Research output: Contribution to journal › Article › peer-review
Apurinic/apyrimidinic endonuclease 1 has major impact in prevention of suicidal covalent DNA–protein crosslink with apurinic/apyrimidinic site in cellular extracts. / Lebedeva, Natalia A.; Dyrkheeva, Nadezhda S.; Rechkunova, Nadejda I. et al.
In: IUBMB Life, Vol. 76, No. 11, 11.2024, p. 987-996.Research output: Contribution to journal › Article › peer-review
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TY - JOUR
T1 - Apurinic/apyrimidinic endonuclease 1 has major impact in prevention of suicidal covalent DNA–protein crosslink with apurinic/apyrimidinic site in cellular extracts
AU - Lebedeva, Natalia A.
AU - Dyrkheeva, Nadezhda S.
AU - Rechkunova, Nadejda I.
AU - Lavrik, Olga I.
N1 - Funding information: Russian Science Foundation,Grant/Award Numbers: 21-64-00017, 22-14-00112; Ministry of Higher Educationand Science
PY - 2024/11
Y1 - 2024/11
N2 - DNA–protein crosslinks (DPC) are common DNA lesions induced by various external and endogenous agents. One of the sources of DPC is the apurinic/apyrimidinic site (AP site) and proteins interacting with it. Some proteins possessing AP lyase activity form covalent complexes with AP site-containing DNA without borohydride reduction (suicidal crosslinks). We have shown earlier that tyrosyl-DNA phosphodiesterase 1 (TDP1) but not AP endonuclease 1 (APE1) is able to remove intact OGG1 from protein–DNA adducts, whereas APE1 is able to prevent the formation of DPC by hydrolyzing the AP site. Here we demonstrate that TDP1 can remove intact PARP2 but not XRCC1 from covalent enzyme–DNA adducts with AP-DNA formed in the absence of APE1. We also analyzed an impact of APE1 and TDP1 on the efficiency of DPC formation in APE1−/− or TDP1−/− cell extracts. Our data revealed that APE1 depletion leads to increased levels of PARP1–DNA crosslinks, whereas TDP1 deficiency has little effect on DPC formation.
AB - DNA–protein crosslinks (DPC) are common DNA lesions induced by various external and endogenous agents. One of the sources of DPC is the apurinic/apyrimidinic site (AP site) and proteins interacting with it. Some proteins possessing AP lyase activity form covalent complexes with AP site-containing DNA without borohydride reduction (suicidal crosslinks). We have shown earlier that tyrosyl-DNA phosphodiesterase 1 (TDP1) but not AP endonuclease 1 (APE1) is able to remove intact OGG1 from protein–DNA adducts, whereas APE1 is able to prevent the formation of DPC by hydrolyzing the AP site. Here we demonstrate that TDP1 can remove intact PARP2 but not XRCC1 from covalent enzyme–DNA adducts with AP-DNA formed in the absence of APE1. We also analyzed an impact of APE1 and TDP1 on the efficiency of DPC formation in APE1−/− or TDP1−/− cell extracts. Our data revealed that APE1 depletion leads to increased levels of PARP1–DNA crosslinks, whereas TDP1 deficiency has little effect on DPC formation.
KW - AP endonuclease 1
KW - DNA–protein crosslinks
KW - apurinic/apyrimidinic site
KW - poly(ADP-ribose) polymerases
KW - tyrosyl-DNA phosphodiesterase 1
KW - DNA-(Apurinic or Apyrimidinic Site) Lyase/metabolism
KW - Phosphoric Diester Hydrolases/metabolism
KW - Humans
KW - DNA/metabolism
KW - Animals
KW - X-ray Repair Cross Complementing Protein 1/metabolism
KW - Cell Extracts/chemistry
KW - DNA Repair
KW - Mice
KW - DNA Adducts/metabolism
KW - DNA-Binding Proteins/genetics
KW - DNA Damage
KW - Poly(ADP-ribose) Polymerases/metabolism
UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85197510442&origin=inward&txGid=00536e9eb862eb737e65d7ec0ddc8c29
UR - https://www.mendeley.com/catalogue/4e620e46-0797-38cc-a164-7cd1d01ff522/
U2 - 10.1002/iub.2890
DO - 10.1002/iub.2890
M3 - Article
C2 - 38963041
VL - 76
SP - 987
EP - 996
JO - IUBMB Life
JF - IUBMB Life
SN - 1521-6543
IS - 11
ER -
ID: 60780640