Degeneration of archenteron in sea urchin embryos caused by α,α′-dipyridyl

Abstract

Degeneration of the archenteron in middle gastrulae occurred in the presence of α,α′-dipyridyl or Zn 2+, inhibitors of prolyl hydroxylase. In the presence of these substances the archenteron degenerated and was eventually destroyed. Adding Fe 2+ to the embryo culture containing α,α′-dipyridyl protected the archenteron from further degeneration, but the collapsed archenteron was not restored to the upright position. At the late gastrula stage, α,α′-dipyridyl did not cause the degeneration of the archenteron. Treatment of the embryos by α,α′-dipyridyl, starting at the swimming blastula stage, resulted in the production of many mesenchyme-like cells but archenteron was not produced in the embryos. Addition of Fe 2+ to α,α′-dipyridyl culture, just before the beginning of gastrulation of normal embryos, resulted in the formation of normal archenteron. α,α′-Dipyridyl inhibited hydroxylation of proline residues of collagen in sea urchin embryos and Fe 2+ prevented the inhibition by α,α′-dipyridyl. Respiration was not inhibited by α,α′-dipyridyl.