impairs procentriole formation.

Functions in Cellular Processes

Role in Mitosis and Cell Division

Centrioles serve as the structural core of centrosomes, which are the primary microtubule-organizing centers (MTOCs) during in animal cells. Each centrosome consists of a pair of centrioles surrounded by pericentriolar material (PCM), a dynamic protein matrix that the centrioles recruit and organize to nucleate . At the onset of mitosis, this recruitment intensifies during centrosome maturation, enabling the centrosomes to efficiently nucleate astral that position the spindle and spindle that attach to kinetochores for segregation. The barrel-shaped centrioles, with their characteristic nine triplet , provide anchoring sites for PCM components, facilitating robust microtubule nucleation essential for spindle assembly.01362-2)30522-2)00289-5) In , the two , each containing a mother-daughter centriole pair, separate and migrate to opposite poles of the cell, establishing the bipolar architecture of the mitotic spindle. This orthogonal arrangement of the mother (older) and daughter (newer) centrioles within each centrosome ensures precise pole positioning, with the mother centriole often orienting appendages toward the poles to stabilize the structure. The resulting bipolar spindle captures and aligns chromosomes at the plate, promoting equal distribution of to daughter cells during , thereby maintaining genomic stability. Disruption of this bipolarity, such as through unequal centrosome separation, can lead to chromosome missegregation and . Centriole integrity contributes to the spindle assembly checkpoint (SAC), a mechanism that delays until all chromosomes are properly attached to the spindle. Aurora A , localized at centrioles and , phosphorylates key regulators to promote PCM expansion and attachment, indirectly supporting SAC signaling by ensuring functional spindle poles; defects in this process can activate the SAC via enhanced Aurora B activity at unattached kinetochores. Experimental evidence from studies in vertebrate cells demonstrates that removing centrioles during impairs centrosome maturation and spindle bipolarity, leading to disorganized arrays and delayed or aberrant segregation, although cells may still form acentrosomal spindles.00276-6) Centriole amplification, resulting in supernumerary centrosomes, frequently causes multipolar spindles that promote unequal segregation, chromosomal instability (CIN), and —a hallmark of cancer progression. In many tumor cells, extra centrioles lead to transient multipolar intermediates that, if not clustered into bipolar structures, result in lagging chromosomes and genomic alterations driving oncogenesis. Recent findings link centriole amplification to cell development, where progenitors tolerate extra centrioles amid high proliferation and DNA damage but eliminate them before maturation, suggesting a controlled role in immune cell expansion without promoting .

Role in Microtubule Organization Center (MTOC)

The centrosome, comprising a pair of centrioles embedded in pericentriolar material (PCM), serves as the primary microtubule-organizing center (MTOC) in animal cells during interphase, where centrioles act as scaffolds to template the recruitment of gamma-tubulin ring complexes (γ-TuRCs) for minus-end-directed microtubule nucleation. This templating mechanism ensures the organized assembly of the cytoplasmic microtubule network essential for intracellular transport and cell architecture. Recent structural studies have revealed that γ-TuRCs associate with specific centriolar proteins, such as those in the PCM scaffold, to form nucleation-competent templates, highlighting the centriole's role in positioning and activating these complexes at the centrosome periphery. Centriole appendages further specialize this MTOC function in : subdistal appendages anchor the minus ends of interphase to stabilize the radial array, while distal appendages contribute to positioning, including the alignment of the Golgi apparatus relative to the network. These appendages, composed of proteins like ODF2 and CEP164, enable precise attachment and orientation without extending into axonemal structures. In contrast to animal cells, where centriole-based dominate organization, and many differentiated animal cells rely on non-centrosomal MTOCs, such as cortical or Golgi-associated sites, which nucleate independently of centrioles using similar γ-TuRC components but lack the centralized templating provided by the .30209-8) Dynamic expansion of the PCM, mediated by recruitment of pericentrin (PCNT), enhances the centrosome's capacity to form microtubule asters during interphase by concentrating nucleation factors and stabilizing microtubule minus ends. Pericentrin forms a scaffold that phase-separates to create a selective environment for γ-TuRC integration, allowing rapid adaptation of the microtubule array to cellular needs like directed transport. Defects in centriole integrity or PCM recruitment, such as those from pericentrin mutations, disrupt this organization, leading to impaired cell polarity and defective vesicular trafficking, as microtubules fail to properly direct cargo movement and maintain asymmetric cellular domains.30589-5)

Role in Ciliogenesis and Basal Bodies

The mother centriole, distinguished by its distal and subdistal appendages, undergoes conversion to a during ciliogenesis by docking at the plasma membrane, where these appendages facilitate attachment and stabilize the structure for assembly. This docking orients the perpendicularly to the membrane, enabling it to template the nine-fold symmetric array of doublets that form the core of the ciliary . The transition involves recruitment of transition zone proteins, which seal the ciliary compartment and prevent diffusion of membrane proteins. Ciliogenesis proceeds through a series of coordinated steps, beginning with membrane invagination around the docked basal body to form a ciliary vesicle, which expands into the ciliary pocket. Intraflagellar transport (IFT) is then initiated at the basal body, where IFT trains—assembled from IFT-A, IFT-B, and BBSome complexes—load cargo proteins and are powered by kinesin-2 motors to anterogradely transport components along the axoneme for cilium elongation. Proteins like IFT88, a core component of the IFT-B complex, are essential for this process, as their depletion disrupts train assembly and leads to shortened or absent cilia. Centriole duplication during the provides the necessary mother-daughter pairs, allowing one to function as a basal body while the other remains cytoplasmic. Primary cilia, which are non-motile sensory organelles, arise from a single basal body derived from the mother centriole and feature a 9+0 microtubule arrangement for signaling functions like Hedgehog pathway reception. In contrast, motile cilia, such as those in respiratory epithelia or sperm flagella, often originate from multiple basal bodies and exhibit a 9+2 axonemal structure with dynein arms for beating and fluid propulsion. While both types rely on basal bodies for templating, motile cilia require additional accessory structures like radial spokes for coordinated motility. A rare de novo pathway enables centriole-independent ciliogenesis in certain multiciliated cells, such as airway epithelia, where deuterosomes act as acentriolar platforms to generate hundreds of basal bodies without relying on pre-existing centrioles. This pathway amplifies basal body production via procentriole assembly on deuterosomes, followed by maturation and docking, ensuring efficient multicilia formation. Defects in basal body conversion and ciliogenesis contribute to ciliopathies, exemplified by Bardet-Biedl syndrome (BBS), where mutations in BBS genes disrupt the BBSome complex's role in IFT and vesicular trafficking to the . This leads to malformed basal bodies, impaired extension, and dysfunctional primary cilia, resulting in phenotypes like retinal degeneration and due to defective signaling. In BBS models, such as knockout mice, primary cilia exhibit altered lengths and mislocalized IFT components like IFT88, underscoring the basal body's critical role in ciliary integrity.

Centriole Duplication and Regulation

Mechanism of Duplication

Centriole duplication is a semi-conservative process tightly coupled to the cell cycle, ensuring that each daughter cell inherits exactly one pair of centrioles. This duplication initiates during the S phase, when a new procentriole buds orthogonally from the proximal end of each existing mother centriole, maintaining the structural hierarchy by ensuring one new structure per template and preventing multiple initiations from the same template. This budding is triggered by the recruitment of key initiation factors to the pericentriolar material surrounding the parental centriole. The core of procentriole assembly begins with the formation of the cartwheel, a central scaffold that imparts the signature nine-fold symmetry to the centriole. SAS-6 proteins oligomerize into a hub-and-spoke structure at the proximal end, creating radial spokes that template the arrangement of nine triplet . This cartwheel then facilitates the recruitment and stabilization of α/β- dimers, which polymerize to extend the microtubule blades orthogonally from the parental centriole wall. The process relies on the coordinated action of PLK4 and STIL, which phosphorylate and SAS-6 to the site of assembly. Structural proteins such as SAS-4 (the ortholog of CPAP in some organisms) further aid in tubulin recruitment during this elongation phase. As the procentriole elongates, its length is precisely controlled to reach approximately 0.5 μm, preventing overextension that could disrupt cellular . CPAP promotes polymerization by binding dimers and adding them to the growing distal end, while capping proteins like CP110 limit further extension by blocking additional incorporation. Ninein contributes to this regulation by anchoring at the subdistal region, ensuring structural integrity and proper scaling during elongation. These mechanisms balance positive and negative regulators to achieve uniform centriole dimensions across cell cycles. The newly formed procentriole remains immature throughout the cell cycle and only matures post-mitosis. During cytokinesis, the procentriole disengages from its parental counterpart and acquires distal appendages for microtubule anchoring and subdistal appendages for pericentriolar material recruitment, transforming it into a functional mother centriole capable of nucleating the mitotic spindle or cilia. This maturation step is essential for the procentriole's role in the next duplication cycle. To enforce the once-per-cycle rule, PLK4 kinase serves as the master regulator, with its levels and activity oscillating to initiate duplication precisely once during while preventing reduplication. PLK4 auto-phosphorylates, recruiting downstream effectors like STIL and SAS-6. Recent 2025 research highlights how the DNA replication machinery transmits dual signals—via Cdc6 inhibition of disengagement and DONSON-mediated coordination of suppression—to license duplication only after origin firing, averting premature or multiple assemblies that could lead to genomic instability. For instance, DONSON facilitates Cdc6 translocation to prevent premature disengagement and coordinates checkpoint signaling to ensure licensing post-DNA origin firing. Additionally, as of 2025, the A-C linker proteins are implicated in maintaining centriole integrity essential for duplication, while SSNA-1 supports post-assembly stability in models like C. elegans. This coupling mirrors licensing, ensuring synchrony between chromosome and centrosome duplication.

Control of Centriole Number

The precise control of centriole number is essential to maintain exactly two centrosomes per cell in most animal cells, ensuring bipolar spindle formation during and preventing genomic instability. This regulation involves licensing factors that initiate duplication strictly once per , coupled to through . The core licensing pathway centers on the PLK4-STIL-SAS-6 axis, where PLK4 phosphorylates and recruits STIL to the centriole wall during , enabling STIL to bind and oligomerize SAS-6 into cartwheel structures that seed procentriole assembly; this activation is limited to once per cycle by autoregulatory feedback loops that degrade excess PLK4 via SCF , preventing unlicensed reinitiation. Cell cycle checkpoints integrate centriole duplication with to enforce this temporal coupling, primarily through the S-phase checkpoint that licenses both processes simultaneously while inhibiting premature or repeated events. For instance, the machinery, including MCM helicase loading, parallels centriole licensing by PLK4, and disruptions in either pathway trigger ATR/ATM-mediated delays to coordinate progression; this ensures duplication occurs only during , avoiding asynchrony that could lead to multipolar spindles. Additionally, post-S phase inhibitory signals, such as pericentriolar material (PCM)-mediated sequestration of duplication factors like PLK4 and SAS-6, restrict access to the centriole distal end, thereby blocking further procentriole budding until the next G1. Deregulation of these controls can trigger overduplication, as seen with PLK4 overexpression, which overrides licensing limits and drives supernumerary centrioles by hyperactivating STIL-SAS-6 recruitment, often forming multiple daughter structures per mother centriole. This amplification is strongly linked to tumorigenesis, as extra centrosomes promote chromosomal instability through multipolar mitoses and , with PLK4 upregulation observed in various cancers including and colorectal tumors. Error correction mechanisms mitigate such excesses, particularly through p53-dependent pathways in , where supernumerary centrioles induce DNA damage responses leading to their clustering, autophagy-mediated degradation, or cell cycle arrest to eliminate extras and restore diploidy. Recent findings highlight context-specific tolerance to amplification; in early B cell development, progenitors frequently exhibit centriole numbers exceeding four due to high proliferative demands and DNA breaks, yet this does not promote oncogenic transformation or impair , as extras are rapidly resolved during maturation without p53-mediated elimination.

Biological and Developmental Roles

In Animal Development

In mammalian fertilization, the inheritance of centrioles exhibits species-specific variations that influence early embryonic development. In most non- mammals, including humans and bovines, the contributes two remodeled centrioles (proximal and distal) to the acentriolar ; the proximal centriole nucleates the first aster and organizes the mitotic spindle in the , while the distal centriole, an atypical structure, functions as the second centriole for subsequent duplication. However, in such as mice and rats, paternal centrioles undergo extensive degradation during , resulting in their absence in mature ; instead, the provides an initial pool of acentrosomal microtubule-organizing centers (MTOCs) derived from maternal contributions, which support organization until de novo centriole formation occurs around the blastula stage. This maternal reliance ensures proper cleavage divisions but highlights evolutionary adaptations in centrosome inheritance across mammals. Centrioles play a pivotal role in establishing left-right (LR) asymmetry during vertebrate embryogenesis through their conversion into basal bodies for motile node cilia. In the mouse node at embryonic day 7.5, centriole-derived basal bodies anchor 9+0 motile cilia that generate a leftward fluid flow, triggering asymmetric calcium signaling and Nodal expression on the left side of the embryo, which directs organ situs. Disruptions in centriole assembly or basal body docking, as seen in mutations affecting intraflagellar transport (IFT) proteins like IFT88 or kinesin motors (e.g., KIF3A), abolish nodal cilia function, leading to randomized LR patterning and situs inversus in up to 50% of affected embryos. This process exemplifies how centrioles integrate motility and signaling to break bilateral symmetry essential for proper heart and gut looping. During neural tube closure, centriole-derived primary cilia serve as signaling hubs for Sonic Hedgehog (Shh) pathway activation, which is critical for ventral neural patterning and preventing defects (NTDs). Primary cilia, anchored by the mother centriole as a , concentrate Shh receptors (Patched and ) and Gli transcription factors, enabling gradient-dependent specification of neural progenitors around embryonic day 8.5 in mice. Defects in centriole-to- transition, such as those in ciliopathy genes like IFT172, impair Shh transduction, resulting in holoprosencephaly-like NTDs and failure of the neural folds to fuse, as evidenced by exencephaly in mutant models. This underscores the centriole's indirect but essential contribution to the biomechanical and molecular events coordinating closure. Centriole integrity is vital for maintaining neural stem and proliferation during development, with defects often leading to . In mouse models, mutations in centriole biogenesis genes like STIL or CDK5RAP2 cause centrosome fragmentation and p53-mediated in radial glial progenitors, significantly reducing the progenitor pool and impairing cortical expansion. Similarly, loss of centriolar proteins such as CETN3 disrupts spindle orientation and symmetric divisions, favoring premature over proliferation and resulting in smaller brains with fewer neurons. These findings highlight how centriole defects shift the balance toward differentiation, limiting tissue growth in a manner conserved across vertebrates. Studies in model organisms like Drosophila melanogaster and Caenorhabditis elegans have elucidated centriole positioning mechanisms critical for gastrulation and tissue organization. In Drosophila, during mesoderm invagination at stage 6, centrioles polarize along the planar cell polarity (PCP) axis via Frizzled-Dishevelled signaling, directing apical constriction and cell sheet bending to form the ventral furrow; disruptions randomize centriole orientation, delaying gastrulation onset by up to 1 hour. In C. elegans, centrioles (as part of centrosomes) position the mitotic spindle in the MS and E precursor cells at the 26-cell stage, ensuring timely apical ingression through PAR polarity-mediated nuclear-centrosome coupling; mutations in SAS-7 impair this positioning, causing ectopic cell retention on the surface and defective gut morphogenesis. These invertebrate models reveal conserved roles for centriole dynamics in coordinating cell shape changes and migration during early patterning.

In Fertility and Reproduction

In , centrioles play a critical role in forming the of the sperm flagellum, enabling motility essential for . During , the distal centriole of the spermatid transforms into the , which nucleates the assembly of the 9+2 structure of the , while the proximal centriole remains associated with the nucleus. This process ensures the mature spermatozoon contains two remodeled centrioles, with the distal one serving as the foundational structure for flagellar beating. Mammalian oocytes, in contrast, lack functional centrioles at maturity, having eliminated them during to prevent multipolar spindles and ensure uniparental inheritance. Upon fertilization, the contributes both the proximal and distal centrioles, which reconstitute the zygotic by recruiting maternal pericentriolar material (PCM); the proximal centriole organizes the sperm aster for pronuclear migration, while the distal centriole functions as an atypical second centriole to initiate embryonic networks. This paternal dominance in centrosome provision is conserved across most mammals, highlighting the asymmetry in contributions to early embryonic organization. Defects in centriole structure or function can lead to , particularly , characterized by reduced sperm motility due to abnormal flagellar assembly. For instance, mutations in centriolar proteins like CEP135 disrupt formation, resulting in oligoasthenoteratozoospermia and impaired fertility in affected individuals. In fertilization (IVF), this centriole asymmetry influences embryo viability; paternal centriole abnormalities may cause failed aster formation or multipolar divisions, increasing risk and underscoring the need for sperm centrosome integrity assessments in clinical protocols. Evolutionarily, centriole elimination in the female germline is a widespread in metazoans, ensuring monopaternal centrosome inheritance to avoid genomic instability while maintaining centrioles in for flagellar development. This differential regulation across , observed in nematodes to mammals, supports uniparental control of zygotic centrosome biogenesis.

Evolutionary and Variant Forms

Evolutionary Origin

The evolutionary origins of centrioles trace back to prokaryotic cytoskeletal elements, with hypotheses suggesting precursors in bacterial cytoskeletal proteins that contributed to the development of microtubule-based structures in early . Centrioles emerged in early eukaryotes around 1.5–2 billion years ago, coinciding with the of and the last eukaryotic common ancestor (LECA), where they likely functioned as basal bodies for flagella before adapting to spindle organization. This co-evolution reflects the integration of prokaryotic-derived cytoskeletal components into a more complex eukaryotic framework, enabling open in . The nine-fold radial symmetry of centrioles is highly conserved across , including animals and many protists, underscoring their ancient origin and role in . However, this structure is absent in (), which rely on decentralized organizing centers, and shows variations in fungi, where centrioles are often simplified or lost in favor of spindle pole bodies. Evidence for de novo centriole assembly in protists, such as Naegleria gruberi, indicates that centrioles can form without pre-existing templates, suggesting flexible evolutionary pathways independent of canonical duplication.

Atypical Centrioles

In , centrioles are absent, and microtubule organization is instead mediated by acentriolar microtubule-organizing centers (MTOCs) that nucleate and anchor during and other cellular processes. These acentriolar MTOCs, often involving gamma-tubulin complexes distributed throughout the or associated with the , enable spindle formation without canonical centriolar structures, reflecting an evolutionary adaptation to plant-specific cytoskeletal demands. In fungi, spindle pole bodies (SPBs) serve as functional analogs to centrioles and centrosomes, organizing for spindle assembly during and , but lack the characteristic microtubule triplets found in animal centrioles. Embedded in the , SPBs are multilayered, disc-shaped protein complexes that recruit gamma-tubulin and other nucleators to generate astral and spindle , demonstrating divergent yet conserved MTOC functionality across eukaryotes. Certain insects exhibit atypical giant centrioles, particularly in spermatocytes, where these elongated structures—measuring up to 1-2 μm in length—deviate from the standard short barrel shape and feature layered microtubule arrangements including singlets, doublets, and irregular spirals rather than uniform triplets. These giant centrioles, organized in pairs per , support meiotic spindle formation and subsequent , with their atypical architecture stabilized by proteins like Ana3 that maintain structural integrity across layers. Recent studies in have revealed that the canonical 9-fold of microtubule triplets is not essential for centriole elongation or stability, as disrupting this still allow proper growth and formation of functional centriole-like structures during duplication. This finding challenges the universality of 9-fold organization, indicating that longitudinal microtubule associations and accessory proteins can compensate for radial asymmetry in specific models. In protozoans like , monocentrioles represent a single-membered variant, with each cell containing only one mature /centriole that organizes the , deviating from the paired centrioles typical in animal cells. This solitary structure assembles via a probasal body intermediate and features nine singlet in its early form, transitioning to support flagellar without a second centriole counterpart. Planarians demonstrate functional atypia through acentriolar regeneration, where pluripotent neoblast s lack centrioles yet drive whole-body regeneration by proliferating and differentiating into all cell types, including ciliated cells that de novo assemble centrioles only upon terminal differentiation. This centriole-independent mechanism in neoblasts enables robust mitotic spindle assembly via alternative MTOCs, underscoring the non-essential role of centrioles in division and tissue repair in this .

History and Terminology

Discovery and Historical Milestones

The discovery of the centriole traces back to the late 19th century, when German biologist first observed these structures within the centrosomes of Ascaris megalocephala (now ) embryos using light microscopy. In his seminal 1888 work, Boveri coined the term "centrosome" to describe the central organizing body of the mitotic spindle and noted the presence of small, paired dots—later identified as centrioles—that appeared to direct chromosome segregation during cell division. These observations, detailed in Zellen-Studien II, established the centriole as a key component of the and laid foundational insights into its role in animal cell , influencing early concepts of cellular . Advancements in the mid-20th century came with the advent of electron microscopy, which revealed the intricate of the centriole. In 1956, Etienne de Harven provided the first electron micrographs depicting the centriole's characteristic ninefold array of triplets, confirming its cylindrical architecture and distinguishing it from surrounding pericentriolar . This breakthrough, building on earlier light microscopy limitations, shifted understanding from vague "dots" to a precise composed of triplet (A, B, and C tubules), essential for its stability and function in spindle organization. By the 1970s, researchers like Greenfield Sluder advanced functional studies through the isolation of centrosomes from embryos, enabling in vitro duplication assays that demonstrated centriole replication as a semi-conservative process tied to the . The molecular era began in the 2000s, identifying key regulators of centriole biogenesis. In 2005, polo-like 4 (PLK4), also known as SAK in , was established as a master initiating centriole duplication by phosphorylating downstream targets to license procentriole formation at the mother centriole base. Shortly after, in 2005, SAS-6 was molecularly characterized as a core cartwheel protein required for establishing the ninefold symmetry during early centriole assembly in both C. elegans and human cells. These discoveries, stemming from genetic screens and RNAi studies, marked a transition from structural to mechanistic insights, highlighting how proteins orchestrate duplication to prevent numerical errors in . Recent milestones have leveraged advanced imaging to visualize dynamic assembly. In 2024, cryo-electron tomography (cryo-ET) enabled a time-series reconstruction of human centriole biogenesis, modeling its 4D architecture across six structural modules from cartwheel formation to microtubule blade completion. Building on this, a 2025 study in Nature Communications elucidated the A-C linker's role in maintaining triplet integrity and regulating duplication, showing how it connects A- and C-tubules to ensure structural cohesion during biogenesis. Overall, imaging evolution—from Boveri's light microscopy to super-resolution techniques like STED and cryo-ET—has progressively unveiled the centriole's nanoscale dynamics, transforming it from a historical curiosity to a precisely understood organelle central to cellular fidelity.

Etymology and Pronunciation

The term "centriole" was first proposed in 1895 by German biologist in his studies on . Boveri derived the name from the New Latin centriolum, a diminutive form of the Latin centrum meaning "center," reflecting the organelle's position at the core of the and its role in organizing cellular processes. This etymology emphasizes the centriole's centrality, akin to the related term "," which had coined in 1888 to denote the broader structure containing one or two centrioles. Early observations of the structure predated the formal naming, with Belgian biologist Edouard Van Beneden describing it in 1883 as a "central corpuscle" in the eggs of the Ascaris, noting its persistence across cell divisions. Prior to Boveri's proposal, he had referred to it informally as a "central granule" in his studies of embryos, highlighting its granular appearance under light microscopy. These historical variants underscore the evolving recognition of the centriole as a distinct entity separate from the surrounding pericentriolar material. In modern scientific literature, "centriole" is standardly pronounced in American English as /ˈsɛntri.oʊl/ and in British English as /ˈsɛntrɪəʊl/, with stress on the first syllable and a clear distinction from similar terms like "centromere," which refers to a chromosomal region and derives from different observational contexts in mitosis. This precise terminology avoids confusion, ensuring the centriole is understood specifically as a cylindrical microtubule-organizing organelle rather than a chromosomal feature.

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