English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Targeting of the Fun30 nucleosome remodeller by the Dpb11 scaffold facilitates cell cycle-regulated DNA end resection

MPS-Authors
/persons/resource/persons80777

Bantele,  Susanne C. S.
Pfander, Boris / DNA Replication and Genome Integrity, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons134055

Gritenaite,  Dalia
Pfander, Boris / DNA Replication and Genome Integrity, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons78499

Pfander,  Boris
Pfander, Boris / DNA Replication and Genome Integrity, Max Planck Institute of Biochemistry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)

e21687-download.pdf
(Publisher version), 3MB

Supplementary Material (public)

e21687-download.figures.pdf
(Supplementary material), 5MB

Citation

Bantele, S. C. S., Ferreira, P., Gritenaite, D., Boos, D., & Pfander, B. (2017). Targeting of the Fun30 nucleosome remodeller by the Dpb11 scaffold facilitates cell cycle-regulated DNA end resection. eLife, 6: e21687. doi:10.7554/eLife.21687.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-ED86-5
Abstract
DNA double strand breaks (DSBs) can be repaired by either recombination-based or direct ligation-based mechanisms. Pathway choice is made at the level of DNA end resection, a nucleolytic processing step, which primes DSBs for repair by recombination. Resection is thus under cell cycle control, but additionally regulated by chromatin and nucleosome remodellers. Here, we show that both layers of control converge in the regulation of resection by the evolutionarily conserved Fun30/SMARCAD1 remodeller. Budding yeast Fun30 and human SMARCAD1 are cell cycle-regulated by interaction with the DSB-localized scaffold protein Dpb11/TOPBP1, respectively. In yeast, this protein assembly additionally comprises the 9-1-1 damage sensor, is involved in localizing Fun30 to damaged chromatin, and thus is required for efficient long-range resection of DSBs. Notably, artificial targeting of Fun30 to DSBs is sufficient to bypass the cell cycle regulation of long-range resection, indicating that chromatin remodelling during resection is underlying DSB repair pathway choice.