Evidence that the DNA mismatch repair system removes 1-nucleotide Okazaki fragment flaps.

Szczegóły
Abstrakt

Tytuł:: Evidence that the DNA mismatch repair system removes 1-nucleotide Okazaki fragment flaps.
Autorzy:: Kadyrova LY; From the Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, Illinois 62901.
Dahal BK; From the Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, Illinois 62901.
Kadyrov FA; From the Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, Illinois 62901 .
Źródło:: The Journal of biological chemistry [J Biol Chem] 2015 Oct 02; Vol. 290 (40), pp. 24051-65. Date of Electronic Publication: 2015 Jul 29.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology
Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology
MeSH Terms:: DNA Mismatch Repair*
DNA/*genetics
DNA Repair Enzymes/*metabolism
MutS DNA Mismatch-Binding Protein/*metabolism
Replication Protein C/*metabolism
DNA/chemistry ; DNA Mutational Analysis ; DNA Replication ; DNA, Circular/chemistry ; Flap Endonucleases/genetics ; Fungal Proteins/metabolism ; Gene Deletion ; Genome ; Humans ; MutL Proteins ; Mutation ; Ploidies ; Proliferating Cell Nuclear Antigen/metabolism ; Protein Structure, Tertiary ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Substrate Specificity
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Grant Information:: R01 GM095758 United States GM NIGMS NIH HHS; R01GM095758 United States GM NIGMS NIH HHS
Contributed Indexing:: Keywords: DNA endonuclease; DNA mismatch repair; DNA replication; Okazaki fragment maturation; cancer; genomic instability; mutL homolog 1 (MLH1)
Substance Nomenclature:: 0 (DNA, Circular)
0 (Fungal Proteins)
0 (MutLalpha protein, human)
0 (Okazaki fragments)
0 (Proliferating Cell Nuclear Antigen)
0 (Saccharomyces cerevisiae Proteins)
9007-49-2 (DNA)
EC 3.1.- (Flap Endonucleases)
EC 3.6.1.3 (MutL Proteins)
EC 3.6.1.3 (MutS DNA Mismatch-Binding Protein)
EC 3.6.4.- (Replication Protein C)
EC 6.5.1.- (DNA Repair Enzymes)
Entry Date(s):: Date Created: 20150731 Date Completed: 20160106 Latest Revision: 20210205
Update Code:: 20240104
PubMed Central ID:: PMC4591796
DOI:: 10.1074/jbc.M115.660357
PMID:: 26224637
: Czasopismo naukowe

The DNA mismatch repair (MMR) system plays a major role in promoting genome stability and suppressing carcinogenesis. In this work, we investigated whether the MMR system is involved in Okazaki fragment maturation. We found that in the yeast Saccharomyces cerevisiae, the MMR system and the flap endonuclease Rad27 act in overlapping pathways that protect the nuclear genome from 1-bp insertions. In addition, we determined that purified yeast and human MutSα proteins recognize 1-nucleotide DNA and RNA flaps. In reconstituted human systems, MutSα, proliferating cell nuclear antigen, and replication factor C activate MutLα endonuclease to remove the flaps. ATPase and endonuclease mutants of MutLα are defective in the flap removal. These results suggest that the MMR system contributes to the removal of 1-nucleotide Okazaki fragment flaps.
(© 2015 by The American Society for Biochemistry and Molecular Biology, Inc.)

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