Cdc14 phosphatase counteracts Cdk-dependent Dna2 phosphorylation to inhibit resection during recombinational DNA repair

Adrián Campos, Facundo Ramos, Lydia Iglesias, Celia Delgado, Eva Merino, Antonio Esperilla-Muñoz, Jaime Correa-Bordes and Andrés Clemente-Blanco ()
Additional contact information
Adrián Campos: Instituto de Biología Funcional y Genómica (IBFG), CSIC-USAL
Facundo Ramos: Instituto de Biología Funcional y Genómica (IBFG), CSIC-USAL
Lydia Iglesias: Instituto de Biología Funcional y Genómica (IBFG), CSIC-USAL
Celia Delgado: Instituto de Biología Funcional y Genómica (IBFG), CSIC-USAL
Eva Merino: Instituto de Biología Funcional y Genómica (IBFG), CSIC-USAL
Antonio Esperilla-Muñoz: Universidad de Extremadura
Jaime Correa-Bordes: Universidad de Extremadura
Andrés Clemente-Blanco: Instituto de Biología Funcional y Genómica (IBFG), CSIC-USAL

Nature Communications, 2023, vol. 14, issue 1, 1-20

Abstract: Abstract Cyclin-dependent kinase (Cdk) stimulates resection of DNA double-strand breaks ends to generate single-stranded DNA (ssDNA) needed for recombinational DNA repair. Here we show in Saccharomyces cerevisiae that lack of the Cdk-counteracting phosphatase Cdc14 produces abnormally extended resected tracts at the DNA break ends, involving the phosphatase in the inhibition of resection. Over-resection in the absence of Cdc14 activity is bypassed when the exonuclease Dna2 is inactivated or when its Cdk consensus sites are mutated, indicating that the phosphatase restrains resection by acting through this nuclease. Accordingly, mitotically activated Cdc14 promotes Dna2 dephosphorylation to exclude it from the DNA lesion. Cdc14-dependent resection inhibition is essential to sustain DNA re-synthesis, thus ensuring the appropriate length, frequency, and distribution of the gene conversion tracts. These results establish a role for Cdc14 in controlling the extent of resection through Dna2 regulation and demonstrate that the accumulation of excessively long ssDNA affects the accurate repair of the broken DNA by homologous recombination.

Date: 2023
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-023-38417-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-38417-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-023-38417-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().