2',3'-Dideoxythymidine 5'-triphosphate inhibition of DNA replication and ultraviolet-induced DNA repair synthesis in human cells: evidence for involvement of DNA polymerase .delta.

Biochemistry ◽  
1987 ◽  
Vol 26 (10) ◽  
pp. 2664-2668 ◽  
Author(s):  
Steven L. Dresler ◽  
Kevin Sean Kimbro
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Dna Polymerase ◽  
Human Cells ◽  
Dna Polymerase Delta ◽  
Repair Synthesis ◽  
Dna Repair Synthesis

In situ enzymology of DNA replication and ultraviolet-induced DNA repair synthesis in permeable human cells

Biochemistry ◽  
1988 ◽  
Vol 27 (19) ◽  
pp. 7247-7254 ◽  
Author(s):  
Steven L. Dresler ◽  
Mark G. Frattini ◽  
Rona M. Robinson-Hill
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Human Cells ◽  
Repair Synthesis ◽  
Dna Repair Synthesis

scholarly journals Aphidicolin does not inhibit DNA repair synthesis in ultraviolet-irradiated HeLa cells. A radioautographic study

1981 ◽  
Vol 199 (2) ◽  
pp. 453-455 ◽  
Author(s):  
N Hardt ◽  
G Pedrali-Noy ◽  
F Focher ◽  
S Spadari
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Dna Synthesis ◽  
Dna Polymerase ◽  
Hela Cells ◽  
Nuclear Dna ◽  
Detectable Effect ◽  
Repair Synthesis ◽  
Dna Polymerase Alpha ◽  
Dna Repair Synthesis

A radioautographic examination of nuclear DNA synthesis in unirradiated and u.v.-irradiated HeLa cells, in the presence and in the absence of aphidicolin, showed that aphidicolin inhibits nuclear DNA replication and has no detectable effect on DNA repair synthesis. Although the results establish that in u.v.-irradiated HeLa cells most of the DNA repair synthesis is not due to DNA polymerase alpha, they do not preclude a significant role for this enzyme in DNA repair processes.

Involvement of DNA polymerase .delta. in DNA repair synthesis in human fibroblasts at late times after ultraviolet irradiation

Biochemistry ◽  
1988 ◽  
Vol 27 (17) ◽  
pp. 6379-6383 ◽  
Author(s):  
Steven L. Dresler ◽  
Bonnie J. Gowans ◽  
Rona M. Robinson-Hill ◽  
Darel J. Hunting
Keyword(s):  
Dna Repair ◽  
Dna Polymerase ◽  
Ultraviolet Irradiation ◽  
Human Fibroblasts ◽  
Dna Polymerase Delta ◽  
Repair Synthesis ◽  
Dna Repair Synthesis

scholarly journals The Base Excision Repair Pathway in the Nematode Caenorhabditis elegans

2020 ◽  
Vol 8 ◽  
Author(s):  
Noha Elsakrmy ◽  
Qiu-Mei Zhang-Akiyama ◽  
Dindial Ramotar
Keyword(s):  
Dna Repair ◽  
Caenorhabditis Elegans ◽  
Dna Polymerase ◽  
Base Excision Repair ◽  
Excision Repair ◽  
Dna Glycosylases ◽  
Repair Synthesis ◽  
C Elegans ◽  
Base Excision ◽  
Dna Repair Synthesis

Exogenous and endogenous damage to the DNA is inevitable. Several DNA repair pathways including base excision, nucleotide excision, mismatch, homologous and non-homologous recombinations are conserved across all organisms to faithfully maintain the integrity of the genome. The base excision repair (BER) pathway functions to repair single-base DNA lesions and during the process creates the premutagenic apurinic/apyrimidinic (AP) sites. In this review, we discuss the components of the BER pathway in the nematode Caenorhabditis elegans and delineate the different phenotypes caused by the deletion or the knockdown of the respective DNA repair gene, as well as the implications. To date, two DNA glycosylases have been identified in C. elegans, the monofunctional uracil DNA glycosylase-1 (UNG-1) and the bifunctional endonuclease III-1 (NTH-1) with associated AP lyase activity. In addition, the animal possesses two AP endonucleases belonging to the exonuclease-3 and endonuclease IV families and in C. elegans these enzymes are called EXO-3 and APN-1, respectively. In mammalian cells, the DNA polymerase, Pol beta, that is required to reinsert the correct bases for DNA repair synthesis is not found in the genome of C. elegans and the evidence indicates that this role could be substituted by DNA polymerase theta (POLQ), which is known to perform a function in the microhomology-mediated end-joining pathway in human cells. The phenotypes observed by the C. elegans mutant strains of the BER pathway raised many challenging questions including the possibility that the DNA glycosylases may have broader functional roles, as discuss in this review.

scholarly journals TRAIP drives replisome disassembly and mitotic DNA repair synthesis at sites of incomplete DNA replication

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Remi Sonneville ◽  
Rahul Bhowmick ◽  
Saskia Hoffmann ◽  
Niels Mailand ◽  
Ian D Hickson ◽  
...  
Keyword(s):  
Dna Repair ◽  
Dna Replication ◽  
Ubiquitin Ligase ◽  
Early Embryo ◽  
Model System ◽  
Replication Forks ◽  
Nematode Caenorhabditis Elegans ◽  
Repair Synthesis ◽  
Dna Repair Synthesis ◽  
Early Mitosis

The faithful segregation of eukaryotic chromosomes in mitosis requires that the genome be duplicated completely prior to anaphase. However, cells with large genomes sometimes fail to complete replication during interphase and instead enter mitosis with regions of incompletely replicated DNA. These regions are processed in early mitosis via a process known as mitotic DNA repair synthesis (MiDAS), but little is known about how cells switch from conventional DNA replication to MiDAS. Using the early embryo of the nematode Caenorhabditis elegans as a model system, we show that the TRAIP ubiquitin ligase drives replisome disassembly in response to incomplete DNA replication, thereby providing access to replication forks for other factors. Moreover, TRAIP is essential for MiDAS in human cells, and is important in both systems to prevent mitotic segregation errors. Our data indicate that TRAIP is a master regulator of the processing of incomplete DNA replication during mitosis in metazoa.

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