Cytochalasin D inhibits basal body migration and ciliary elongation in quail oviduct epithelium

Boisvieux‐Ulrich, Emmanuelle; Lainé, Marie-Christine; Sandoz, Daniel

doi:10.1007/bf01740770

Cited by 106 publications

(92 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Because a well-organized actin cytoskeleton is required for the migration and docking of the basal bodies to the apical plasma membrane, and for cilia elongation (Boisvieux-Ulrich et al, 1990;Pan et al, 2007;Ravanelli and Klingensmith, 2011;Tamm and Tamm, 1988), a sept7b-dependent disruption of actin organization could contribute to the defects in ciliogenesis. Alternatively, the reduced number of basal bodies upon sept7b knockdown could also lead to reduced cortical actin, as a dense apical actin cap has been shown to form around basal bodies after their apical docking (Pan et al, 2007;Werner et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Sept7bis essential for pronephric function and development of left-right asymmetry in zebrafish embryogenesis

Dash

Lehtonen

Wasik

et al. 2014

Journal of Cell Science

View full text Add to dashboard Cite

The conserved septin family of filamentous small GTPases plays important roles in mitosis, cell migration and cell morphogenesis by forming scaffolds and diffusion barriers. Recent studies in cultured cells in vitro indicate that a septin complex of septin 2, 7 and 9 is required for ciliogenesis and cilia function, but septin function in ciliogenesis in vertebrate organs in vivo is not understood. We show that sept7b is expressed in ciliated cells in different tissues during early zebrafish development. Knockdown of sept7b by using morpholino antisense oligonucleotides caused misorientation of basal bodies and cilia, reduction of apical actin and the shortening of motile cilia in Kupffer's vesicle and pronephric tubules. This resulted in pericardial and yolk sac edema, body axis curvature and hydrocephaly. Notably, in sept7b morphants we detected strong leftright asymmetry defects in the heart and lateral plate mesoderm (situs inversus), reduced fluid flow in the kidney, the formation of kidney cysts and loss of glomerular filtration barrier function. Thus, sept7b is essential during zebrafish development for pronephric function and ciliogenesis, and loss of expression of sept7b results in defects that resemble human ciliopathies.

show abstract

Section: Discussionmentioning

confidence: 99%

Sept7bis essential for pronephric function and development of left-right asymmetry in zebrafish embryogenesis

Dash

Lehtonen

Wasik

et al. 2014

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…5b, arrows). In addition, the microvilli, which interspaced the axonema, appeared to be reduced in length as well as in number, compared with the WT samples from the same litter, reminiscent of actin organization or Rho GTPase activity defect 32,33 . Thus, in mutant cells basal bodies multiply normally but fail to migrate apically, suggesting a defect in transport and/or docking at the apical membrane.…”

Section: Cyld Interacts With Cap350 At the Centrosome/basal Bodiesmentioning

confidence: 96%

The deubiquitinating enzyme CYLD controls apical docking of basal bodies in ciliated epithelial cells

et al. 2014

View full text Add to dashboard Cite

CYLD is a tumour suppressor gene mutated in familial cylindromatosis, a genetic disorder leading to the development of skin appendage tumours. It encodes a deubiquitinating enzyme that removes Lys63-or linear-linked ubiquitin chains. CYLD was shown to regulate cell proliferation, cell survival and inflammatory responses, through various signalling pathways. Here we show that CYLD localizes at centrosomes and basal bodies via interaction with the centrosomal protein CAP350 and demonstrate that CYLD must be both at the centrosome and catalytically active to promote ciliogenesis independently of NF-kB. In transgenic mice engineered to mimic the smallest truncation found in cylindromatosis patients, CYLD interaction with CAP350 is lost disrupting CYLD centrosome localization, which results in cilia formation defects due to impairment of basal body migration and docking. These results point to an undiscovered regulation of ciliogenesis by Lys63 ubiquitination and provide new perspectives regarding CYLD function that should be considered in the context of cylindromatosis.

show abstract

“…These structures extend laterally to basal bodies, point to the effective stroke of cilia beats [32][33] and are considered a landmark of cilia polarity 34 . In WT ( During assembly of motile cilia, basal bodies (bb) form deep in the cytoplasm and are transported to the apical surface via actin-dependent mechanisms 33,[35][36] . To study how Celsr2 inactivation influences ependymal ciliogenesis, we performed sections perpendicular to the ventricular surface to examine by TEM the position of bb relatively to the apical surface of ependymal cells at P10.…”

Section: Celsr2mentioning

confidence: 99%

“…Studies of ciliogenesis in the quail oviduct showed that localization of basal bodies to the apical cell domain depends on actin dynamics 35 . In line with this, ciliogenesis is defective in Foxj1 mutant mice, due to abnormal basal body anchoring to the actin-based apical cytoskeleton, and failure of RhoA-mediated apical actin enrichment [44][45][46][47] .…”

mentioning

confidence: 99%

Lack of cadherins Celsr2 and Celsr3 impairs ependymal ciliogenesis, leading to fatal hydrocephalus

et al. 2010

View full text Add to dashboard Cite

Cilia are organelles that protrude from the apical surface of most eukaryotic cells. According to their structure and motility, they are classified into three groups 1 . Primary monocilia, present in most cells, lack a central pair of microtubules (9+0 structure), and play several roles in mechanosensation and cell signaling. Nodal cilia have a 9+0 structure but, unlike primary cilia, they move and generate an asymmetric distribution of morphogenetic cues in the node, thereby contributing to laterality 2 . The third group is composed of motile 9+2 cilia that cover epithelial cells lining airways, reproductive tracts, and cerebral ventricles. Motile cilia play crucial functions in clearing mucus and debris in the airways and may assist the transit of sperm and eggs in genital tracts [3][4] . In the early postnatal mammalian brain, neuroepithelial cells that line the cerebral ventricles leave the cell cycle and differentiate into a monolayer of ependymal cells. At the end of maturation, the apical surface of ependymal cells bears dozens of cilia that beat in coordinate manner to facilitate the circulation of the cerebrospinal fluid (CSF), from sites of production in choroid plexuses to sites of absorption in subarachnoid spaces. In mice, mutations in genes involved in the assembly or structure of ependymal cilia, such as Mdnah5 5 , Ift88 (also known as Tg737 or Polaris) 6 , and Hy3 7-8 affect cilia genesis, CSF dynamics, and result in hydrocephalus. Thus far, however, little is known about the genetic factors that govern ependymal cilia polarization and the relationship between the polarity and the development and function of these organelles.Planar cell polarity (PCP), also known as tissue polarity, controls the polarization of epithelial cells in a plane perpendicular to their apicobasal axis. It was initially described in Drosophila, where it affects the stereotypic arrangement of cuticular hairs, sensory bristles, and Supplementary Fig. 1a, b). RT-PCR and (Supplementary Fig. 1c).Using the knocked-in beta-galactosidase reporter, we monitored the expression of Celsr2 in heterozygous mice. Consistent with published data [24][25][26] , Celsr2 expression was detected in all brain areas, from E11.5 to P5 (Fig. 1a-h). Celsr2 mutant mice develop progressive hydrocephalusCelsr2 mutant mice were viable and fertile, except for some females that had vaginal atresia. At birth, their brain did not display any flagrant morphological abnormality, suggesting that Celsr2 is not critical for cerebral embryonic development. However, a progressive ventricular dilation appeared between P5 and P10 with variable severity between animals, and became evident at P21 (Fig. 2a,b).The lateral ventricles were enlarged, and the septum had an abnormal triangular shape, due to 6 6 reduction of the dorsal part of the lateral septum. We did not observe any stenosis or constriction at the level of the foramen of Monro or of the aqueduct. The subcommissural organ (SCO), a structure thought to play a role in non-communicating hydrocephalus, was...

show abstract

Cytochalasin D inhibits basal body migration and ciliary elongation in quail oviduct epithelium

Cited by 106 publications

References 41 publications

Sept7bis essential for pronephric function and development of left-right asymmetry in zebrafish embryogenesis

Sept7bis essential for pronephric function and development of left-right asymmetry in zebrafish embryogenesis

The deubiquitinating enzyme CYLD controls apical docking of basal bodies in ciliated epithelial cells

Lack of cadherins Celsr2 and Celsr3 impairs ependymal ciliogenesis, leading to fatal hydrocephalus

Contact Info

Product

Resources

About