Shaping the Vertebrate Body Plan by Polarized Embryonic Cell Movements

Keller, Ray

doi:10.1126/science.1079478

Cited by 670 publications

(573 citation statements)

References 54 publications

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“…The rapid expansion of ectodermal surface to cover the embryo and engulf the endoderm that is required during epiboly is achieved by the radial intercalation of several cell layers in the blastocoel roof (BCR), causing its thinning. [24][25][26][27] In contrast to control-injected embryos, we noticed that the BCR of xRIPK4Mo atg -depleted embryos showed impaired thinning of the ectodermal cell layers (Figure 4d), suggesting that this is the onset of a disrupted epibolic movement hampering gastrulation.…”

Section: G H and I)mentioning

confidence: 99%

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

et al. 2014

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Receptor-interacting protein kinase 4 (RIPK4)-deficient mice have epidermal defects and fusion of all external orifices. These are similar to Bartsocas-Papas syndrome and popliteal pterygium syndrome (PPS) in humans, for which causative mutations have been documented in the RIPK4 and IRF6 (interferon regulatory factor 6) gene, respectively. Although genetically distinct, these syndromes share the anomalies of marked pterygia, syndactyly, clefting and hypoplastic genitalia. Despite the strong resemblance of these two syndromes, no molecular connection between the transcription factor IRF6 and the kinase RIPK4 was known and the mechanism underlying the phenotype was unclear. Here we describe that RIPK4 deficiency in mice causes epithelial fusions associated with abnormal periderm development and aberrant ectopic localization of E-cadherin on the apical membrane of the outer peridermal cell layers. In Xenopus, RIPK4 depletion causes the absence of ectodermal epiboly and concomitant gastrulation defects that phenocopy ectopic expression of dominant-negative IRF6. We found that IRF6 controls RIPK4 expression and that wild-type, but not kinase-dead, RIPK4 can complement the gastrulation defect in Xenopus caused by IRF6 malfunctioning. In contrast to the mouse, we observed only minor effects on cadherin membrane expression in Xenopus RIPK4 morphants. However, gastrulation defects were associated with a virtual absence of cortical actin in the ectodermal cells that face the blastocoel cavity and this was phenocopied in embryos expressing dominant-negative IRF6. A role for RIPK4 in actin cytoskeleton organization was also revealed in mouse epidermis and in human epithelial HaCaT cells. In conclusion, we showed that in mice RIPK4 is implicated in cortical actin organization and in E-cadherin localization or function, which can explain the characteristic epithelial fusions observed in PPSs. In addition, we provide a novel molecular link between IRF6 and RIPK4 that unifies the different PPSs to a common molecular pathway.

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Section: G H and I)mentioning

confidence: 99%

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

et al. 2014

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“…We and others have observed the onset of Math1 in columns of cells spanning the depth of the cochlear epithelium within the primordial organ of Corti (Chen et al, 2002;Kiernan et al, 2005a;Wang et al, 2005;Fig. 2B,C), and we have hypothesized that these columns of cells are the early hair cell precursors in a multi-cell layered primordial organ of Corti at E14.5. Subsequently, cellular intercalation movements, characteristic of convergent extension (Keller, 2002), lead to the extension of the organ of Corti and the formation of a single hair cell layer during terminal differentiation (Chen et al, 2002;Montcouquiol et al, 2003;McKenzie et al, 2004;Wang et al, 2005). At the basal region of the cochlea, the presumptive hair cell precursors marked by the expression of Math1 were seen as two columns of cells, presumably at the inner hair cell and the first row of outer hair cell locations (Fig.…”

Section: Hes6 Expression Delineates the Morphogenesis Of The Hair Celmentioning

confidence: 99%

Basic helix–loop–helix gene Hes6 delineates the sensory hair cell lineage in the inner ear

et al. 2006

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The basic helix-loop-helix (bHLH) gene Hes6 is known to promote neural differentiation in vitro. Here, we report the expression and functional studies of Hes6 in the inner ear. The expression of Hes6 appears to be parallel to that of Math1 (also known as Atoh1), a bHLH gene necessary and sufficient for hair cell differentiation. Hes6 is expressed initially in the presumptive hair cell precursors in the cochlea. Subsequently, the expression of Hes6 is restricted to morphologically differentiated hair cells. Similarly, the expression of Hes6 in the vestibule is in the hair cell lineage. Hes6 is dispensable for hair cell differentiation, and its expression in inner ear hair cells is abolished in the Math1-null animals. Furthermore, the introduction of Hes6 into the cochlea in vitro is not sufficient to promote sensory or neuronal differentiation. Therefore, Hes6 is downstream of Math1 and its expression in the inner ear delineates the sensory lineage. However, the role of Hes6 in the inner ear remains elusive.

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“…This morphogenic process of body axis elongation begins with a thinning and lateral elongation of postinvoluted prospective notochordal and somatic mesoderm and the overlying posterior neural plate. The following mediolateral intercalation of cells results in a narrower and longer array of these tissues in the frog embryo (Keller, 1984(Keller, , 1986(Keller, , 2002Keller et al, 1991Keller et al, , 2000.…”

Section: Morphogenesis Of the Initial Primitive Streakmentioning

confidence: 99%

Induction and patterning of the primitive streak, an organizing center of gastrulation in the amniote

Matsukawa

Poh

Kelly

et al. 2004

Developmental Dynamics

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The primitive streak is the organizing center for amniote gastrulation. It defines the future embryonic midline and serves as a conduit of cell migration for germ layer formation. The migration patterns of endodermal and mesodermal precursors through the streak have been studied in great detail. Additional new breakthroughs recently have revealed the cell biological and molecular mechanisms that govern streak induction and patterning. These findings include (1) identification of the ontogeny and inductive signals of streak precursors, (2) the potential cellular mechanism of streak extension, and (3) the molecular and functional diversification along the anterior-posterior and mediolateral axes within the primitive streak. These findings indicate that amniote embryos initiate gastrulation by using both evolutionarily conserved and divergent mechanisms. The data also provide a foundation for understanding how the midline axis is defined and maintained during gastrulation of the amniotes. Developmental Dynamics 229:422-432, 2004.

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Shaping the Vertebrate Body Plan by Polarized Embryonic Cell Movements

Cited by 670 publications

References 54 publications

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

Basic helix–loop–helix gene Hes6 delineates the sensory hair cell lineage in the inner ear

Induction and patterning of the primitive streak, an organizing center of gastrulation in the amniote

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