Conversion of deletions during recombination in pneumococcal transformation.

Abstract Genetic analysis of 16 deletions obtained in the amiA locus of pneumococcus is described. When present on donor DNA, all deletions increased drastically the frequency of wild-type recombinants in two-point crosses. This effect was maximal for deletions longer than 200 bases. It was reduced for heterologies shorter than 76 bases and did not exist for very short deletions. In three-point crosses in which the deletion was localized between two point mutations, we demonstrated that this excess of wild-type recombinants was the result of a genetic conversion. This conversion extended over several scores of bases outside the deletion. Conversion takes place during the heteroduplex stage of recombination. Therefore, in pneumococcal transformation, long heterologies participated in this heteroduplex configuration. As this conversion did not require an active DNA polymerase A gene it is proposed that the mechanism of conversion is not a DNA repair synthesis but involves breakage and ligation between DNA molecules. Conversion of deletions did not require the Hex system of correction of mismatched bases. It differs also from localized conversion. It appears that it is a process that evolved to correct errors of replication which lead to long heterologies and which are not eliminated by other systems.

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DNA replication and UV-induced DNA repair synthesis in human fibroblasts are much less sensitive than DNA polymerase α to inhibition by butylphenyl-deoxyguanosine triphosphate

Nucleic Acids Research ◽

10.1093/nar/14.17.7093 ◽

1986 ◽

Vol 14 (17) ◽

pp. 7093-7102 ◽

Cited By ~ 55

Author(s):

Steven L. Dresler ◽

Mark G. Frattini

Keyword(s):

Dna Repair ◽

Dna Replication ◽

Dna Polymerase ◽

Human Fibroblasts ◽

Repair Synthesis ◽

Dna Polymerase Α ◽

Dna Repair Synthesis ◽

Deoxyguanosine Triphosphate

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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 ◽

10.1021/bi00384a002 ◽

1987 ◽

Vol 26 (10) ◽

pp. 2664-2668 ◽

Cited By ~ 33

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

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The Base Excision Repair Pathway in the Nematode Caenorhabditis elegans

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2020.598860 ◽

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.

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DNA repair synthesis during base excision repair in vitro is catalyzed by DNA polymerase epsilon and is influenced by DNA polymerases alpha and delta in Saccharomyces cerevisiae.

Molecular and Cellular Biology ◽

10.1128/mcb.13.2.1051 ◽

1993 ◽

Vol 13 (2) ◽

pp. 1051-1058 ◽

Cited By ~ 78

Author(s):

Z Wang ◽

X Wu ◽

E C Friedberg

Keyword(s):

Dna Repair ◽

Dna Polymerase ◽

Base Excision Repair ◽

Excision Repair ◽

Repair Synthesis ◽

Dna Polymerase Epsilon ◽

Nuclear Extracts ◽

Polymerase Epsilon ◽

Base Excision ◽

Dna Repair Synthesis

Base excision repair is an important mechanism for correcting DNA damage produced by many physical and chemical agents. We have examined the effects of the REV3 gene and the DNA polymerase genes POL1, POL2, and POL3 of Saccharomyces cerevisiae on DNA repair synthesis is nuclear extracts. Deletional inactivation of REV3 did not affect repair synthesis in the base excision repair pathway. Repair synthesis in nuclear extracts of pol1, pol2, and pol3 temperature-sensitive mutants was normal at permissive temperatures. However, repair synthesis in pol2 nuclear extracts was defective at the restrictive temperature of 37 degrees C and could be complemented by the addition of purified yeast DNA polymerase epsilon. Repair synthesis in pol1 nuclear extracts was proficient at the restrictive temperature unless DNA polymerase alpha was inactivated prior to the initiation of DNA repair. Thermal inactivation of DNA polymerase delta in pol3 nuclear extracts enhanced DNA repair synthesis approximately 2-fold, an effect which could be specifically reversed by the addition of purified yeast DNA polymerase delta to the extract. These results demonstrate that DNA repair synthesis in the yeast base excision repair pathway is catalyzed by DNA polymerase epsilon but is apparently modulated by the presence of DNA polymerases alpha and delta.

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

Biochemical Journal ◽

10.1042/bj1990453 ◽

1981 ◽

Vol 199 (2) ◽

pp. 453-455 ◽

Cited By ~ 14

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.

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