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Lookup NU author(s): Vasil Raykov,
Dr Laura Maringele
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Inverted chromosome duplications or palindromes are linked with genetic disorders and malignant transformation. They are considered by-products of DNA double-strand break (DSB) repair: the homologous recombination (HR) and the nonhomologous end joining (NHEJ). Palindromes near chromosome ends are often triggered by telomere losses. An important question is to what extent their formation depends upon DSB repair mechanisms. Here we addressed this question using yeast genetics and comparative genomic hybridization. We induced palindrome formation by passaging cells lacking any form of telomere maintenance (telomerase and telomere recombination). Surprisingly, we found that DNA ligase 4, essential for NHEJ, did not make a significant contribution to palindrome formation induced by telomere losses. Moreover RAD51, important for certain HR-derived mechanisms, had little effect. Furthermore RAD52, which is essential for HR in yeast, appeared to decrease the number of palindromes in cells proliferating without telomeres. This study also uncovered an important role for Rev3 and Rev7 (but not for Pol32) subunits of polymerase in the survival of cells undergoing telomere losses and forming palindromes. We propose a model called short-inverted repeat-induced synthesis in which DNA synthesis, rather than DSB repair, drives the inverted duplication triggered by telomere dysfunction.
Author(s): Raykov V, Marvin ME, Louis EJ, Maringele L
Publication type: Article
Publication status: Published
Print publication date: 01/08/2016
Online publication date: 11/08/2016
Acceptance date: 06/08/2016
Date deposited: 26/07/2017
ISSN (print): 0016-6731
ISSN (electronic): 1943-2631
Publisher: Genetics Society of America
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