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. Author manuscript; available in PMC: 2015 Apr 24.
Published in final edited form as: Dev Biol. 2009 Jan 23;328(2):234–244. doi: 10.1016/j.ydbio.2009.01.017

Fig. 2.

Fig. 2

Morphogenesis defects in zygotic mutants for Wnt/β-catenin asymmetry pathway members. (A) Gene structure for sys-1, pop-1, and wrm-1 indicating the regions deleted in the alleles used for this study. Indicated protein domains are: red, armadillo repeats; green, β-catenin binding domain; and blue, HMG Box. (B–D) Dorsal and (E–G) ventral views of (B, E) sys-1(q736), (C, F) pop-1(q772) and (D, G) wrm-1(ok738) mutant embryos. Wnt/β-catenin asymmetry pathway members display variable defects in dorsal intercalation, including dorsal cells that fail to complete intercalation (arrowheads, B–D) and dorsal cells that migrate in groups (arrows, C). When gastrulation appears complete, leading cells (asterisks, E–G) in Wnt/β-catenin mutant embryos often migrate properly; however, pocket cells fail to meet at the ventral midline (arrow E–G). Head enclosure also fails in wrm-1(ok738) mutant embryos (arrowheads, G). Scale bar=10 μm.