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Field | Value |
---|---|
Namespace | Biological process |
Short description | Mitotic recombination-dependent replication fork processing |
Full defintion | Replication fork processing that includes recombination between DNA near the arrested fork and homologous sequences. Proteins involved in homologous recombination are required for replication restart. |
Subterm of |
The relationship of GO:1990426 with other GO terms.
Relationship type | GO terms |
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Is a | |
Regulates | n.a. |
Part of | n.a. |
Positively regulates | n.a. |
Negatively regulates | n.a. |
A force layout showing the ancestor tree for GO:1990426, and its immediate children. If you wish to explore the tree dynamically, please use the GO Explorer.
This table contains additional metadata associated with the GO entry's definition field.
Field | Value |
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GOC | mah |
PMID | Recovery of arrested replication forks by homologous recombination is error-prone. PLoS Genet. 2012; 8 (10): e1002976.PMID: 23093942 Homologous recombination is a universal mechanism that allows repair of DNA and provides support for DNA replication. Homologous recombination is therefore a major pathway that suppresses non-homology-mediated genome instability. Here, we report that recovery of impeded replication forks by homologous recombination is error-prone. Using a fork-arrest-based assay in fission yeast, we demonstrate that a single collapsed fork can cause mutations and large-scale genomic changes, including deletions and translocations. Fork-arrest-induced gross chromosomal rearrangements are mediated by inappropriate ectopic recombination events at the site of collapsed forks. Inverted repeats near the site of fork collapse stimulate large-scale genomic changes up to 1,500 times over spontaneous events. We also show that the high accuracy of DNA replication during S-phase is impaired by impediments to fork progression, since fork-arrest-induced mutation is due to erroneous DNA synthesis during recovery of replication forks. The mutations caused are small insertions/duplications between short tandem repeats (micro-homology) indicative of replication slippage. Our data establish that collapsed forks, but not stalled forks, recovered by homologous recombination are prone to replication slippage. The inaccuracy of DNA synthesis does not rely on PCNA ubiquitination or trans-lesion-synthesis DNA polymerases, and it is not counteracted by mismatch repair. We propose that deletions/insertions, mediated by micro-homology, leading to copy number variations during replication stress may arise by progression of error-prone replication forks restarted by homologous recombination. |
GO predictions are based solely on the InterPro-to-GO mappings published by EMBL-EBI, which are in turn based on the mapping of predicted domains to the InterPro dataset. The InterPro-to-GO mapping was last updated on , while the GO metadata was last updated on .
Transcript | Name | Description | GO terms | GO count |
---|---|---|---|---|
– | PREDICTED: DNA repair protein RAD51 homolog 1-like [Cicer arietinum] gi|502150634|ref|XP_004508049.1| | 6 | ||
– | DNA repair protein RAD51 like 1; TAIR: AT5G20850.1 RAS associated with diabetes protein 51; Swiss-Prot: sp|P94102|RAD51_ARATH DNA repair protein RAD51 homolog 1; TrEMBL-Plants: tr|A0A151SSM0|A0A151SSM0_CAJCA DNA repair protein RAD51 isogeny 1; Found in the gene: LotjaGi4g1v0319500 | 6 |
A list of co-occurring GO terms within the L. japonicus gene space:
GO term | Namespace | Name | Observations | Saturation (%) |
---|---|---|---|---|
Biological process | Mitotic recombination-dependent replication fork processing | 1 | 50.00 |