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Contributions of recombination and repair proteins to telomere maintenance in telomerase‐positive and negative Ustilago maydis Ustilago maydis

机译:重组和修复蛋白在端粒酶阳性和阴性Ustilago maydis Ustilago maydis中的贡献

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摘要

Summary Homologous recombination and repair factors are known to promote both telomere replication and recombination‐based telomere extension. Herein, we address the diverse contributions of several recombination/repair proteins to telomere maintenance in? Ustilago maydis , a fungus that bears strong resemblance to mammals with respect to telomere regulation and recombination mechanisms. In telomerase‐positive U. maydis , deletion of rad51 and blm separately caused shortened but stably maintained telomeres, whereas deletion of both engendered similar telomere loss, suggesting that the repair proteins help to resolve similar problems in telomere replication. In telomerase‐negative cells, the loss of Rad51 or Brh2 caused accelerated senescence and failure to generate survivors on semi‐solid medium. However, slow growing survivors can be isolated through continuous liquid culturing, and these survivors exhibit type II‐like as well as ALT‐like telomere features. In contrast, the trt1Δ blmΔ double mutant gives rise to survivors as readily as the trt1Δ single mutant, and like the single mutant survivors, exhibit almost exclusively type I‐like telomere features. In addition, we observed direct physical interactions between Blm and two telomere‐binding proteins, which may thus recruit or regulate Blm at telomeres. Our findings provide the basis for further analyzing the interplays between telomerase, telomere replication, and telomere recombination.
机译:发明内容已知同源重组和修复因子促进端粒复制和基于重组的端粒延伸。在此,我们解决了几种重组/修复蛋白的各种贡献,以重组维护? Ustilago maydis,一种与哺乳动物相对于端粒调节和重组机制相比强烈相似的真菌。在端粒酶阳性U. maydis中,缺失Rad51和Blm分别引起缩短但稳定地保持的端粒,而缺失具有合成的类似的端粒损失,表明修复蛋白有助于解决端粒复制中的类似问题。在端粒酶阴性细胞中,RAD51或BRH2的损失导致加速衰老和未在半固体培养基上产生幸存者。然而,可以通过连续液体培养分离缓慢生长的幸存者,并且这些幸存者表现出II型类似的以及Alt样的端粒特征。相反,TRT1ΔBLMδ双突变体使幸存者易于作为TRT1δ单突变体,并且与单个突变幸存者一样,几乎完全型I形端粒体特征。此外,我们观察到BLM和两种端粒结合蛋白之间的直接物理相互作用,这可以因此可以在端粒募集或调节BLM。我们的研究结果为进一步分析了端粒酶,端粒复制和端粒重组之间的相互作用提供了依据。

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  • 来源
    《Molecular Microbiology》 |2018年第1期|共13页
  • 作者单位

    Department of Microbiology &

    ImmunologyW. R. Hearst Microbiology Research Center Weill Medical;

    Department of Microbiology &

    ImmunologyW. R. Hearst Microbiology Research Center Weill Medical;

    Department of Microbiology &

    ImmunologyW. R. Hearst Microbiology Research Center Weill Medical;

    Department of Microbiology &

    ImmunologyW. R. Hearst Microbiology Research Center Weill Medical;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
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