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C16orf72/HAPSTR1/TAPR1 functions with BRCA1/Senataxin to modulate replication-associated R-loops and confer resistance to PARP disruption

Abstract:
While the toxicity of PARP inhibitors to cells with defects in homologous recombination (HR) is well established, other synthetic lethal interactions with PARP1/PARP2 disruption are poorly defined. To inform on these mechanisms we conducted a genome-wide screen for genes that are synthetic lethal with PARP1/2 gene disruption and identified C16orf72/HAPSTR1/TAPR1 as a novel modulator of replication-associated R-loops. C16orf72 is critical to facilitate replication fork restart, suppress DNA damage and maintain genome stability in response to replication stress. Importantly, C16orf72 and PARP1/2 function in parallel pathways to suppress DNA:RNA hybrids that accumulate at stalled replication forks. Mechanistically, this is achieved through an interaction of C16orf72 with BRCA1 and the RNA/DNA helicase Senataxin to facilitate their recruitment to RNA:DNA hybrids and confer resistance to PARP inhibitors. Together, this identifies a C16orf72/Senataxin/BRCA1-dependent pathway to suppress replication-associated R-loop accumulation, maintain genome stability and confer resistance to PARP inhibitors.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-023-40779-9

Authors

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Institution:
University of Oxford
Division:
MSD
Department:
Biochemistry
Role:
Author
ORCID:
0000-0003-2554-1025
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Biochemistry
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Biochemistry
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Biochemistry
Role:
Author


More from this funder
Funder identifier:
https://ror.org/029chgv08
Grant:
102348/Z/13/Z
More from this funder
Funder identifier:
https://ror.org/03x94j517
Grant:
MR/P028284/1
MR/P018963/1
MR/V00896X/1
MR/W017350/1


Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
14
Issue:
1
Article number:
5003
Publication date:
2023-09-17
Acceptance date:
2023-08-10
DOI:
EISSN:
2041-1723


Language:
English
Keywords:
Pubs id:
1506391
Local pid:
pubs:1506391
Deposit date:
2023-08-10
ARK identifier:

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