Abstract
Gastrulation is the process by which the germ layers become positioned in an embryo. C. elegans gastrulation serves as a model for studying the molecular mechanisms of diverse cellular and developmental phenomena, including morphogenesis, cell polarization, cell-cell signaling, actomyosin contraction and cell-cell adhesion. One distinct advantage of studying these phenomena in C. elegans is that genetic tools can be combined with high resolution live cell imaging and direct manipulations of the cells involved. Here we review what is known to date about the cellular and molecular mechanisms that function in C. elegans gastrulation.
Highlights
Polarization of gastrulating cellsThe cell movements of gastrulation begin at the 26-cell stage when the two endodermal precursors, Ea and Ep, move from the surface of the embryo into a small interior cavity called the blastocoel (Sulston et al, 1983)
Gastrulation in C. elegans when small groups of cells ingress at various times into the small blastocoel space
PAR proteins found on the apical surface are required for the apical accumulation of myosin in ingressing cells and ingressions are inefficient in PAR-depleted embryos
Summary
The cell movements of gastrulation begin at the 26-cell stage when the two endodermal precursors, Ea and Ep, move from the surface of the embryo into a small interior cavity called the blastocoel (Sulston et al, 1983). A blastocoel-like cavity can form when a single cell (the AB blastomere) is isolated from the embryo and allowed to divide in culture (Figure 1B; Nance and Priess, 2002) This observation suggests that cell contacts induce an apical-basal polarization in cells that causes their different surfaces to develop different adhesive properties. To establish that the role of PAR-3 in apical-basal polarity is direct and not a secondary consequence of earlier defects in anterior-posterior polarity, PAR-3 was depleted from early embryonic cells by fusion to a protein domain (the ZF1 domain of PIE-1; Nance et al, 2003) This domain promotes protein degradation beginning at the four-cell stage (Reese et al, 2000; Nance et al, 2003). The target molecules that mediate the cell adhesion functions of PAR-3 and PAR-6 have yet to be identified
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