Towards an understanding of yolk syncytial layer formation in the zebrafish embryo.
The transformation of the single-celled zygote into a complex, multi-cellular organism begins with the process of cleavage. The yolk-rich embryos of birds, reptiles, prototherian mammals and teleosts initially undergo a pattern of meroblastic (or partial) cleavage. This results in a blastoderm with marginal cells that retain cytoplasmic connections to the yolk when the central cells cellularize after several rounds of division. A consequence of this cellularization is the formation of a small, almost imperceptible cavity separating the central blastomeres from the yolk-mass. This study demonstrated the presence of extracellular space beneath the blastoderm of the early zebrafish embryo, which corresponds to this cavity.
The hallmark of meroblastic cleavage is the formation of the periblast from the marginal blastomeres, which contribute their nuclei and cytoplasm to the yolk cell cortex resulting in the formation of a syncytium. In teleosts, detailed descriptive studies have revealed that the periblast or yolk syncytial layer (YSL) is formed by the “collapse” of marginal blastomeres onto the yolk cell. However, little is known about the molecular mechanism that underlies the formation of this important structure. In this thesis, I demonstrated by time-lapse confocal microscopy, in a transgenic line that expresses membrane-targeted GFP, that the YSL forms as a result of the absence of cytokinesis between daughter nuclei at the tenth mitotic division and the regression of pre-exsiting marginal cell membranes thus converting the former margin of the blastoderm into a true syncytium. Moreover, disruption of components of the cytoskeleton induced the formation of an expanded YSL, which is enlarged at the expense of the blastoderm. Depolymerization of microtubules with nocodazole, blocking the polymerization of actin using cytochalasin D and inhibiting the activation of Rho kinase (Rock), a known actin cytoskeleton regulator and myosin activator, with Y27632 all resulted in the same phenotype – the expansion of the YSL. Since these elements are components of the cytokinetic machinery, it suggests that the YSL normally forms as a result of inhibition of cytokinesis in the marginal blastomeres.
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