Toggle Main Menu Toggle Search

Open Access padlockePrints

Telomere Dysfunction Triggers Palindrome Formation Independently of Double-Strand Break Repair Mechanisms

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.

Publication metadata

Author(s): Raykov V, Marvin ME, Louis EJ, Maringele L

Publication type: Article

Publication status: Published

Journal: Genetics

Year: 2016

Volume: 203

Issue: 4

Pages: 1659-1668

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


DOI: 10.1534/genetics.115.183020


Altmetrics provided by Altmetric


Funder referenceFunder name
81164Wellcome Trust