Ku is required for telomeric C-rich strand maintenance but not for end-to-end chromosome fusions in Arabidopsis.
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abstract
Telomere dysfunction arising from mutations in telomerase or in telomere capping proteins leads to end-to-end chromosome fusions. Paradoxically, the Ku7080 heterodimer, essential for nonhomologous end-joining double-strand break repair, is also found at telomeres, and in mammals it is required to prevent telomere fusion. Previously, we showed that inactivation of Ku70 in Arabidopsis results in telomere lengthening. Here, we have demonstrated that this telomere elongation is telomerase dependent. Further, we found that the terminal 3' G overhang was significantly extended in ku70 mutants and in plants deficient in both Ku70 and the catalytic subunit of telomerase (TERT), implying that Ku is needed for proper maintenance of the telomeric C-rich strand. Consistent with inefficient C-strand maintenance, telomere shortening was accelerated in ku70 tert double mutants, and the onset of a terminal sterile phenotype was reached two to three times faster than in tert single mutants. Unexpectedly, abundant anaphase bridges were found in terminal plants harboring critically shortened telomeres, indicating that Ku is not required for the formation of end-to-end chromosome fusions in telomerase-deficient Arabidopsis. Together, these findings define Ku70 as a gene in higher eukaryotes required for maintenance of the telomeric C-rich strand and underscore the complexity and diversity of molecular interactions at telomeres.
