scholarly journals Cellular heredity in haploid cultures of somatic cells. Progress report, August 1978-September 1979. [Correlation between uv mutagenesis and DNA repair in cultured haploid frog cells (ICR 2A)]

1979 ◽  
Author(s):  
J. Freed
Keyword(s):  
Dna Repair ◽  
Somatic Cells ◽  
Progress Report ◽  
Uv Mutagenesis

scholarly journals A role for XLF in DNA repair and recombination in human somatic cells

DNA Repair ◽  
2014 ◽  
Vol 15 ◽  
pp. 39-53 ◽  
Author(s):  
Farjana Jahan Fattah ◽  
Junghun Kweon ◽  
Yongbao Wang ◽  
Eu Han Lee ◽  
Yinan Kan ◽  
...  
Keyword(s):  
Dna Repair ◽  
Somatic Cells

scholarly journals The SRS2 suppressor of rad6 mutations of Saccharomyces cerevisiae acts by channeling DNA lesions into the RAD52 DNA repair pathway.

Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 817-831 ◽  
Author(s):  
R H Schiestl ◽  
S Prakash ◽  
L Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Repair ◽  
Gamma Ray ◽  
Dna Lesions ◽  
Recombinational Repair ◽  
Repair Pathway ◽  
Uv Mutagenesis ◽  
Uv Sensitivity ◽  
Suppressor Mutations ◽  
Induced Mutagenesis

Abstract rad6 mutants of Saccharomyces cerevisiae are defective in the repair of damaged DNA, DNA damage induced mutagenesis, and sporulation. In order to identify genes that can substitute for RAD6 function, we have isolated genomic suppressors of the UV sensitivity of rad6 deletion (rad6 delta) mutations and show that they also suppress the gamma-ray sensitivity but not the UV mutagenesis or sporulation defects of rad6. The suppressors show semidominance for suppression of UV sensitivity and dominance for suppression of gamma-ray sensitivity. The six suppressor mutations we isolated are all alleles of the same locus and are also allelic to a previously described suppressor of the rad6-1 nonsense mutation, SRS2. We show that suppression of rad6 delta is dependent on the RAD52 recombinational repair pathway since suppression is not observed in the rad6 delta SRS2 strain containing an additional mutation in either the RAD51, RAD52, RAD54, RAD55 or RAD57 genes. Possible mechanisms by which SRS2 may channel unrepaired DNA lesions into the RAD52 DNA repair pathway are discussed.

scholarly journals Features of DNA Repair in the Early Stages of Mammalian Embryonic Development

Genes ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1138 ◽  
Author(s):  
Evgenia V. Khokhlova ◽  
Zoia S. Fesenko ◽  
Julia V. Sopova ◽  
Elena I. Leonova
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Embryonic Development ◽  
Somatic Cells ◽  
Genomic Integrity ◽  
Embryonic Period ◽  
Early Stages ◽  
Mammalian Embryos ◽  
Disparate Data ◽  
Mammalian Embryonic Development

Cell repair machinery is responsible for protecting the genome from endogenous and exogenous effects that induce DNA damage. Mutations that occur in somatic cells lead to dysfunction in certain tissues or organs, while a violation of genomic integrity during the embryonic period often leads to death. A mammalian embryo’s ability to respond to damaged DNA and repair it, as well as its sensitivity to specific lesions, is still not well understood. In this review, we combine disparate data on repair processes in the early stages of preimplantation development in mammalian embryos.

Polymerases and UV mutagenesis in Escherichia coli

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 572-577 ◽  
Author(s):  
B. A. Bridges ◽  
Helen Bates ◽  
Firdaus Sharif
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Nucleic Acid ◽  
Gene Product ◽  
Ultraviolet Light ◽  
Dna Polymerase ◽  
Dna Polymerase Iii ◽  
Uv Mutagenesis ◽  
Α Subunit ◽  
Polymerase Iii

Evidence for and against the involvement of the known nucleic acid polymerases in UV mutagenesis in Escherichia coli is reviewed. There is no evidence that rules out the participation of any of them when they are present but only one, the α subunit of DNA polymerase III holoenzyme (polC gene product) has been shown to be essential. It is argued that the PolC protein that functions in UV mutagenesis may not be immediately recognizable as one of the normal cellular polymerases or polymerase complexes.Key words: polymerases, ultraviolet light, mutagenesis, DNA repair, misincorporation.

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