9 + 0 and 9 + 2 cilia are randomly dispersed in the mouse node

Odate, Toru; Takeda, Sén; Narita, Keishi; Kawahara, Toru

doi:10.1093/jmicro/dfv352

Cited by 10 publications

(8 citation statements)

References 18 publications

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“…To translate AP polarity to LR polarity, the clockwise rotation rather than the planar beating of ciliary motion pattern is indispensable and we speculate that this is the reason why the mouse node cilia have lost radial spokes during evolution. Avery recent study reports the presence of minor population of cells in the mouse node containing cilia of 9þ2 structure (Odate et al 2016). It is tempting to propose that the mouse embryo might still be evolving toward the loss of 9þ2 arrangement.…”

Section: Clockwise Rotation Of the Mouse Node Ciliamentioning

confidence: 99%

“…These cilia show planar beating and generate directional fluid flow. In contrast, the 9þ0 type motile cilia present in the node cavity of the mouse embryo possess nine doublet microtubules with dynein arms but lack the central microtubules and radial spokes (Nonaka et al 1998;Takeda et al 1999;Hirokawa et al 2006;Shinohara et al 2015;Odate et al 2016). The driving force of ciliary bending is generated by sliding of dynein arms between the peripheral doublet microtubules of the axoneme (Summers et al 1971;Fox et al 1987).…”

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confidence: 99%

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Cilia in Left–Right Symmetry Breaking

Shinohara

Hamada

2017

Cold Spring Harb Perspect Biol

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Visceral organs of vertebrates show left-right (L-R) asymmetry with regard to their position and morphology. Cilia play essential role in generating L-R asymmetry. A number of genes required for L-R asymmetry have now been identified in vertebrates, including human, many of which contribute to the formation and motility of cilia. In the mouse embryo, breaking of L-R symmetry occurs in the ventral node, where two types of cilia (motile and immotile) are present. Motile cilia are located at the central region of the node, and generate a leftward fluid flow. These motile cilia at the node are unique in that they rotate in the clockwise direction, unlike other immotile cilia such as airway cilia that show planar beating. The second type of cilia essential for L-R asymmetry is immotile cilia that are peripherally located immotile cilia. They sense a flow-dependent signal, which is either chemical or mechanical in nature. Although Ca signaling is implicated in flow sensing, the precise mechanism remains unknown.

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Section: Clockwise Rotation Of the Mouse Node Ciliamentioning

confidence: 99%

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confidence: 99%

Cilia in Left–Right Symmetry Breaking

Shinohara

Hamada

2017

Cold Spring Harb Perspect Biol

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“…The axoneme of motile cilia is made up of a microtubule-based cytoskeleton arranged in an organized 9 + 2 pattern, with the exception of motile nodal cilia largely lacking central pair microtubules [34,91]. The sliding of the microtubules against each other enables ciliary motility and requires additional structural components, namely: inner and outer dynein arms, the outer dynein arm docking complex, the nexin dynein regulatory complex (N-DRC), and radial spokes (Figure 4A).…”

Section: Motile Cilia Structurementioning

confidence: 99%

Ciliary Dyneins and Dynein Related Ciliopathies

Antony

Brunner

Schmidts

2021

Cells

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Although ubiquitously present, the relevance of cilia for vertebrate development and health has long been underrated. However, the aberration or dysfunction of ciliary structures or components results in a large heterogeneous group of disorders in mammals, termed ciliopathies. The majority of human ciliopathy cases are caused by malfunction of the ciliary dynein motor activity, powering retrograde intraflagellar transport (enabled by the cytoplasmic dynein-2 complex) or axonemal movement (axonemal dynein complexes). Despite a partially shared evolutionary developmental path and shared ciliary localization, the cytoplasmic dynein-2 and axonemal dynein functions are markedly different: while cytoplasmic dynein-2 complex dysfunction results in an ultra-rare syndromal skeleto-renal phenotype with a high lethality, axonemal dynein dysfunction is associated with a motile cilia dysfunction disorder, primary ciliary dyskinesia (PCD) or Kartagener syndrome, causing recurrent airway infection, degenerative lung disease, laterality defects, and infertility. In this review, we provide an overview of ciliary dynein complex compositions, their functions, clinical disease hallmarks of ciliary dynein disorders, presumed underlying pathomechanisms, and novel developments in the field.

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“…Cilia with varied ultrastructure have also been identified within the node. Cilia with 9 + 2 and 9 + 4 structures have been found in the zebrafish, mouse, and rabbit embryonic node but their function and movement pattern are not yet known; it is presumed they would beat rather than spin (due to the presence of central microtubules) [ 63 , 64 , 65 , 66 , 67 ]. Motility requires transcription factor FOXJ1, among others, and functional IDA and ODA motor complexes [ 68 ].…”

Section: Motile Cilia In the Embryonic Node During Human Embryogenesismentioning

confidence: 99%

Impact of Motile Ciliopathies on Human Development and Clinical Consequences in the Newborn

Hyland

Brody

2021

Cells

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Motile cilia are hairlike organelles that project outward from a tissue-restricted subset of cells to direct fluid flow. During human development motile cilia guide determination of the left-right axis in the embryo, and in the fetal and neonatal periods they have essential roles in airway clearance in the respiratory tract and regulating cerebral spinal fluid flow in the brain. Dysregulation of motile cilia is best understood through the lens of the genetic disorder primary ciliary dyskinesia (PCD). PCD encompasses all genetic motile ciliopathies resulting from over 60 known genetic mutations and has a unique but often underrecognized neonatal presentation. Neonatal respiratory distress is now known to occur in the majority of patients with PCD, laterality defects are common, and very rarely brain ventricle enlargement occurs. The developmental function of motile cilia and the effect and pathophysiology of motile ciliopathies are incompletely understood in humans. In this review, we will examine the current understanding of the role of motile cilia in human development and clinical considerations when assessing the newborn for suspected motile ciliopathies.

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9 + 0 and 9 + 2 cilia are randomly dispersed in the mouse node

Cited by 10 publications

References 18 publications

Cilia in Left–Right Symmetry Breaking

Cilia in Left–Right Symmetry Breaking

Ciliary Dyneins and Dynein Related Ciliopathies

Impact of Motile Ciliopathies on Human Development and Clinical Consequences in the Newborn

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