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Avoiding chromosome pathology when replication forks collide

机译：复制叉碰撞时避免染色体病理

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摘要

沿一个DNA链向相反方向运动的两个复制叉之rn间的碰撞，预计会经常发生在具有多个复制起rn源的真核细胞中。Christian Rudolph等人利用rn一个细菌系统来观察这种碰撞对细胞的影响。rn他们发现，碰撞点可被用来独立于一个活性来rn源重新启动复制，这可能具有潜在的致病效rn应。RecG转位酶和几种核酸外切酶能防止这rn种事件的发生，从而维持基因组的稳定性。%Chromosome duplication normally initiates through the assembly of replication fork complexes at defined origins. DNA synthesis by any one fork is thought to cease when it meets another travelling in the opposite direction, at which stage the replication machinery may simply dissociate before the nascent strands are finally ligated. But what actually happens is not clear. Here we present evidence consistent with the idea that every fork collision has the potential to threaten genomic integrity. In Escherichia coli this threat is kept at bay by RecG DNA translocase and by single-strand DNA exonu-cleases. Without RecG, replication initiates where forks meet through a replisome assembly mechanism normally associated with fork repair, replication restart and recombination, establishing new forks with the potential to sustain cell growth and division without an active origin. This potential is realized when roadblocks to fork progression are reduced or eliminated. It relies on the chromosome being circular, reinforcing the idea that replication initiation is triggered repeatedly by fork collision. The results reported raise the question of whether replication fork collisions have pathogenic potential for organisms that exploit several origins to replicate each chromosome.
机译：沿一个DNA链向相反方向运动的两个复制叉之rn间的碰撞，预计会经常发生在具有多个复制起rn源的真核细胞中。Christian Rudolph等人利用rn一个细菌系统来观察这种碰撞对细胞的影响。rn他们发现，碰撞点可被用来独立于一个活性来rn源重新启动复制，这可能具有潜在的致病效rn应。RecG转位酶和几种核酸外切酶能防止这rn种事件的发生，从而维持基因组的稳定性。%Chromosome duplication normally initiates through the assembly of replication fork complexes at defined origins. DNA synthesis by any one fork is thought to cease when it meets another travelling in the opposite direction, at which stage the replication machinery may simply dissociate before the nascent strands are finally ligated. But what actually happens is not clear. Here we present evidence consistent with the idea that every fork collision has the potential to threaten genomic integrity. In Escherichia coli this threat is kept at bay by RecG DNA translocase and by single-strand DNA exonu-cleases. Without RecG, replication initiates where forks meet through a replisome assembly mechanism normally associated with fork repair, replication restart and recombination, establishing new forks with the potential to sustain cell growth and division without an active origin. This potential is realized when roadblocks to fork progression are reduced or eliminated. It relies on the chromosome being circular, reinforcing the idea that replication initiation is triggered repeatedly by fork collision. The results reported raise the question of whether replication fork collisions have pathogenic potential for organisms that exploit several origins to replicate each chromosome.

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  • 来源
    《Nature》 |2013年第7464期|608-611b2|共5页
  • 作者

    Christian J. Rudolph; Amy L. Upton; Anna Stockum1; Conrad A Nieduszynski; Robert G. Lloyd;

  • 作者单位

    Centre for Genetics and Genomics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK,Division of Biosciences, School of Health Sciences and Social Care, Brunei University, Uxbridge, London UB8 3PH, UK;

    Centre for Genetics and Genomics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK,Division of Biosciences, School of Health Sciences and Social Care, Brunei University, Uxbridge, London UB8 3PH, UK,Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK, Division of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK;

    Centre for Genetics and Genomics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK,Present addresses: Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK, Division of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK;

    Centre for Genetics and Genomics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK;

    Centre for Genetics and Genomics, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK;

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