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Question

Lithium chloride treatment in frog embryos leads to:

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Explanation

Lithium chloride is classic dorsalizing agent acting as direct inhibitor of glycogen synthase kinase-3 beta, serine-threonine kinase that phosphorylates beta-catenin for proteasomal degradation. In normal Xenopus embryos GSK3 keeps ventral beta-catenin low, while dorsal Wnt signaling inhibits it. Lithium mimics Wnt activation everywhere, stabilizing beta-catenin ubiquitously, driving ectopic expression of Siamois, Twin, goosecoid and chordin around entire marginal zone. Consequently ventral mesoderm converts to dorsal organizer fate, yielding hyperdorsalized embryos with expanded notochord and neural tissue. This illustrates conserved developmental logic of morphogen gradients patterning embryonic axes through Wnt and BMP antagonism.

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