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首页> 外文期刊>Molecular and Cellular Biology >Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification
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Telomerase- and Rad52-Independent Immortalization of Budding Yeast by an Inherited-Long-Telomere Pathway of Telomeric Repeat Amplification

机译：端粒重复重复序列的继承-长-端粒途径不依赖端粒酶和Rad52使酵母永生化。

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In the absence of telomerase, telomeres erode, provoking accumulation of DNA damage and death by senescence. Rare survivors arise, however, due to Rad52-based amplification of telomeric sequences by homologous recombination. The present study reveals that in budding yeast cells, postsenescence survival relying on amplification of the TG1-3 telomeric repeats can take place in the absence of Rad52 when overelongated telomeres are present during senescence (hence its designation ILT, for inherited-long-telomere, pathway). By growth competition, the Rad52-independent pathway was almost as efficient as the Rad51- and Rad52-dependent pathway that predominates in telomerase-negative cells. The ILT pathway could also be triggered by increased telomerase accessibility before telomerase removal, combined with loss of telomere protection, indicating that prior accumulation of recombination proteins was not required. The ILT pathway was dependent on Rad50 and Mre11 but not on the Rad51 recombinase and Rad59, thus making it distinct from both the type II (budding yeast ALT [alternative lengthening of telomeres]) and type I pathways amplifying the TG1-3 repeats and subtelomeric sequences, respectively. The ILT pathway also required the Rad1 endonuclease and Elg1, a replication factor C (RFC)-like complex subunit, but not Rad24 or Ctf18 (two subunits of two other RFC-like complexes), the Dnl4 ligase, Yku70, or Nej1. Possible mechanisms for this Rad52-independent pathway of telomeric repeat amplification are discussed. The effects of inherited long telomeres on Rad52-dependent recombination are also reported.
机译：在没有端粒酶的情况下，端粒会腐蚀，引起DNA损伤的积累和衰老导致死亡。然而，由于通过同源重组基于Rad52的端粒序列扩增，因此出现了罕见的幸存者。本研究表明，在发芽的酵母细胞中，当衰老过程中存在过度伸长的端粒时，依赖于TG 1-3 端粒重复序列的扩增可以进行衰老后存活（因此其名称为ILT） ，用于继承的长端粒途径）。通过生长竞争，Rad52依赖性途径几乎与端粒酶阴性细胞中占主导地位的Rad51和Rad52依赖性途径一样有效。还可以通过在端粒酶去除之前增加端粒酶的可及性，以及端粒保护的丧失，来触发ILT途径，这表明不需要重组蛋白的预先积累。 ILT途径依赖于Rad50和Mre11，但不依赖于Rad51重组酶和Rad59，因此使其不同于II型（芽孢酵母ALT [端粒的替代长度]）和I型途径，它们会扩增TG <1-> 3 重复序列和亚端粒序列。 ILT途径还需要Rad1核酸内切酶和Elg1，一个复制因子C（RFC）样的复杂亚基，但不需要Rad24或Ctf18（两个其他RFC样复合物的两个亚基），Dnl4连接酶，Yku70或Nej1。讨论了端粒重复扩增此Rad52独立途径的可能机制。还报道了遗传的长端粒对Rad52依赖重组的影响。

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