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Slow down, enzymes at work

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Damage that severs both strands of a DNA molecule creates what's called a double-stranded break, or DSB... Sugimura et al. tested whether PARP-1 inhibits the movement of replication forks along the DNA molecule... In vitro studies suggested that it did, but in vivo evidence was lacking... In human cells, replication fork speed doubled after addition of RNAi that targeted PARP-1, the scientists found... A PARP-1 inhibitor had a similar effect... Cells deploy two mechanisms for mending DSBs—non-homologous end-joining (NHEJ) and homologous recombination (HR)... The team found that the replication forks decelerate in cells that can't perform NHEJ, but not in cells where HR is defective... That result suggests that replication fork slowing occurs because HR is at work repairing the break... PARP-1 helps delay the fork's progress, the researchers determined, by allowing HR proteins access to the DNA but obstructing the protein Ku70, which is necessary for NHEJ and can block HR.

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PARP-1 (green) associates with replicating regions of the genome (red and blue) and will slow fork progression during double-strand break repair.
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fig1: PARP-1 (green) associates with replicating regions of the genome (red and blue) and will slow fork progression during double-strand break repair.


Slow down, enzymes at work
PARP-1 (green) associates with replicating regions of the genome (red and blue) and will slow fork progression during double-strand break repair.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2606954&req=5

fig1: PARP-1 (green) associates with replicating regions of the genome (red and blue) and will slow fork progression during double-strand break repair.

View Article: PubMed Central

AUTOMATICALLY GENERATED EXCERPT
Please rate it.

Damage that severs both strands of a DNA molecule creates what's called a double-stranded break, or DSB... Sugimura et al. tested whether PARP-1 inhibits the movement of replication forks along the DNA molecule... In vitro studies suggested that it did, but in vivo evidence was lacking... In human cells, replication fork speed doubled after addition of RNAi that targeted PARP-1, the scientists found... A PARP-1 inhibitor had a similar effect... Cells deploy two mechanisms for mending DSBs—non-homologous end-joining (NHEJ) and homologous recombination (HR)... The team found that the replication forks decelerate in cells that can't perform NHEJ, but not in cells where HR is defective... That result suggests that replication fork slowing occurs because HR is at work repairing the break... PARP-1 helps delay the fork's progress, the researchers determined, by allowing HR proteins access to the DNA but obstructing the protein Ku70, which is necessary for NHEJ and can block HR.

No MeSH data available.


Related in: MedlinePlus