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Tytuł pozycji:

Mck1 defines a key S-phase checkpoint effector in response to various degrees of replication threats.

Tytuł:
Mck1 defines a key S-phase checkpoint effector in response to various degrees of replication threats.
Autorzy:
Li X; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Jin X; State Key Laboratory of Subtropical Silviculture, Zhejiang A&F University, Lin'an, Hangzhou, China.; Department of Chemistry and Molecular Biology, University of Gothenburg, Medicinaregatan, Gothenburg, Sweden.
Sharma S; Department of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.
Liu X; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Zhang J; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Niu Y; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Li J; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Li Z; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Zhang J; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Cao Q; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Hou W; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Du LL; National Institute of Biological Sciences, Beijing, China.
Liu B; State Key Laboratory of Subtropical Silviculture, Zhejiang A&F University, Lin'an, Hangzhou, China.; Department of Chemistry and Molecular Biology, University of Gothenburg, Medicinaregatan, Gothenburg, Sweden.
Lou H; State Key Laboratory of Agro-Biotechnology and Beijing Advanced Innovation Center for Food Nutrition and Human Health, MOA Key Laboratory of Soil Microbiology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
Źródło:
PLoS genetics [PLoS Genet] 2019 Aug 05; Vol. 15 (8), pp. e1008136. Date of Electronic Publication: 2019 Aug 05 (Print Publication: 2019).
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: San Francisco, CA : Public Library of Science, c2005-
MeSH Terms:
Cell Cycle Proteins/*metabolism
Gene Expression Regulation, Fungal/*physiology
Glycogen Synthase Kinase 3/*metabolism
Protein Serine-Threonine Kinases/*metabolism
S Phase Cell Cycle Checkpoints/*genetics
Saccharomyces cerevisiae/*physiology
Saccharomyces cerevisiae Proteins/*metabolism
Cell Cycle Proteins/genetics ; DNA Damage ; DNA Replication/drug effects ; Gene Expression Regulation, Fungal/drug effects ; Gene Knockout Techniques ; Glycogen Synthase Kinase 3/genetics ; Hydroxyurea/toxicity ; Nucleotides/metabolism ; Phosphorylation ; Promoter Regions, Genetic/genetics ; Protein Serine-Threonine Kinases/genetics ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Ribonucleotide Reductases/genetics ; Ribonucleotide Reductases/metabolism ; S Phase Cell Cycle Checkpoints/drug effects ; Saccharomyces cerevisiae/drug effects ; Saccharomyces cerevisiae Proteins/genetics
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Substance Nomenclature:
0 (Cell Cycle Proteins)
0 (Nucleotides)
0 (RFX1 protein, S cerevisiae)
0 (Repressor Proteins)
0 (Saccharomyces cerevisiae Proteins)
EC 1.17.4.- (Ribonucleotide Reductases)
EC 2.7.1.- (DUN1 protein, S cerevisiae)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
EC 2.7.11.26 (Glycogen Synthase Kinase 3)
EC 2.7.12.1 (MCK1 protein, S cerevisiae)
X6Q56QN5QC (Hydroxyurea)
Entry Date(s):
Date Created: 20190806 Date Completed: 20200107 Latest Revision: 20211204
Update Code:
20240105
PubMed Central ID:
PMC6695201
DOI:
10.1371/journal.pgen.1008136
PMID:
31381575
Czasopismo naukowe
The S-phase checkpoint plays an essential role in regulation of the ribonucleotide reductase (RNR) activity to maintain the dNTP pools. How eukaryotic cells respond appropriately to different levels of replication threats remains elusive. Here, we have identified that a conserved GSK-3 kinase Mck1 cooperates with Dun1 in regulating this process. Deleting MCK1 sensitizes dun1Δ to hydroxyurea (HU) reminiscent of mec1Δ or rad53Δ. While Mck1 is downstream of Rad53, it does not participate in the post-translational regulation of RNR as Dun1 does. Mck1 phosphorylates and releases the Crt1 repressor from the promoters of DNA damage-inducible genes as RNR2-4 and HUG1. Hug1, an Rnr2 inhibitor normally silenced, is induced as a counterweight to excessive RNR. When cells suffer a more severe threat, Mck1 inhibits HUG1 transcription. Consistently, only a combined deletion of HUG1 and CRT1, confers a dramatic boost of dNTP levels and the survival of mck1Δdun1Δ or mec1Δ cells assaulted by a lethal dose of HU. These findings reveal the division-of-labor between Mck1 and Dun1 at the S-phase checkpoint pathway to fine-tune dNTP homeostasis.
Competing Interests: The authors have declared that no competing interests exist.
Comment in: PLoS Genet. 2019 Oct 31;15(10):e1008372. (PMID: 31671089)
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