Abstract
Early stage treatment of the sea urchin embryo with zinc ions is known to prevent its gastrulation. The treated embryo, termed “animalized” and classically regarded as a permanent blastula with possibly exaggerated ectodermal differentiation, can be viewed, instead, as being in a state of reversibly suspended differentiation. This proposition is supported by the following observations: (1) An embryo exposed to Zn 2+ through its blastula stages and resuspended in fresh sea water retains the simple blastula morphology for at least 4 days; however, if the Zn 2+ is also depleted by a chelator during this period, development resumes and reaches the pluteus stage. (2) A suppression of ectodermal differentiation in the zinc-animalized embryo can be inferred from the blockage of the developmental initiation of Spec 1 and CyIIIa actin mRNA accumulation, since the genes encoding them are specifically expressed in differentiated (aboral) ectoderm. (3) Chelation allows the zinc-blocked accumulation of these ectodermal mRNAs to proceed. The later the treatment with chelator, the more slowly these mRNA accumulations resume, and the longer the interval between them and the subsequent morphological differentiation. (4) The enhancement of some early ectodermal functions in the zinc-animalized embryo is indicated by the increased concentrations of mRNAs, encoded by a set of genes, Blast j1 and Spec 3, that normally display peak levels in the blastula. The association of these genes with ectoderm is based on their being specifically expressed, albeit at low levels, in the pluteus ectoderm, and their being suppressed when presumptive ectoderm is made to differentiate as endoderm in the case of the embryo treated with lithium. The program of cell division in the zinc-animalized embryo remains essentially normal. Differentiation becomes reversibly suspended, with the enhancement of certain early mRNA expressions and the reversible suppression of certain late mRNA expressions, characteristic of differentiated tissues.
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