APOBEC3C, a nucleolar protein induced by genotoxins, is excluded from DNA damage sites.

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License: CC BY-NC-ND 4.0
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Under indefinite embargo.
UNIL restricted access
State: Public
Version: Supplementary document
License: Not specified
Serval ID
serval:BIB_549304C0D4F3
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
APOBEC3C, a nucleolar protein induced by genotoxins, is excluded from DNA damage sites.
Journal
The FEBS journal
Author(s)
Constantin D., Dubuis G., Conde-Rubio MDC, Widmann C.
ISSN
1742-4658 (Electronic)
ISSN-L
1742-464X
Publication state
Published
Issued date
02/2022
Peer-reviewed
Oui
Volume
289
Number
3
Pages
808-831
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
The human genome contains 11 APOBEC (apolipoprotein B mRNA editing catalytic polypeptide-like) cytidine deaminases classified into four families. These proteins function mainly in innate antiviral immunity and can also restrict endogenous retrotransposable element multiplication. The present study focuses on APOBEC3C (A3C), a member of the APOBEC3 subfamily. Some APOBEC3 proteins use their enzymatic activity on genomic DNA, inducing mutations and DNA damage, while other members facilitate DNA repair. Our results show that A3C is highly expressed in cells treated with DNA-damaging agents. Its expression is regulated by p53. Depletion of A3C slightly decreases proliferation and does not affect DNA repair via homologous recombination or nonhomologous end joining. The A3C interactomes obtained from control cells and cells exposed to the genotoxin etoposide indicated that A3C is a nucleolar protein. This was confirmed by the detection of either endogenous or ectopic A3C in nucleoli. Interestingly, we show that A3C is excluded from areas of DNA breaks in live cells. Our data also indicate that the C-terminal part of A3C is responsible for its nucleolar localization and exclusion from DNA damage sites.
Keywords
Cell Nucleolus/genetics, Cytidine Deaminase/genetics, DNA Breaks, Double-Stranded/drug effects, DNA Damage/drug effects, DNA Damage/genetics, DNA End-Joining Repair/genetics, DNA Repair/drug effects, DNA Repair/genetics, Etoposide/pharmacology, Gene Expression Regulation/drug effects, Genome, Human/genetics, Homologous Recombination/genetics, Humans, Multigene Family/genetics, Mutagens/pharmacology, Mutation/genetics, Tumor Suppressor Protein p53/genetics, APOBEC3C, DNA repair, cancer biology, nucleolus, p53
Pubmed
Web of science
Open Access
Yes
Create date
27/09/2021 11:41
Last modification date
23/03/2023 7:10
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