CRL4DCAF12 regulation of MCMBP ensures optimal licensing of DNA
replication

J 2025

CRL4DCAF12 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

CRL4DCAF12 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 POLASEK-SEDLACKOVA a Lukas CERMAK

Vydání

Nature Communications, Nature Research, 2025, 2041-1723

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10608 Biochemistry and molecular biology

Stát vydavatele

Německo

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 15.700 v roce 2024

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14310/25:00142586

Organizační jednotka

Přírodovědecká fakulta

Klíčová slova anglicky

Replisome; Tumour-suppressor proteins; Ubiquitin ligases

Štítky

14314010, rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 18. 11. 2025 10:04, Mgr. Marie Novosadová Šípková, DiS.

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.

Návaznosti

90250, velká výzkumná infrastruktura

Název: Czech-BioImaging III

Citovat

YADAV, Anoop Kumar; Alikhan ABDIROV; Katarina ONDRUSKOVA; Simran NEGI; Kristina JAMRICHOVA; Karolina KOLAROVA; Nikol DIBUS; Jana KREJCI; Hana POLASEK-SEDLACKOVA a Lukas CERMAK. CRL4DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication. Nature Communications. Nature Research, 2025, roč. 16, č. 1, s. 1-17. ISSN 2041-1723. Dostupné z: https://doi.org/10.1038/s41467-025-64258-5.

@article{2533732,
   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 PolasekandSedlackova, Hana and Cermak, Lukas},
   article_number = {1},
   doi = {https://doi.org/10.1038/s41467-025-64258-5},
   keywords = {Replisome; Tumour-suppressor proteins; Ubiquitin ligases},
   language = {eng},
   issn = {2041-1723},
   journal = {Nature Communications},
   title = {CRL4DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication},
   url = {https://www.nature.com/articles/s41467-025-64258-5},
   volume = {16},
   year = {2025}
}

TY  - JOUR
ID  - 2533732
AU  - Yadav, Anoop Kumar - Abdirov, Alikhan - Ondruskova, Katarina - Negi, Simran - Jamrichova, Kristina - Kolarova, Karolina - Dibus, Nikol - Krejci, Jana - Polasek-Sedlackova, Hana - Cermak, Lukas
PY  - 2025
TI  - CRL4DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication
JF  - Nature Communications
VL  - 16
IS  - 1
SP  - 1-17
EP  - 1-17
PB  - Nature Research
SN  - 20411723
KW  - Replisome
KW  - Tumour-suppressor proteins
KW  - Ubiquitin ligases
UR  - https://www.nature.com/articles/s41467-025-64258-5
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 POLASEK-SEDLACKOVA a Lukas CERMAK. CRL4DCAF12 regulation of MCMBP ensures optimal licensing of DNA replication. \textit{Nature Communications}. Nature Research, 2025, roč.~16, č.~1, s.~1-17. ISSN~2041-1723. Dostupné z: https://doi.org/10.1038/s41467-025-64258-5.

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