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The bacterial MRE11–RAD50 and DNA2–WRN homologs process replication forks at distinct and separate loci on the chromosome.

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Title: The bacterial MRE11–RAD50 and DNA2–WRN homologs process replication forks at distinct and separate loci on the chromosome.
Authors: Spolek, Raymond L.1 (AUTHOR), Christian, Paden Y. H.1 (AUTHOR), Courcelle, Charmain T.1 (AUTHOR), Courcelle, Justin1 (AUTHOR) justc@pdx.edu
Source: FEBS Letters. Feb2026, Vol. 600 Issue 4, p451-466. 16p.
Subjects: Replication fork, Locus (Genetics), BRCA genes, DNA repair, Bacteria, Genetic mutation, Double-strand DNA breaks
Abstract: Human BRCA2 protects the DNA when replication forks stall, whereas MRE11–RAD50 and DNA2–WRN process or partially degrade these substrates. When mutated, these genes result in distinct genetic instabilities and cancers, arguing they have unique, not redundant, functions. Escherichia coli encodes functional homologs of MRE11–RAD50 (SbcC–SbcD), DNA2–WRN (RecJ–RecQ), and BRCA2 (RecF). Here, we use 2‐dimensional gels, pulse‐labelling, and replication‐profiling analysis to show the bacterial homologs act at distinct substrates and loci on the chromosome. Whereas RecF and RecJ–RecQ protect and process DNA at arrested replication forks to facilitate repair, RecBCD and SbcC–SbcD protect and process DNA at sites where forks converge. Comparing the assays used in E. coli to human cells, we consider whether these cellular roles may be functionally conserved.Impact statementBRCA2, MRE11‐RAD50, and WRN‐DNA2 encode human proteins that process replication forks and result in distinct genetic instabilities and cancers when mutated. Here, we show their bacterial homologs act on unique replication fork substrates—those at DNA damage sites or as replication completes, and discuss their possible functional conservation in humans. [ABSTRACT FROM AUTHOR]
Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
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DbLabel: Engineering Source
An: 191803825
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  Data: The bacterial MRE11–RAD50 and DNA2–WRN homologs process replication forks at distinct and separate loci on the chromosome.
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  Data: <searchLink fieldCode="JN" term="%22FEBS+Letters%22">FEBS Letters</searchLink>. Feb2026, Vol. 600 Issue 4, p451-466. 16p.
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  Data: <searchLink fieldCode="DE" term="%22Replication+fork%22">Replication fork</searchLink><br /><searchLink fieldCode="DE" term="%22Locus+%28Genetics%29%22">Locus (Genetics)</searchLink><br /><searchLink fieldCode="DE" term="%22BRCA+genes%22">BRCA genes</searchLink><br /><searchLink fieldCode="DE" term="%22DNA+repair%22">DNA repair</searchLink><br /><searchLink fieldCode="DE" term="%22Bacteria%22">Bacteria</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+mutation%22">Genetic mutation</searchLink><br /><searchLink fieldCode="DE" term="%22Double-strand+DNA+breaks%22">Double-strand DNA breaks</searchLink>
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  Data: Human BRCA2 protects the DNA when replication forks stall, whereas MRE11–RAD50 and DNA2–WRN process or partially degrade these substrates. When mutated, these genes result in distinct genetic instabilities and cancers, arguing they have unique, not redundant, functions. Escherichia coli encodes functional homologs of MRE11–RAD50 (SbcC–SbcD), DNA2–WRN (RecJ–RecQ), and BRCA2 (RecF). Here, we use 2‐dimensional gels, pulse‐labelling, and replication‐profiling analysis to show the bacterial homologs act at distinct substrates and loci on the chromosome. Whereas RecF and RecJ–RecQ protect and process DNA at arrested replication forks to facilitate repair, RecBCD and SbcC–SbcD protect and process DNA at sites where forks converge. Comparing the assays used in E. coli to human cells, we consider whether these cellular roles may be functionally conserved.Impact statementBRCA2, MRE11‐RAD50, and WRN‐DNA2 encode human proteins that process replication forks and result in distinct genetic instabilities and cancers when mutated. Here, we show their bacterial homologs act on unique replication fork substrates—those at DNA damage sites or as replication completes, and discuss their possible functional conservation in humans. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of FEBS Letters is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1002/1873-3468.70211
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        Text: English
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        PageCount: 16
        StartPage: 451
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      – SubjectFull: Replication fork
        Type: general
      – SubjectFull: Locus (Genetics)
        Type: general
      – SubjectFull: BRCA genes
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      – SubjectFull: DNA repair
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      – SubjectFull: Bacteria
        Type: general
      – SubjectFull: Genetic mutation
        Type: general
      – SubjectFull: Double-strand DNA breaks
        Type: general
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      – TitleFull: The bacterial MRE11–RAD50 and DNA2–WRN homologs process replication forks at distinct and separate loci on the chromosome.
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            NameFull: Spolek, Raymond L.
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            NameFull: Christian, Paden Y. H.
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              M: 02
              Text: Feb2026
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              Y: 2026
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