Degeneration of archenteron in sea urchin embryos caused by alpha,alpha'-dipyridyl.
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.
D015082:2,2'-Dipyridyl / Q000494:pharmacology*; D000818:Animals; D003094:Collagen / Q000378:metabolism; D005260:Female; D005296:Ferrous Compounds / Q000494:pharmacology; D005775:Gastrula / Q000187:drug effects* / Q000378:metabolism; D006900:Hydroxylation; D010101:Oxygen Consumption / Q000187:drug effects; D011392:Proline / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology*; D012617:Sea Urchins / Q000196:embryology*; D013431:Sulfates / Q000494:pharmacology; D015032:Zinc / Q000494:pharmacology; D019287:Zinc Sulfate
D005296:Ferrous Compounds; D011725:Pyridines; D013431:Sulfates; C020748:ferrous sulfate; D015082:2,2'-Dipyridyl; D019287:Zinc Sulfate; D003094:Collagen; D011392:Proline; D015032:Zinc