How we are shaped: The biomechanics of gastrulation

Keller, Ray; Davidson, Lance A.; Shook, David

doi:10.1046/j.1432-0436.2003.710301.x

Cited by 453 publications

(394 citation statements)

References 193 publications

(264 reference statements)

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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%

“…During gastrulation in Xenopus, involution of the mesoderm through the blastopore is coupled to epiboly movements where the BCR shows rapid thinning via radial intercalation of the deep animal ectodermal cells. 26,27 This requires dynamic cadherinmediated interactions between the neighboring interdigitating cells. 40 During this process, a decrease in C-cadherinmediated adhesiveness has been reported.…”

Section: G H and I)mentioning

confidence: 99%

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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%

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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“…While amphibian body axis elongation and amniote primitive streak formation both rise from an extension, it has been pointed out that the early onset of extension in amphibian gastrulation shows no similarity to primitive streak extension in the amniote (Keller et al, 2003). For example, while the frog tissue thins and extends, the primitive streak thickens during extension.…”

Section: Morphogenesis Of the Initial Primitive Streakmentioning

confidence: 99%

“…Indeed, cells of chicken gastrulae, including those of the developing streak (Wei and Mikawa, 2000a), actively proliferate with a mitotic index of ϳ2-4 hr (Sanders et al, 1993), whereas no cell division takes place in tissues elongating by convergence and extension in the frog embryo Keller et al, 2000). Therefore, it appears that a typical convergence and extension mechanism alone may not be sufficient for initial primitive streak formation in the chick and in other amniotes (reviewed in Keller, 2002;Keller et al, 2003).…”

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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“…Odell et al, 1981;Cummings, 1990). This modelling approach has been used to describe, for example, gastrulation (Keller et al, 2003), and sea urchin invagination (Davidson et al, 1995). However, for colorectal crypt budding and fission to be initiated by changes in the Wnt cascade the folding must be driven by hyperproliferation, or by changes in cell motility and adhesion, and not by such apical contractions.…”

Section: Introductionmentioning

confidence: 99%

Biomechanical Modelling of Colorectal Crypt Budding and Fission

Edwards

Chapman

2007

Bull. Math. Biol.

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This paper presents a biomechanical model for the small pits, called crypts, that line the colon. A continuum approach is adopted, with the crypt epithelium modelled as a growing beam attached to the underlying lamina by cell bonds, which generate tension within the layer. These cell attachments are assumed to be viscoelastic thus allowing for cell progression along the crypt. It is shown that any combination of: an increase in net proliferation (i.e. cell production minus apoptosis), an enlargement of the proliferative compartment, an increase in the strength of the cellular attachment to the underlying lamina, or a change in the rate of cell growth or cell bonding may generate buckling of the tissue. These changes can all be generated by an activating mutation of the Wnt cascade, which is generally accepted to be the first genetic change in colorectal cancer, with subsequent deformation, budding, and crypt fission an observed feature of the adenomatous crypt.

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How we are shaped: The biomechanics of gastrulation

Cited by 453 publications

References 193 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

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

Biomechanical Modelling of Colorectal Crypt Budding and Fission

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