Vannier Jean-Baptiste, Depeiges Annie, White Charles, Gallego Maria Eugenia
UMR 6547 CNRS/Université Blaise Pascal, Aubière cedex, France.
EMBO J. 2006 Oct 4;25(19):4577-85. doi: 10.1038/sj.emboj.7601345. Epub 2006 Sep 21.
We describe two roles for the Rad50 protein in telomere maintenance and the protection of chromosome ends. Using fluorescence in situ hybridisation (FISH) and fibre-FISH analyses, we show that absence of AtRad50 protein leads to rapid shortening of a subpopulation of chromosome ends and subsequently chromosome-end fusions lacking telomeric repeats. In the absence of telomerase, mutation of atrad50 has a synergistic effect on the number of chromosome end fusions. Surprisingly, this 'deprotection' of the shortened telomeres does not result in increased exonucleolytic degradation, but in a higher proportion of anaphase bridges containing telomeric repeats in atrad50/tert plants, compared to tert mutant plants. Absence of AtRad50 thus facilitates the action of recombination on these shortened telomeres. We propose that this protective role of Rad50 protein on shortened telomeres results from its action in constraining recombination to sister chromatids and thus avoiding end-to-end interactions.
我们阐述了Rad50蛋白在端粒维持和染色体末端保护中的两种作用。通过荧光原位杂交（FISH）和纤维FISH分析，我们发现AtRad50蛋白的缺失会导致一部分染色体末端迅速缩短，随后出现缺乏端粒重复序列的染色体末端融合。在没有端粒酶的情况下，atrad50的突变对染色体末端融合的数量具有协同作用。令人惊讶的是，这种对缩短端粒的“去保护”并没有导致核酸外切酶降解增加，而是与tert突变体植株相比，在atrad50/tert植株中含有端粒重复序列的后期桥的比例更高。因此，AtRad50的缺失促进了重组作用于这些缩短的端粒。我们认为，Rad50蛋白对缩短端粒的这种保护作用源于其将重组限制在姐妹染色单体上的作用，从而避免了端对端的相互作用。
