CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of
DNA replication

J 2025

CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication

YADAV, Anoop Kumar; Alikhan ABDIROV; Katarina ONDRUSKOVA; Simran NEGI; Kristina JAMRICHOVA et al.

Základní údaje

Originální název

CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication

Autoři

YADAV, Anoop Kumar; Alikhan ABDIROV; Katarina ONDRUSKOVA; Simran NEGI ; Kristina JAMRICHOVA; Karolina KOLAROVA; Nikol DIBUS; Jana KREJCI; Hana POLÁŠEK-SEDLÁČKOVÁ a Lukas CERMAK

Vydání

NATURE COMMUNICATIONS, BERLIN, NATURE PORTFOLIO, 2025

Další údaje

Typ výsledku

Článek v odborném periodiku

Označené pro přenos do RIV

DOI

https://doi.org/10.1038/s41467-025-64258-5

UT WoS

001603687300022

Změněno: 7. 2. 2026 23:50, Mgr. Hana Polášek-Sedláčková, Ph.D.

Anotace

V originále

The minichromosome maintenance (MCM2-7) protein complexes are central drivers of genome duplication. Distinct protein pools, parental and nascent MCMs, and their precise equilibrium are essential to sustain error-free DNA replication. However, the mechanism responsible for generating these pools and maintaining their equilibrium remains largely unexplored. Here, we identified CRL4DCAF12 as a factor controlling the assembly of nascent MCM complexes. During MCM biogenesis, MCMBP facilitates the assembly and transport of newly synthesized MCM3-7 subcomplexes into the nucleus. Once in the nucleus, the MCM2 subunit must be incorporated into the MCM3-7 subcomplex, while MCMBP needs to be removed. CRL4DCAF12 facilitates the degradation of MCMBP and thereby regulates the assembly of MCM2-7 complexes. The absence of CRL4DCAF12 adversely affects the level of chromatin-bound nascent MCMs, resulting in accelerated replication forks and replication stress. Collectively, our findings uncovered the molecular mechanism underlying nascent MCM production essential to counteract genome instability.

Citovat

YADAV, Anoop Kumar; Alikhan ABDIROV; Katarina ONDRUSKOVA; Simran NEGI; Kristina JAMRICHOVA; Karolina KOLAROVA; Nikol DIBUS; Jana KREJCI; Hana POLÁŠEK-SEDLÁČKOVÁ a Lukas CERMAK. CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication. Online. NATURE COMMUNICATIONS. BERLIN: NATURE PORTFOLIO, 2025, roč. 16, č. 1, s. 1-17. Dostupné z: https://doi.org/10.1038/s41467-025-64258-5.

@article{2553285,
   author = {Yadav, Anoop Kumar and Abdirov, Alikhan and Ondruskova, Katarina and Negi, Simran and Jamrichova, Kristina and Kolarova, Karolina and Dibus, Nikol and Krejci, Jana and PolášekandSedláčková, Hana and Cermak, Lukas},
   article_location = {BERLIN},
   article_number = {1},
   doi = {https://doi.org/10.1038/s41467-025-64258-5},
   journal = {NATURE COMMUNICATIONS},
   title = {CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication},
   volume = {16},
   year = {2025}
}

TY  - JOUR
ID  - 2553285
AU  - Yadav, Anoop Kumar - Abdirov, Alikhan - Ondruskova, Katarina - Negi, Simran - Jamrichova, Kristina - Kolarova, Karolina - Dibus, Nikol - Krejci, Jana - Polášek-Sedláčková, Hana - Cermak, Lukas
PY  - 2025
TI  - CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication
JF  - NATURE COMMUNICATIONS
VL  - 16
IS  - 1
SP  - 1-17
EP  - 1-17
PB  - NATURE PORTFOLIO
N2  - The minichromosome maintenance (MCM2-7) protein complexes are central drivers of genome duplication. Distinct protein pools, parental and nascent MCMs, and their precise equilibrium are essential to sustain error-free DNA replication. However, the mechanism responsible for generating these pools and maintaining their equilibrium remains largely unexplored. Here, we identified CRL4DCAF12 as a factor controlling the assembly of nascent MCM complexes. During MCM biogenesis, MCMBP facilitates the assembly and transport of newly synthesized MCM3-7 subcomplexes into the nucleus. Once in the nucleus, the MCM2 subunit must be incorporated into the MCM3-7 subcomplex, while MCMBP needs to be removed. CRL4DCAF12 facilitates the degradation of MCMBP and thereby regulates the assembly of MCM2-7 complexes. The absence of CRL4DCAF12 adversely affects the level of chromatin-bound nascent MCMs, resulting in accelerated replication forks and replication stress. Collectively, our findings uncovered the molecular mechanism underlying nascent MCM production essential to counteract genome instability.
ER  -

YADAV, Anoop Kumar; Alikhan ABDIROV; Katarina ONDRUSKOVA; Simran NEGI; Kristina JAMRICHOVA; Karolina KOLAROVA; Nikol DIBUS; Jana KREJCI; Hana POLÁŠEK-SEDLÁČKOVÁ a Lukas CERMAK. CRL4-DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication. Online. \textit{NATURE COMMUNICATIONS}. BERLIN: NATURE PORTFOLIO, 2025, roč.~16, č.~1, s.~1-17. Dostupné z: https://doi.org/10.1038/s41467-025-64258-5.

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