首页> 外文期刊>Developmental dynamics: an official publication of the American Association of Anatomists >Dual mechanisms governing muscle cell death in tadpole tail during amphibian metamorphosis.
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Dual mechanisms governing muscle cell death in tadpole tail during amphibian metamorphosis.

机译:在两栖动物变态过程中控制t尾肌细胞死亡的双重机制。

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摘要

The tadpole tail, which is twice as long as the body, is induced to resorb completely by thyroid hormone within several days during the anuran metamorphosis. To investigate the underlying mechanism, we undertook two approaches. First, we examined the effect of dominant-negative thyroid hormone receptor (DNTR) on muscle cell death in vitro. The overexpression of DNTR suppressed the death of a tail-derived myoblastic cell line induced by thyroid hormone. Second, tadpole tails were injected with a reporter gene and the DNTR expression construct, and the reporter gene expression in muscle cells was followed during the spontaneous metamorphosis. DNTR overexpression inhibited a decrease of the reporter gene expression that began at stage 57 in the control tadpoles but only delayed massive muscle cell death at stage 63 when tails shrink very rapidly. Some remained even a few weeks after the metamorphosis, although most DNTR-overexpressing cells died by the end of the metamorphosis. These results led us to propose that thyroid hormone induces the suicide of muscle cells (the cell-autonomous death) in the tail between stage 57 and 62 and that both the murder and suicide mechanisms execute muscle cell death in stage 62-64 to remove muscle promptly and completely. Developmental Dynamics 227:246-255, 2003.
机译:an的尾巴长两倍于身体,在无色变态的几天内被甲状腺激素完全吸收。为了研究潜在的机制,我们采取了两种方法。首先,我们检查了显性阴性甲状腺激素受体(DNTR)对体外肌肉细胞死亡的影响。 DNTR的过表达抑制了甲状腺激素诱导的源自尾的成肌细胞系的死亡。其次,向t尾部注射报告基因和DNTR表达构建体,并在自发性变态过程中追踪肌细胞中报告基因的表达。 DNTR的过量表达抑制了对照组t从57阶段开始的报告基因表达的下降,但仅在63阶段尾巴迅速收缩时才延迟了大规模的肌肉细胞死亡。尽管大多数过度表达DNTR的细胞在变态结束时就死亡了,但在变态后的几周内仍保留了一些。这些结果使我们提出,甲状腺激素在57至62期之间导致尾巴中的肌细胞自杀(细胞自主死亡),而谋杀和自杀机制均在62-64期执行了肌细胞死亡以去除肌肉。及时而完整。发展动态227:246-255,2003年。

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