Organelle DNA rearrangement mapping reveals U-turn-like inversions as a major source of genomic instability in Arabidopsis and humans
Identifieur interne : 000616 ( Main/Exploration ); précédent : 000615; suivant : 000617Organelle DNA rearrangement mapping reveals U-turn-like inversions as a major source of genomic instability in Arabidopsis and humans
Auteurs : Éric Zampini ; Étienne Lepage ; Samuel Tremblay-Belzile ; Sébastien Truche ; Normand BrissonSource :
- Genome Research [ 1088-9051 ] ; 2015.
Abstract
Failure to maintain organelle genome stability has been linked to numerous phenotypes, including variegation and cytosolic male sterility (CMS) in plants, as well as cancer and neurodegenerative diseases in mammals. Here we describe a next-generation sequencing approach that precisely maps and characterizes organelle DNA rearrangements in a single genome-wide experiment. In addition to displaying global portraits of genomic instability, it surprisingly unveiled an abundance of short-range rearrangements in
Url:
DOI: 10.1101/gr.188573.114
PubMed: 25800675
PubMed Central: 4417113
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Failure to maintain organelle genome stability has been linked to numerous phenotypes, including variegation and cytosolic male sterility (CMS) in plants, as well as cancer and neurodegenerative diseases in mammals. Here we describe a next-generation sequencing approach that precisely maps and characterizes organelle DNA rearrangements in a single genome-wide experiment. In addition to displaying global portraits of genomic instability, it surprisingly unveiled an abundance of short-range rearrangements in <italic>Arabidopsis thaliana</italic>
and human organelles. Among these, short-range U-turn-like inversions reach 25% of total rearrangements in wild-type <italic>Arabidopsis</italic>
plastids and 60% in human mitochondria. Furthermore, we show that replication stress correlates with the accumulation of this type of rearrangement, suggesting that U-turn-like rearrangements could be the outcome of a replication-dependent mechanism. We also show that U-turn-like rearrangements are mostly generated using microhomologies and are repressed in plastids by Whirly proteins WHY1 and WHY3. A synergistic interaction is also observed between the genes for the plastid DNA recombinase <italic>RECA1</italic>
and those encoding plastid Whirly proteins, and the triple mutant <italic>why1why3reca1</italic>
accumulates almost 60 times the WT levels of U-turn-like rearrangements. We thus propose that the process leading to U-turn-like rearrangements may constitute a RecA-independent mechanism to restart stalled forks. Our results reveal that short-range rearrangements, and especially U-turn-like rearrangements, are a major factor of genomic instability in organelles, and this raises the question of whether they could have been underestimated in diseases associated with mitochondrial dysfunction.</p>
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<name sortKey="Zampini, Eric" sort="Zampini, Eric" uniqKey="Zampini E" first="Éric" last="Zampini">Éric Zampini</name>
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