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Pré-Publication, Document De Travail Année : 2023

The RecBC complex protects the nascent DNA in the presence of single stranded DNA gaps

Gaëlle Philippin
Élodie Chrabaszcz
  • Fonction : Auteur
Maialen Iturralde
  • Fonction : Auteur
Mauro Modesti
Luisa Laureti

Résumé

Following the encounter with an unrepaired DNA lesion, replication is halted and can restart downstream of the lesion leading to the formation of a single-stranded DNA (ssDNA) gap. To complete replication, this ssDNA gap is filled in by one of the two known lesion tolerance pathways: the error-prone Translesion Synthesis (TLS) or the error-free Homology Directed Gap Repair (HDGR). In the present work, we show a role for the RecBC complex that is distinct from its canonical function in homologous recombination at double strand breaks: RecBC (independently of the RecD subunit) is required to protect the 3'-end of the nascent DNA at the lesion site, in order to promote efficient lesion bypass. In the absence of RecBC, the nuclease ExoI can access and degrade the nascent DNA, thus strongly inhibiting the action of the TLS DNA polymerases and also affecting the HDGR mechanism. RecBC is recruited only when post-replicatively ssDNA gaps are formed and are covered by the single-stranded binding protein (SSB). This protective role of RecBC is reminiscent of BRCA2's role in human cells, once again highlighting the evolutionary conservation of DNA replication mechanisms across all living organisms.
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Dates et versions

hal-04271493 , version 1 (06-11-2023)

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Gaëlle Philippin, Élodie Chrabaszcz, Maialen Iturralde, Mauro Modesti, Vincent Pagès, et al.. The RecBC complex protects the nascent DNA in the presence of single stranded DNA gaps. 2023. ⟨hal-04271493⟩

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