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非洲爪蟾成纤维细胞生长因子受体在发育过程中的时间调控:3'非翻译区的一个翻译抑制元件。

Temporal regulation of the Xenopus FGF receptor in development: a translation inhibitory element in the 3' untranslated region.

作者信息

Robbie E P, Peterson M, Amaya E, Musci T J

机构信息

Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco 94143-0556, USA.

出版信息

Development. 1995 Jun;121(6):1775-85. doi: 10.1242/dev.121.6.1775.

Abstract

Early frog embryogenesis depends on a maternal pool of mRNA to execute critical intercellular signalling events. FGF receptor-1, which is required for normal development, is stored as a stable, untranslated maternal mRNA transcript in the fully grown immature oocyte, but is translationally activated at meiotic maturation. We have identified a short cis-acting element in the FGF receptor 3' untranslated region that inhibits translation of synthetic mRNA. This inhibitory element is sufficient to inhibit translation of heterologous reporter mRNA in the immature oocyte without changing RNA stability. Deletion of the poly(A) tract or polyadenylation signal sequences does not affect translational inhibition by this element. At meiotic maturation, we observe the reversal of translational repression mediated by the inhibitory element, mimicking that seen with endogenous maternal FGF receptor mRNA at meiosis. In addition, the activation of synthetic transcripts at maturation does not appear to require poly(A) lengthening. We also show that an oocyte cytoplasmic protein specifically binds the 3' inhibitory element, suggesting that translational repression of Xenopus FGF receptor-1 maternal mRNA in the oocytes is mediated by RNA-protein interactions. These data describe a mechanism of translational control that appears to be independent of poly(A) changes.

摘要

早期青蛙胚胎发育依赖于母源mRNA库来执行关键的细胞间信号传导事件。正常发育所必需的成纤维细胞生长因子受体1(FGF receptor-1),在完全成熟的未成熟卵母细胞中作为一种稳定的、未翻译的母源mRNA转录本储存,但在减数分裂成熟时被翻译激活。我们在FGF受体3'非翻译区鉴定出一个短的顺式作用元件,它能抑制合成mRNA的翻译。这个抑制元件足以在未成熟卵母细胞中抑制异源报告基因mRNA的翻译,而不改变RNA的稳定性。删除多聚腺苷酸尾或多聚腺苷酸化信号序列不影响该元件介导的翻译抑制。在减数分裂成熟时,我们观察到由抑制元件介导的翻译抑制的逆转,这与减数分裂时内源性母源FGF受体mRNA的情况相似。此外,成熟时合成转录本的激活似乎不需要多聚腺苷酸延长。我们还表明,一种卵母细胞胞质蛋白特异性结合3'抑制元件,这表明非洲爪蟾FGF受体-1母源mRNA在卵母细胞中的翻译抑制是由RNA-蛋白质相互作用介导的。这些数据描述了一种似乎独立于多聚腺苷酸变化的翻译控制机制。

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