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Tytuł pozycji:

A novel cell-cycle-regulated interaction of the Bloom syndrome helicase BLM with Mcm6 controls replication-linked processes.

Tytuł:
A novel cell-cycle-regulated interaction of the Bloom syndrome helicase BLM with Mcm6 controls replication-linked processes.
Autorzy:
Shastri VM; Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL 33620, USA.
Subramanian V; Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL 33620, USA.
Schmidt KH; Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL 33620, USA.; Cancer Biology and Evolution Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.
Źródło:
Nucleic acids research [Nucleic Acids Res] 2021 Sep 07; Vol. 49 (15), pp. 8699-8713.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: 1992- : Oxford : Oxford University Press
Original Publication: London, Information Retrieval ltd.
MeSH Terms:
Minichromosome Maintenance Complex Component 6/*metabolism
RecQ Helicases/*metabolism
S Phase/*genetics
Binding Sites ; Cell Line ; DNA Repair ; G1 Phase ; Humans ; Minichromosome Maintenance Complex Component 6/chemistry ; Mutation ; Protein Interaction Domains and Motifs ; RecQ Helicases/chemistry
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Grant Information:
R01 GM081425 United States GM NIGMS NIH HHS; R01 GM139296 United States GM NIGMS NIH HHS
Substance Nomenclature:
EC 3.6.1.- (Bloom syndrome protein)
EC 3.6.4.12 (MCM6 protein, human)
EC 3.6.4.12 (Minichromosome Maintenance Complex Component 6)
EC 3.6.4.12 (RecQ Helicases)
Entry Date(s):
Date Created: 20210809 Date Completed: 20210910 Latest Revision: 20220716
Update Code:
20240105
PubMed Central ID:
PMC8421143
DOI:
10.1093/nar/gkab663
PMID:
34370039
Czasopismo naukowe
The Bloom syndrome DNA helicase BLM contributes to chromosome stability through its roles in double-strand break repair by homologous recombination and DNA replication fork restart during the replication stress response. Loss of BLM activity leads to Bloom syndrome, which is characterized by extraordinary cancer risk and small stature. Here, we have analyzed the composition of the BLM complex during unperturbed S-phase and identified a direct physical interaction with the Mcm6 subunit of the minichromosome maintenance (MCM) complex. Using distinct binding sites, BLM interacts with the N-terminal domain of Mcm6 in G1 phase and switches to the C-terminal Cdt1-binding domain of Mcm6 in S-phase, with a third site playing a role for Mcm6 binding after DNA damage. Disruption of Mcm6-binding to BLM in S-phase leads to supra-normal DNA replication speed in unperturbed cells, and the helicase activity of BLM is required for this increased replication speed. Upon disruption of BLM/Mcm6 interaction, repair of replication-dependent DNA double-strand breaks is delayed and cells become hypersensitive to DNA damage and replication stress. Our findings reveal that BLM not only plays a role in the response to DNA damage and replication stress, but that its physical interaction with Mcm6 is required in unperturbed cells, most notably in S-phase as a negative regulator of replication speed.
(© The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.)

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