scholarly journals Preferential repair of UV damage in highly transcribed DNA diminishes UV-induced intrachromosomal recombination in mammalian cells.

1994 ◽  
Vol 14 (1) ◽  
pp. 391-399 ◽  
Author(s):  
W P Deng ◽  
J A Nickoloff
Keyword(s):  
Dna Damage ◽  
Mammalian Cells ◽  
Uv Light ◽  
Uv Damage ◽  
Dna Damage And Repair ◽  
Intrachromosomal Recombination ◽  
Dna Damaging Agents ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

The relationships among transcription, recombination, DNA damage, and repair in mammalian cells were investigated. We monitored the effects of transcription on UV-induced intrachromosomal recombination between neomycin repeats including a promoterless allele and an inducible heteroallele regulated by the mouse mammary tumor virus promoter. Although transcription and UV light separately stimulated recombination, increasing transcription levels reduced UV-induced recombination. Preferential repair of UV damage in transcribed strands was shown in highly transcribed DNA, suggesting that recombination is stimulated by unrepaired UV damage and that increased DNA repair in highly transcribed alleles removes recombinogenic lesions. This study indicates that the genetic consequences of DNA damage depend on transcriptional states and provides a basis for understanding tissue- and gene-specific responses to DNA-damaging agents.

scholarly journals Preferential repair of UV damage in highly transcribed DNA diminishes UV-induced intrachromosomal recombination in mammalian cells

1994 ◽  
Vol 14 (1) ◽  
pp. 391-399
Author(s):  
W P Deng ◽  
J A Nickoloff
Keyword(s):  
Dna Damage ◽  
Mammalian Cells ◽  
Uv Light ◽  
Uv Damage ◽  
Dna Damage And Repair ◽  
Intrachromosomal Recombination ◽  
Dna Damaging Agents ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

The relationships among transcription, recombination, DNA damage, and repair in mammalian cells were investigated. We monitored the effects of transcription on UV-induced intrachromosomal recombination between neomycin repeats including a promoterless allele and an inducible heteroallele regulated by the mouse mammary tumor virus promoter. Although transcription and UV light separately stimulated recombination, increasing transcription levels reduced UV-induced recombination. Preferential repair of UV damage in transcribed strands was shown in highly transcribed DNA, suggesting that recombination is stimulated by unrepaired UV damage and that increased DNA repair in highly transcribed alleles removes recombinogenic lesions. This study indicates that the genetic consequences of DNA damage depend on transcriptional states and provides a basis for understanding tissue- and gene-specific responses to DNA-damaging agents.

scholarly journals Detection of DNA Damage in Prokaryotes by Terminal Deoxyribonucleotide Transferase-Mediated dUTP Nick End Labeling

2000 ◽  
Vol 66 (3) ◽  
pp. 1001-1006 ◽  
Author(s):  
Forest Rohwer ◽  
Farooq Azam
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Dna Repair ◽  
Uv Light ◽  
Fluorescein Isothiocyanate ◽  
Protein Synthesis Inhibitors ◽  
Dna Damage And Repair ◽  
Dna Damaging Agents ◽  
Bacteriophage Infection ◽  
Dna Ends

ABSTRACT Numerous agents can damage the DNA of prokaryotes in the environment (e.g., reactive oxygen species, irradiation, and secondary metabolites such as antibiotics, enzymes, starvation, etc.). The large number of potential DNA-damaging agents, as well as their diverse modes of action, precludes a simple test of DNA damage based on detection of nucleic acid breakdown products. In this study, free 3′-OH DNA ends, produced by either direct damage or excision DNA repair, were used to assess DNA damage. Terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling (TUNEL) is a procedure in which 3′-OH DNA ends are enzymatically labeled with dUTP-fluorescein isothiocyanate using TdT. Cells labeled by this method can be detected using fluorescence microscopy or flow cytometry. TUNEL was used to measure hydrogen peroxide-induced DNA damage in the archaeonHaloferax volcanii and the bacterium Escherichia coli. DNA repair systems were implicated in the hydrogen peroxide-dependent generation of 3′-OH DNA ends by the finding that the protein synthesis inhibitors chloramphenicol and diphtheria toxin blocked TUNEL labeling of E. coli and H. volcanii, respectively. DNA damage induced by UV light and bacteriophage infection was also measured using TUNEL. This methodology should be useful in applications where DNA damage and repair are of interest, including mutant screening and monitoring of DNA damage in the environment.

scholarly journals Heregulin Co-opts PR Transcriptional Action Via Stat3 Role As a Coregulator to Drive Cancer Growth

2015 ◽  
Vol 29 (10) ◽  
pp. 1468-1485 ◽  
Author(s):  
Cecilia J. Proietti ◽  
Franco Izzo ◽  
María Celeste Díaz Flaqué ◽  
Rosalía Cordo Russo ◽  
Leandro Venturutti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Cancer Growth ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

Abstract Accumulated findings have demonstrated the presence of bidirectional interactions between progesterone receptor (PR) and the ErbB family of receptor tyrosine kinases signaling pathways in breast cancer. We previously revealed signal transducer and activator of transcription 3 (Stat3) as a nodal convergence point between said signaling pathways proving that Stat3 is activated by one of the ErbBs' ligands, heregulin (HRG)β1 via ErbB2 and through the co-option of PR as a signaling molecule. Here, we found that HRGβ1 induced Stat3 recruitment to the promoters of the progestin-regulated cell cycle modulators Bcl-XL and p21CIP1 and also stimulated Stat3 binding to the mouse mammary tumor virus promoter, which carries consensus progesterone response elements. Interestingly, HRGβ1-activated Stat3 displayed differential functions on PR activity depending on the promoter bound. Indeed, Stat3 was required for PR binding in bcl-X, p21CIP1, and c-myc promoters while exerting a PR coactivator function on the mouse mammary tumor virus promoter. Stat3 also proved to be necessary for HRGβ1-induced in vivo tumor growth. Our results endow Stat3 a novel function as a coregulator of HRGβ1-activated PR to promote breast cancer growth. These findings underscore the importance of understanding the complex interactions between PR and other regulatory factors, such as Stat3, that contribute to determine the context-dependent transcriptional actions of PR.

Antisense RNA of proto-oncogene c-fos blocks renewed growth of quiescent 3T3 cells

1987 ◽  
Vol 7 (2) ◽  
pp. 639-649
Author(s):  
K Nishikura ◽  
J M Murray
Keyword(s):  
Growth Factor ◽  
Antisense Rna ◽  
Platelet Derived Growth Factor ◽  
3T3 Cells ◽  
Mammary Tumor Virus ◽  
Quiescent Cells ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter ◽  
Stimulation Of

Mouse 3T3 cells were transformed with an antisense c-fos gene fused to a mouse mammary tumor virus promoter. In transformants that integrated a large number of antisense c-fos sequences, the usual large increase in c-fos mRNA and protein following stimulation of quiescent cells by platelet-derived growth factor was blocked in the presence of dexamethasone. These cells subsequently also failed to show the stimulation of DNA synthesis normally induced by platelet-derived growth factor. Appropriate expression of c-fos appears to be a prerequisite for reentry of quiescent cells into the cell cycle.

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