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首页> 外文期刊>Development >SoxB1 downregulation in vegetal lineages of sea urchin embryos is achieved by both transcriptional repression and selective protein turnover.
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SoxB1 downregulation in vegetal lineages of sea urchin embryos is achieved by both transcriptional repression and selective protein turnover.

机译:海胆胚胎的植物谱系中的SoxB1下调是通过转录抑制和选择性蛋白更新实现的。

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摘要

Patterning of cell fates along the sea urchin animal-vegetal embryonic axis requires the opposing functions of nuclear beta-catenin/TCF-Lef, which activates the endomesoderm gene regulatory network, and SoxB1, which antagonizes beta-catenin and limits its range of function. A crucial aspect of this interaction is the temporally controlled downregulation of SoxB1, first in micromeres and then in macromere progeny. We show that SoxB1 is regulated at the level of protein turnover in these lineages. This mechanism is dependent on nuclear beta-catenin function. It can be activated by Pmar1, but not by Krl, both of which function downstream of beta-catenin/TCF-Lef. At least partially distinct, lineage-specific mechanisms operate, as turnover in the macromeres depends on entry of SoxB1 into nuclei, and on redundant destruction signals, neither of which is required in micromeres. Neither of these turnover mechanisms operates in mesomere progeny, which give rise to ectoderm. However, in mesomeres, SoxB1 appearsto be subject to negative autoregulation that helps to maintain tight regulation of SoxB1 mRNA levels in presumptive ectoderm. Between the seventh and tenth cleavage stages, beta-catenin not only promotes degradation of SoxB1, but also suppresses accumulation of its message in macromere-derived blastomeres. Collectively, these different mechanisms work to regulate precisely the levels of SoxB1 in the progeny of different tiers of blastomeres arrayed along the animal-vegetal axis.
机译:沿着海胆动物-植物胚胎轴的细胞命运模式需要核β-catenin/ TCF-Lef的相反功能,后者激活内胚层基因调控网络,而SoxB1拮抗β-catenin并限制其功能范围。这种相互作用的一个至关重要的方面是暂时控制SoxB1的下调,首先是在小绒毛动物中,然后是大绒毛动物后代。我们表明,在这些谱系中,SoxB1在蛋白质更新的水平上受到调节。该机制取决于核β-连环蛋白功能。它可以由Pmar1激活,但不能由Krl激活,两者均在β-catenin/ TCF-Lef的下游起作用。至少部分不同的,特定于谱系的机制起作用,因为大分子的转换取决于SoxB1进入细胞核以及冗余的破坏信号,而在微分子中都不是必需的。这些周转机制都不在减数分裂后代中起作用,后者引起外胚层。但是,在子宫内膜中,SoxB1似乎受到负的自动调节,这有助于维持推测的外胚层中SoxB1 mRNA的严格调节。在第七和第十个切割阶段之间,β-连环蛋白不仅促进SoxB1的降解,而且还抑制了其信息在大麦衍生的卵裂球中的积累。集体地,这些不同的机制起作用以精确地调节沿动物-植物轴排列的不同级别的卵裂球的后代中SoxB1的水平。

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