Telomere stability and development of ctc1 mutants are rescued by inhibition of EJ recombination pathways in a telomerase-dependent manner.
Bottom Line: In this work, we set out to specifically test this hypothesis in the plant, Arabidopsis.It is thus the chromosomal fusions, per se, which are the underlying cause of the severe developmental defects.This rescue is mediated by telomerase-dependent telomere extension, revealing a competition between telomerase and end-joining recombination proteins for access to deprotected telomeres.
Affiliation: Génétique, Reproduction et Développement, UMR CNRS 6293, Clermont Université, INSERM U1103, Aubière, France firstname.lastname@example.org.Show MeSH
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Mentions: Strikingly, the absence of all three EJ pathways leads to almost complete rescue of telomere-deprotected plants (Figure 1). While 18.9% of second generation (and 37.9% of third generation) of ctc1 mutant plants are completely sterile and show severe morphological defects, only 4.6% in the second generation (and 3.4% of third generation) plants deficient for the CST complex and the three known EJ pathways show this dramatic phenotype. This improved phenotype in ctc1 ku80 xrcc1 xpf plants is stable at least up to the fifth generation (data not shown). The absence of increased cell cycle arrest and cell death in this quadruple mutant is in accord with this wild-type phenotype (Supplementary Figure S1). An effect is also seen in ctc1 ku80 xrcc1 mutants, however this is not stable in subsequent generations, with 5.5% and 22.4% affected plants in second and third generations respectively (Figure 1A and B). That these effects are not simply due to the absence of the EJ pathways themselves is confirmed by the wild-type phenotype of second and third generation ku80 xrcc1 xpf plants.
Affiliation: Génétique, Reproduction et Développement, UMR CNRS 6293, Clermont Université, INSERM U1103, Aubière, France email@example.com.