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卡哈尔体数量的控制由卷曲螺旋蛋白的C末端介导。

Control of Cajal body number is mediated by the coilin C-terminus.

作者信息

Shpargel Karl B, Ospina Jason K, Tucker Karen E, Matera A Gregory, Hebert Michael D

机构信息

Department of Genetics, Center for Human Genetics and Program in Cell Biology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106-4955, USA.

出版信息

J Cell Sci. 2003 Jan 15;116(Pt 2):303-12. doi: 10.1242/jcs.00211.

Abstract

Cajal bodies (CBs) are nuclear suborganelles implicated in the post-transcriptional maturation of small nuclear and small nucleolar RNAs. The number of CBs displayed by various cell lines and tissues varies, and factors that control CB numbers within a given cell have yet to be described. In this report, we show that specific regions within the C-terminus of coilin, the CB marker protein, are responsible for regulating the number of nuclear foci. Despite the fact that the coilin N-terminal domain is responsible for its self-oligomerization activity, truncation or mutation of predicted sites of phosphorylation in the conserved C-terminal region leads to a striking alteration in the number of nuclear bodies. Similarly, coilin constructs from various species display differential propensities to form nuclear foci when expressed in heterologous backgrounds. We mapped the domain responsible for this variability to the coilin C-terminus utilizing chimeric proteins. Furthermore, the activities responsible for regulating coilin self-association must reside in the nucleus, as constructs lacking critical nuclear localization sequences fail to form foci in the cytoplasm. Factors controlling the putative signal transduction cascade that phosphorylates coilin are also discussed. The results point to a model whereby phosphorylation of the coilin C-terminus regulates the availability of the N-terminal self-interaction domain.

摘要

卡哈尔体(CBs)是细胞核亚细胞器,与小核RNA和小核仁RNA的转录后成熟有关。不同细胞系和组织中显示的卡哈尔体数量各不相同,且尚未明确控制特定细胞内卡哈尔体数量的因素。在本报告中,我们表明卡哈尔体标记蛋白卷曲螺旋蛋白(coilin)C末端的特定区域负责调节核仁的数量。尽管卷曲螺旋蛋白的N末端结构域负责其自身寡聚化活性,但保守C末端区域中预测的磷酸化位点的截断或突变会导致核体数量发生显著变化。同样,来自不同物种的卷曲螺旋蛋白构建体在异源背景中表达时,形成核仁的倾向也不同。我们利用嵌合蛋白将导致这种变异性的结构域定位到卷曲螺旋蛋白的C末端。此外,负责调节卷曲螺旋蛋白自缔合的活性必定存在于细胞核中,因为缺乏关键核定位序列的构建体无法在细胞质中形成核仁。我们还讨论了控制使卷曲螺旋蛋白磷酸化的假定信号转导级联反应的因素。研究结果指向一个模型,即卷曲螺旋蛋白C末端的磷酸化调节N末端自我相互作用结构域的可用性。

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