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Embryonic Induction Essay Research Paper Vertebrate embryos

Embryonic Induction Essay, Research Paper Vertebrate embryos rely extensively upon inductive interactions to diversify the number of different kinds of cells in the embryo. Induction is the process by which one group of cells produces a signal that determines the fate of a second group of cells. This implies both the capacity to produce a signal (ligand) by the inducing cells and the competence of the responding cells to receive and interpret the signal via a signal transduction pathway.

Embryonic Induction Essay, Research Paper

Vertebrate embryos rely extensively upon inductive interactions to diversify the number of different kinds of cells in the embryo. Induction is the process by which one group of cells produces a signal that determines the fate of a second group of cells. This implies both the capacity to produce a signal (ligand) by the inducing cells and the competence of the responding cells to receive and interpret the signal via a signal transduction pathway.

Amphibians are the most extensively studied vertebrates for investigations into embryonic induction. Most contemporary investigations have utilized Xenopus. The two major inductive events during early Xenopus development (Slack, 1994, Fig. 1) are:

mesoderm induction

neural induction

Mesoderm Induction: An Overview

Mesoderm induction occurs over an extended period of time in the equatorial region of the embryo from about the 32-cell stage to the beginning of gastrulation. The requirement of induction for production of mesoderm is evident by comparing the embryonic fate map (which shows the fates of regions of the embryo during normal development) to the specification map (which shows what tissue explants can do in isolation) during cleavage stages.

The fate map shows that about half of the mesoderm arises from cells above the equatorial pigment boundary, whereas no cells from above the pigment boundary will form muscle or notochord in isolation. This implies that cells above this boundary require contact with cells below the boundary (the vegetal cells) to produce mesoderm, and that is what is observed when animal and vegetal explants are combined using the procedure first developed by Nieuwkoop.

(See Browder et al., 1991, Figs. 12.1-12.4; Gilbert, 1997, Fig. 15.14; Kalthoff, 1996, Figs. 6.2 and 9.19; Wolpert et al., 1998, Figs. 3.16, 3.22 and 3.25)

The vegetal cells are not equal in their inductive capacities. The dorsal vegetal cells (the Nieuwkoop Center) induce axial mesoderm of the dorsal midline (notochord and segmented muscle), whereas the remaining vegetal cells induce ventrolateral mesoderm (mesothelium, mesenchyme, blood cells).

(See Gilbert, Fig. 15.16; Kalthoff, Fig. 9.20; Wolpert, 1998, Fig. 3.27)

These observations have led to the proposal that there are two mesoderm-inducing signals:

a general vegetal signal that operates around the circumference and induces ventral mesoderm; and

a dorsal vegetal signal (emanating from the Niewkoop center) that induces the axial mesoderm (i.e., Spemann’s organizer).

The general vegetal signal apparently remains operational in ventralized embryos produced by UV irradiation of fertilized eggs; these radially symmetrical embryos have the normal amount of mesoderm, but all of it is ventral in character. The dorsal vegetal signal is dependent upon dorsalization factors.

The ventral mesoderm becomes further diversified into subdomains. This diversification is apparently due to a third signal that dorsalizes the ventral mesoderm closest to the organizer. Evidence in favor of this hypothesis again comes from a comparison of the fate map and specification map: About 60% of muscle is derived from ventral mesoderm (Slack, 1994). However, explanted ventral mesoderm forms little or no muscle (Dale and Slack, 1987). Muscle is formed by ventral mesoderm when it is juxtaposed with the organizer. This dorsalization of the ventral mesoderm occurs during gastrulation.

(See Browder et al., Fig. 12.5, Gilbert, Fig. 15.17; Kalthoff, Fig. 9.23; Wolpert et al., 1998, Fig. 3.26)

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