LiCl exposure causes sea urchin animal pole cells to become:
Exposure to lithium chloride inhibits GSK-three beta globally, mimicking vegetal Wnt signaling throughout embryo. In normal sea urchin embryos, animal pole cells maintain active GSK-three that degrades beta-catenin, preserving ectodermal fate expressing spec1 and other ectoderm markers. LiCl blocks degradation, causing beta-catenin accumulation even animally, converting presumptive ectoderm to endoderm and mesoderm fates. Animal caps isolated from LiCl treated embryos express gut marker Endo16 and skeletogenic marker Msp130, failing to form ciliated ectoderm. Phenotype illustrates vegetalizing effect, producing embryos with exaggerated endomesoderm, expanded archenteron, and radialized skeleton patterning defects.
Ref: Gilbert, Developmental Biology, 12th ed., Chapter 10: LiCl vegetalizes animal pole to mesoderm endoderm.