Differentiation 1983 Jan 01;252:106-12. doi: 10.1111/j.1432-0436.1984.tb01346.x.

Degeneration of archenteron in sea urchin embryos caused by alpha,alpha''-dipyridyl.

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Degeneration of the archenteron in middle gastrulae occurred in the presence of alpha,alpha''-dipyridyl or Zn2+, inhibitors of prolyl hydroxylase. In the presence of these substances the archenteron degenerated and was eventually destroyed. Adding Fe2+ to the embryo culture containing alpha,alpha''-dipyridyl protected the archenteron from further degeneration, but the collapsed archenteron was not restored to the upright position. At the late gastrula stage, alpha,alpha''-dipyridyl did not cause the degeneration of the archenteron. Treatment of the embryos by alpha,alpha''-dipyridyl, starting at the swimming blastula state, resulted in the production of many mesenchyme-like cells but archenteron was not produced in the embryos. Addition of Fe2+ to alpha, alpha''-dipyridyl culture, just before the beginning of gastrulation of normal embryos, resulted in the formation of normal archenteron. alpha,alpha''-Dipyridyl inhibited hydroxylation of proline residues of collagen in sea urchin embryos and Fe2+ prevented the inhibition by alpha,alpha''-dipyridyl. Respiration was not inhibited by alpha,alpha''-dipyridyl.

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Genes referenced: LOC100887844 pelp1