Analysis of axis induction mutant embryos reveals morphogenetic events associated with zebrafish yolk extension formation

Abstract

We analyze patterning and morphogenetic events during somitogenesis in hecate mutant embryos, which exhibit early axis induction defects. The posterior region, in the absence of a dorsal axis, is capable of forming organized gene expression patterns. The aberrant morphogenesis of mutant embryos is associated with anteriorly directed cell movements, underlying the enveloping layer, from the posterior region. In both wild-type and mutant embryos, these changes result in an accumulation of cells, whose location correlates with a constriction in the posterior yolk cell, which in the wild-type corresponds to the yolk extension. The region encompassing the constriction corresponds to a region of expression of zangptl2 in the yolk syncytial layer, which expands anteriorly together with the anteriorly migrating tail bud-derived cell population.

ApoA-II Directs Morphogenetic Movements of Zebrafish Embryo by Preventing Chromosome Fusion during Nuclear Division in Yolk Syncytial Layer

“…We find that disruption of apoa2 function induced the disordered microfilament arrays in the YSL. However, previous studies and our observations show that microfilament bundles appear after 50% epiboly (39). In apoa2-disrupted embryos, the YSN disorders occur just after the multiple nuclei appear in the yolk cell and induce YSL disorganization, indicating that the disorder of microfilament bundles is the consequence of the YSN disorganization.…”

“…Embryonic gastrulation undergoes correctly along the expansion. Microfilaments forming a concentric ring in eYSL are proposed to generate a constrictive force that would drive expansion of the YSL (16,39). We find that disruption of apoa2 function induced the disordered microfilament arrays in the YSL.…”

Ontogeny and phylogeny of the yolk extension in embryonic Cypriniform fishes

“…Second, another homeobox gene, HoxA13b, shows a morphant phenotype of failure to form the yolk extension (Crow et al, 2009). Third, a maternal-effect gene, hecate (hec), displays a thickened, abnormal yolk extension in mutants (Lyman-Gingerich et al, 2006). Fourth, a signaling gene, retinoic acid binding protein 4 (rbp4), when inhibited pharmacologically or with morpholino injection, either results in failure of the yolk extension to form in some embryos, or the formation of a thickened, abnormal yolk extension in others (Li et al, 2007).…”

“…The deepest layer is the YSL, which is the cortex of the syncytial yolk cell. Lyman-Gingerich et al (2006) describe a third layer of cells between the EVL and the YSL. They propose that this middle cell layer is contractile, and is responsible for formation of the yolk extension.…”

“…The formation of the yolk extension is a particularly useful embryonic trait to examine the issue of modularity for several reasons: (1) yolk extension formation is easy to observe in the embryo; (2) the yolk extension forms as a result of coordinated morphogenetic cell behaviors (Lyman-Gingerich et al, 2006); and (3) yolk extension formation occurs in only a subset of teleostean fishes. An evolutionary analysis of yolk extension formation can exploit the diversity of extant ray-finned (actinopterygian) fishes, which allows the phylogenetic distribution of this putative developmental module to be examined across many taxa.…”