RPA shields inherited DNA lesions for post-mitotic DNA synthesis

The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of herit...

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Veröffentlicht in:Nature communications Jg. 12; H. 1; S. 3827 - 15
Hauptverfasser: Lezaja, Aleksandra, Panagopoulos, Andreas, Wen, Yanlin, Carvalho, Edison, Imhof, Ralph, Altmeyer, Matthias
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London Nature Publishing Group UK 22.06.2021
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631/337/1427
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Cancer
Cell cycle
Cell Cycle - genetics
Cell Line
Cell Line, Tumor
Deoxyribonucleic acid
DNA
DNA - genetics
DNA - metabolism
DNA biosynthesis
DNA Damage
DNA Repair
DNA Replication - genetics
Fragility
Genomes
HeLa Cells
Humanities and Social Sciences
Humans
Lesions
Microscopy, Confocal
Mitosis - genetics
multidisciplinary
Protein A
Proteins
Repair
Replication
Replication protein A
Replication Protein A - genetics
Replication Protein A - metabolism
Science
Science (multidisciplinary)
Shielding
Shields
Single-stranded DNA
Synthesis
Telomere - genetics
Telomere - metabolism
Telomeres
Time-Lapse Imaging - methods
Tumor Suppressor p53-Binding Protein 1 - genetics
Tumor Suppressor p53-Binding Protein 1 - metabolism
Yeast
Zebrafish
ISSN:2041-1723, 2041-1723
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Abstract The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of heritable DNA lesions, which is marked by replication protein A (RPA), a protein primarily known for shielding single-stranded DNA in S/G2. We demonstrate that post-mitotic RPA foci occur at low frequency during unperturbed cell cycle progression, originate from the previous cell cycle, and are exacerbated upon replication stress. RPA-marked inherited ssDNA lesions are found at telomeres, particularly of ALT-positive cancer cells. We reveal that RPA protects these replication remnants in G1 to allow for post-mitotic DNA synthesis (post-MiDAS). Given that ALT-positive cancer cells exhibit high levels of replication stress and telomere fragility, targeting post-MiDAS might be a new therapeutic opportunity. Single-stranded DNA during DNA replication and repair in S/G2 needs protection by replication protein A (RPA). Here the authors reveal that RPA also shields inherited single-stranded DNA in G1, representing replication remnants from the previous cell cycle, to allow for post-mitotic DNA synthesis.
AbstractList The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of heritable DNA lesions, which is marked by replication protein A (RPA), a protein primarily known for shielding single-stranded DNA in S/G2. We demonstrate that post-mitotic RPA foci occur at low frequency during unperturbed cell cycle progression, originate from the previous cell cycle, and are exacerbated upon replication stress. RPA-marked inherited ssDNA lesions are found at telomeres, particularly of ALT-positive cancer cells. We reveal that RPA protects these replication remnants in G1 to allow for post-mitotic DNA synthesis (post-MiDAS). Given that ALT-positive cancer cells exhibit high levels of replication stress and telomere fragility, targeting post-MiDAS might be a new therapeutic opportunity. Single-stranded DNA during DNA replication and repair in S/G2 needs protection by replication protein A (RPA). Here the authors reveal that RPA also shields inherited single-stranded DNA in G1, representing replication remnants from the previous cell cycle, to allow for post-mitotic DNA synthesis.
The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of heritable DNA lesions, which is marked by replication protein A (RPA), a protein primarily known for shielding single-stranded DNA in S/G2. We demonstrate that post-mitotic RPA foci occur at low frequency during unperturbed cell cycle progression, originate from the previous cell cycle, and are exacerbated upon replication stress. RPA-marked inherited ssDNA lesions are found at telomeres, particularly of ALT-positive cancer cells. We reveal that RPA protects these replication remnants in G1 to allow for post-mitotic DNA synthesis (post-MiDAS). Given that ALT-positive cancer cells exhibit high levels of replication stress and telomere fragility, targeting post-MiDAS might be a new therapeutic opportunity.
The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of heritable DNA lesions, which is marked by replication protein A (RPA), a protein primarily known for shielding single-stranded DNA in S/G2. We demonstrate that post-mitotic RPA foci occur at low frequency during unperturbed cell cycle progression, originate from the previous cell cycle, and are exacerbated upon replication stress. RPA-marked inherited ssDNA lesions are found at telomeres, particularly of ALT-positive cancer cells. We reveal that RPA protects these replication remnants in G1 to allow for post-mitotic DNA synthesis (post-MiDAS). Given that ALT-positive cancer cells exhibit high levels of replication stress and telomere fragility, targeting post-MiDAS might be a new therapeutic opportunity.Single-stranded DNA during DNA replication and repair in S/G2 needs protection by replication protein A (RPA). Here the authors reveal that RPA also shields inherited single-stranded DNA in G1, representing replication remnants from the previous cell cycle, to allow for post-mitotic DNA synthesis.
Single-stranded DNA during DNA replication and repair in S/G2 needs protection by replication protein A (RPA). Here the authors reveal that RPA also shields inherited single-stranded DNA in G1, representing replication remnants from the previous cell cycle, to allow for post-mitotic DNA synthesis.
The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of heritable DNA lesions, which is marked by replication protein A (RPA), a protein primarily known for shielding single-stranded DNA in S/G2. We demonstrate that post-mitotic RPA foci occur at low frequency during unperturbed cell cycle progression, originate from the previous cell cycle, and are exacerbated upon replication stress. RPA-marked inherited ssDNA lesions are found at telomeres, particularly of ALT-positive cancer cells. We reveal that RPA protects these replication remnants in G1 to allow for post-mitotic DNA synthesis (post-MiDAS). Given that ALT-positive cancer cells exhibit high levels of replication stress and telomere fragility, targeting post-MiDAS might be a new therapeutic opportunity.The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping checkpoint control. How such inherited lesions affect genome function and integrity is not well understood. Here, we identify a new class of heritable DNA lesions, which is marked by replication protein A (RPA), a protein primarily known for shielding single-stranded DNA in S/G2. We demonstrate that post-mitotic RPA foci occur at low frequency during unperturbed cell cycle progression, originate from the previous cell cycle, and are exacerbated upon replication stress. RPA-marked inherited ssDNA lesions are found at telomeres, particularly of ALT-positive cancer cells. We reveal that RPA protects these replication remnants in G1 to allow for post-mitotic DNA synthesis (post-MiDAS). Given that ALT-positive cancer cells exhibit high levels of replication stress and telomere fragility, targeting post-MiDAS might be a new therapeutic opportunity.
ArticleNumber 3827
Author Wen, Yanlin
Panagopoulos, Andreas
Carvalho, Edison
Lezaja, Aleksandra
Imhof, Ralph
Altmeyer, Matthias
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  givenname: Edison
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  surname: Carvalho
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  surname: Altmeyer
  fullname: Altmeyer, Matthias
  email: matthias.altmeyer@uzh.ch
  organization: Department of Molecular Mechanisms of Disease, University of Zurich
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34158486$$D View this record in MEDLINE/PubMed
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PublicationPlace_xml – name: London
– name: England
PublicationTitle Nature communications
PublicationTitleAbbrev Nat Commun
PublicationTitleAlternate Nat Commun
PublicationYear 2021
Publisher Nature Publishing Group UK
Nature Publishing Group
Nature Portfolio
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
– name: Nature Portfolio
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Snippet The paradigm that checkpoints halt cell cycle progression for genome repair has been challenged by the recent discovery of heritable DNA lesions escaping...
Single-stranded DNA during DNA replication and repair in S/G2 needs protection by replication protein A (RPA). Here the authors reveal that RPA also shields...
SourceID doaj
pubmedcentral
proquest
pubmed
crossref
springer
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Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 3827
SubjectTerms 14/63
49
49/47
631/337/1427
631/337/1427/2566
631/80
631/80/103/560
631/80/641/151
Cancer
Cell cycle
Cell Cycle - genetics
Cell Line
Cell Line, Tumor
Deoxyribonucleic acid
DNA
DNA - genetics
DNA - metabolism
DNA biosynthesis
DNA Damage
DNA Repair
DNA Replication - genetics
Fragility
Genomes
HeLa Cells
Humanities and Social Sciences
Humans
Lesions
Microscopy, Confocal
Mitosis - genetics
multidisciplinary
Protein A
Proteins
Repair
Replication
Replication protein A
Replication Protein A - genetics
Replication Protein A - metabolism
Science
Science (multidisciplinary)
Shielding
Shields
Single-stranded DNA
Synthesis
Telomere - genetics
Telomere - metabolism
Telomeres
Time-Lapse Imaging - methods
Tumor Suppressor p53-Binding Protein 1 - genetics
Tumor Suppressor p53-Binding Protein 1 - metabolism
Yeast
Zebrafish
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Title RPA shields inherited DNA lesions for post-mitotic DNA synthesis
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