沿一個DNA鏈向相反方向運動的兩個復(fù)制叉之間的碰撞，預(yù)計會經(jīng)常發(fā)生在具有多個復(fù)制起源的真核細胞中,。Christian Rudolph等人利用一個細菌系統(tǒng)來觀察這種碰撞對細胞的影響。他們發(fā)現(xiàn),，碰撞點可被用來獨立于一個活性來源重新啟動復(fù)制,，這可能具有潛在的致病效應(yīng)。RecG轉(zhuǎn)位酶和幾種核酸外切酶能防止這種事件的發(fā)生,，從而維持基因組的穩(wěn)定性,。（生物谷 Bioon.com）
生物谷推薦的英文摘要
Nature doi:10.1038/nature12312
Avoiding chromosome pathology when replication forks collide
Christian J. Rudolph, Amy L. Upton, Anna Stockum, Conrad A. Nieduszynski & Robert G. Lloyd
Chromosome duplication normally initiates through the assembly of replication fork complexes at defined origins1, 2. 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 translocase3 and by single-strand DNA exonucleases. Without RecG, replication initiates where forks meet through a replisome assembly mechanism normally associated with fork repair, replication restart and recombination4, 5, 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.
