Degeneration of archenteron in sea urchin embryos caused by α,α′-dipyridyl

Processes of gastrulation in the sea urchin embryo have been intensively studied to reveal the mechanisms involved in the invagination of a monolayered epithelium. It is widely accepted that the invagination proceeds in two steps (primary and secondary invagination) until the archenteron reaches the apical plate, and that the constituent cells of the resulting archenteron are exclusively derived from the veg2 tier of blastomeres formed at the 60-cell stage. However, recent studies have shown that the recruitment of the archenteron cells lasts as late as the late prism stage, and some descendants of veg1 blastomeres are also recruited into the archenteron. In this review, we first illustrate the current outline of sea urchin gastrulation. Second, several factors, such as cytoskeletons, cell contact and extracellular matrix, will be discussed in relation to the cellular and mechanical basis of gastrulation. Third, differences in the manner of gastrulation among sea urchin species will be described; in some species, the archenteron does not elongate stepwise but continuously. In those embryos, bottle cells are scarcely observed, and the archenteron cells are not rearranged during invagination unlike in typical sea urchins. Attention will be also paid to some other factors, such as the turgor pressure of blastocoele and the force generated by blastocoele wall. These factors, in spite of their significance, have been neglected in the analysis of sea urchin gastrulation. Lastly, we will discuss how behavior of pigment cells defines the manner of gastrulation, because pigment cells recently turned out to be the bottle cells that trigger the initial inward bending of the vegetal plate.

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“…1997). Inhibitors of prolyl hydroxylase (Mizoguchi et al . 1983) and collagen deposition (Wessel & McClay 1987) prevent gastrulation.…”

Section: Factors Involved In Gastrulationmentioning

confidence: 99%

Gastrulation in the sea urchin embryo: A model system for analyzing the morphogenesis of a monolayered epithelium

Kominami

Takata

2004

Dev Growth Differ

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“…1981;Wessel & McClay 1987;Karakiulakis et al . 1993) Inhibitor of proline and lysine hydroxylation (Mizoguchi et al . 1983;Mizoguchi et al .…”

Section: Gastrulationmentioning

confidence: 99%

“…1993) Inhibitor of proline and lysine hydroxylation (Mizoguchi et al . 1983;Mizoguchi et al . 1983;Karakiulakis et al .…”

Section: Gastrulationmentioning

confidence: 99%

Inhibition of mitogen activated protein kinase signaling affects gastrulation and spiculogenesis in the sea urchin embryo

Kumano

Foltz

2003

Dev Growth Differ

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The mitogen activated protein (MAP) kinase signaling cascade has been implicated in a wide variety of events during early embryonic development. We investigated the profile of MAP kinase activity during early development in the sea urchin, Strongylocentrotus purpuratus, and tested if disruption of the MAP kinase signaling cascade has any effect on developmental events. MAP kinase undergoes a rapid, transient activation at the early blastula stage. After returning to basal levels, the activity again peaks at early gastrula stage and remains high through the pluteus stage. Immunostaining of early blastula stage embryos using antibodies revealed that a small subset of cells forming a ring at the vegetal plate exhibited active MAP kinase. In gastrula stage embryos, no specific subset of cells expressed enhanced levels of active enzyme. If the signaling cascade was inhibited at any time between the one cell and early blastula stage, gastrulation was delayed, and a significant percentage of embryos underwent exogastrulation. In embryos treated with MAP kinase signaling inhibitors after the blastula stage, gastrulation was normal but spiculogenesis was affected. The data suggest that MAP kinase signaling plays a role in gastrulation and spiculogenesis in sea urchin embryos.

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“…Inhibition of collagen processing dramatically affects embryonic development in the sea urchin embryo. Inhibitors of proline and lysine hydroxylation arrest the sea urchin embryo at the early blastula stage, blocking the cell movements necessary for gastrulation (Mizoguchi & Yasumasu 1983; Mizoguchi et al 1983; Karakiulakis et al 1993). Inhibition of proline and lysine hydroxylation using α,α′‐dipyridyl blocks calcium deposition into growing spicules in primary mesenchyme cell (PMC) culture (Mintz et al 1981).…”

Section: Introductionmentioning

confidence: 99%

Inhibitors of procollagen C‐terminal proteinase block gastrulation and spicule elongation in the sea urchin embryo

Huggins

Lennarz

2001

Dev Growth Differ

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In the sea urchin embryo, inhibition of collagen processing and deposition affects both gastrulation and embryonic skeleton (spicule) formation. It has been found that cell-free extracts of gastrula-stage embryos of Strongylocentrotus purpuratus contain a procollagen C-terminal proteinase (PCP) activity. A rationally designed non-peptidic organic hydroxamate, which is a potent and specific inhibitor of human recombinant PCP (FG-HL1), inhibited both the sea urchin PCP as well as purified chick embryo tendon PCP. In the sea urchin embryo, FG-HL1 inhibited gastrulation and blocked spicule elongation, but not spicule nucleation. A related compound with a terminal carboxylate rather than a hydroxamate (FG-HL2) did not inhibit either chick PCP or sea urchin PCP activity in a procollagen-cleavage assay. However, FG-HL2 did block spicule elongation without affecting spicule nucleation or gastrulation. Neither compound was toxic, because their effects were reversible on removal. It was shown that the inhibition of gastrulation and spicule elongation were independent of tissue specification events, because both the endoderm specific marker Endo1 and the primary mesenchyme cell specific marker SM50 were expressed in embryos treated with FG-HL1 and FG-HL2. These results suggest that disruption of the fibrillar collagen deposition in the blastocoele blocks the cell movements of gastrulation and may disrupt the positional information contained within the extracellular matrix, which is necessary for spicule formation.

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Degeneration of archenteron in sea urchin embryos caused by α,α′-dipyridyl

Cited by 7 publications

References 13 publications

Gastrulation in the sea urchin embryo: A model system for analyzing the morphogenesis of a monolayered epithelium

Gastrulation in the sea urchin embryo: A model system for analyzing the morphogenesis of a monolayered epithelium

Inhibition of mitogen activated protein kinase signaling affects gastrulation and spiculogenesis in the sea urchin embryo

Inhibitors of procollagen C‐terminal proteinase block gastrulation and spicule elongation in the sea urchin embryo

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