Remodeling of insulin producing β-cells during Xenopus laevis metamorphosis

摘要: Abstract Insulin-producing β-cells are present as single cells or in small clusters distributed throughout the pancreas of Xenopus laevis tadpole. During metamorphic climax when exocrine dedifferentiates to progenitor cells, undergo two changes. Insulin mRNA is down regulated at beginning (NF62) and reexpressed again near end climax. Secondly, aggregate form islets. increase insulin cluster size not caused by cell proliferation acinar-to-β-cell transdifferentiation, but rather due aggregation pre-existing β-cells. The total number does change during 8 days Thyroid hormone (TH) induction premetamorphic tadpoles causes an islet while prolonged treatment with goitrogen methimazole inhibits this increase. Expression a dominant negative thyroid receptor (TRDN) driven elastase promoter only protects transgenic tadpole from TH-induced dedifferentiation also prevents These do however normal loss resynthesis same stage controls. In contrast TRDN transgene regulation mRNA, islets like results demonstrate that TH controls remodeling through cell–cell interaction dedifferentiating acinar autonomous program temporarily shuts off gene.