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Telomere stability and development of ctc1 mutants are rescued by inhibition of EJ recombination pathways in a telomerase-dependent manner.

Amiard S, Olivier M, Allain E, Choi K, Smith-Unna R, Henderson IR, White CI, Gallego ME - Nucleic Acids Res. (2014)

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.

View Article: PubMed Central - PubMed

Affiliation: Génétique, Reproduction et Développement, UMR CNRS 6293, Clermont Université, INSERM U1103, Aubière, France megalleg@univ-bpclermont.fr.

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Knockout of EJ recombination rescues ctc1 mutants. (A) The phenotypes of the mutants are analysed six weeks after germination. Growth phenotypes are classified as ‘wild type-like’ (class 1) or stunted, abnormal/fasciated (class 2). Bar at lower left = 1 cm. (B) Percentages of plants of class 1 (blue fill) and class 2 (red fill) phenotypes for second and third generation ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants. (C) Table presenting the percentage of anaphases with chromosomal bridges observed after cytogenetic analysis of flower pistil nuclei (from three different plants in each case) of ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants in generation 2 and 3.
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Figure 1: Knockout of EJ recombination rescues ctc1 mutants. (A) The phenotypes of the mutants are analysed six weeks after germination. Growth phenotypes are classified as ‘wild type-like’ (class 1) or stunted, abnormal/fasciated (class 2). Bar at lower left = 1 cm. (B) Percentages of plants of class 1 (blue fill) and class 2 (red fill) phenotypes for second and third generation ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants. (C) Table presenting the percentage of anaphases with chromosomal bridges observed after cytogenetic analysis of flower pistil nuclei (from three different plants in each case) of ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants in generation 2 and 3.

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.


Telomere stability and development of ctc1 mutants are rescued by inhibition of EJ recombination pathways in a telomerase-dependent manner.

Amiard S, Olivier M, Allain E, Choi K, Smith-Unna R, Henderson IR, White CI, Gallego ME - Nucleic Acids Res. (2014)

Knockout of EJ recombination rescues ctc1 mutants. (A) The phenotypes of the mutants are analysed six weeks after germination. Growth phenotypes are classified as ‘wild type-like’ (class 1) or stunted, abnormal/fasciated (class 2). Bar at lower left = 1 cm. (B) Percentages of plants of class 1 (blue fill) and class 2 (red fill) phenotypes for second and third generation ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants. (C) Table presenting the percentage of anaphases with chromosomal bridges observed after cytogenetic analysis of flower pistil nuclei (from three different plants in each case) of ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants in generation 2 and 3.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4231758&req=5

Figure 1: Knockout of EJ recombination rescues ctc1 mutants. (A) The phenotypes of the mutants are analysed six weeks after germination. Growth phenotypes are classified as ‘wild type-like’ (class 1) or stunted, abnormal/fasciated (class 2). Bar at lower left = 1 cm. (B) Percentages of plants of class 1 (blue fill) and class 2 (red fill) phenotypes for second and third generation ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants. (C) Table presenting the percentage of anaphases with chromosomal bridges observed after cytogenetic analysis of flower pistil nuclei (from three different plants in each case) of ctc1, ctc1 ku80 xrcc1, ctc1 ku80 xrcc1 xpf and ku80 xrcc1 xpf mutants in generation 2 and 3.
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.

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.

View Article: PubMed Central - PubMed

Affiliation: Génétique, Reproduction et Développement, UMR CNRS 6293, Clermont Université, INSERM U1103, Aubière, France megalleg@univ-bpclermont.fr.

Show MeSH
Related in: MedlinePlus