In Vivo Binding of Recombination Proteins to Non-DSB DNA Lesions and to Replication Forks

González-Prieto, Román; Cabello-Lobato, María J.; Prado, Félix

doi:10.1007/978-1-0716-0644-5_31

Cited by 3 publications

(2 citation statements)

References 14 publications

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“…In this assay, cells expressing a chimera of the protein of interest fused to MNase are permeabilized with digitonin and treated with Ca 2+ ions for different periods to activate the nuclease; then, total DNA is extracted and analyzed for the presence of specific cuts. We have used this method to follow the binding of repair factors to ssDNA gaps scattered throughout the genome as those generated by MMS (González‐Prieto et al , 2013, 2020). Here, total DNA is analyzed on an agarose gel.…”

Section: Resultsmentioning

confidence: 99%

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Non‐recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance

et al. 2020

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DNA damage tolerance relies on homologous recombination (HR) and translesion synthesis (TLS) mechanisms to fill in the ssDNA gaps generated during passing of the replication fork over DNA lesions in the template. Whereas TLS requires specialized polymerases able to incorporate a dNTP opposite the lesion and is error-prone, HR uses the sister chromatid and is mostly error-free. We report that the HR protein Rad52-but not Rad51 and Rad57acts in concert with the TLS machinery (Rad6/Rad18-mediated PCNA ubiquitylation and polymerases Rev1/Pol f) to repair MMS and UV light-induced ssDNA gaps through a non-recombinogenic mechanism, as inferred from the different phenotypes displayed in the absence of Rad52 and Rad54 (essential for MMS-and UVinduced HR); accordingly, Rad52 is required for efficient DNA damage-induced mutagenesis. In addition, Rad52, Rad51, and Rad57, but not Rad54, facilitate Rad6/Rad18 binding to chromatin and subsequent DNA damage-induced PCNA ubiquitylation. Therefore, Rad52 facilitates the tolerance process not only by HR but also by TLS through Rad51/Rad57-dependent and-independent processes, providing a novel role for the recombination proteins in maintaining genome integrity.

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Section: Resultsmentioning

confidence: 99%

“…Chromatin endogenous cleavage (ChEC) of Rad6‐MN cells was performed as reported (González‐Prieto et al , 2013, 2020). For cleavage induction, digitonin‐permeabilized cells were incubated with 2 mM CaCl 2 at 30°C under gentle agitation.…”

Section: Methodsmentioning

confidence: 99%

Non‐recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance

et al. 2020

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Physical interactions between MCM and Rad51 facilitate replication fork lesion bypass and ssDNA gap filling by non-recombinogenic functions

Cabello-Lobato¹,

González-Garrido²,

Cano-Linares³

et al. 2021

Cell Reports

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In Vivo Binding of Recombination Proteins to Non-DSB DNA Lesions and to Replication Forks

Cited by 3 publications

References 14 publications

Non‐recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance

Non‐recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance

Physical interactions between MCM and Rad51 facilitate replication fork lesion bypass and ssDNA gap filling by non-recombinogenic functions

Parental histone distribution and location of the replication obstacle at nascent strands control homologous recombination

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