Gamma-ray induced strand breakage of Bacillus subtilis DNA irradiated in vivo

1971 ◽  
Vol 17 (5) ◽  
pp. 575-583 ◽  
Author(s):  
David L. Dugle ◽  
Janet R. Dugle
Keyword(s):  
Bacillus Subtilis ◽  
Survival Data ◽  
Gamma Ray ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Subtilis Strain ◽  
Strand Breaks ◽  
Strand Breakage ◽  
Total Dna

Evidence is presented for the isolation of DNA having a molecular weight of 31 ± 5 × 108 from Bacillus subtilis strain 23 Thy− cells. This accounts for the total DNA content of the genome. Single-strand and double-strand breaks induced by 60Co gamma rays were measured by sucrose density centrifugation. The occurrence of repair of single-strand and possibly double-strand breaks at 0 °C is inferred from survival data and the effects of pre- or post-irradiation heating.

scholarly journals Artificial and Solar UV Radiation Induces Strand Breaks and Cyclobutane Pyrimidine Dimers in Bacillus subtilis Spore DNA

2000 ◽  
Vol 66 (1) ◽  
pp. 199-205 ◽  
Author(s):  
Tony A. Slieman ◽  
Wayne L. Nicholson
Keyword(s):  
Bacillus Subtilis ◽  
Uv Irradiation ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Complex Spectrum ◽  
Cyclobutane Pyrimidine Dimers ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Pyrimidine Dimers ◽  
Solar Uv

ABSTRACT The loss of stratospheric ozone and the accompanying increase in solar UV flux have led to concerns regarding decreases in global microbial productivity. Central to understanding this process is determining the types and amounts of DNA damage in microbes caused by solar UV irradiation. While UV irradiation of dormant Bacillus subtilis endospores results mainly in formation of the “spore photoproduct” 5-thyminyl-5,6-dihydrothymine, genetic evidence indicates that an additional DNA photoproduct(s) may be formed in spores exposed to solar UV-B and UV-A radiation (Y. Xue and W. L. Nicholson, Appl. Environ. Microbiol. 62:2221–2227, 1996). We examined the occurrence of double-strand breaks, single-strand breaks, cyclobutane pyrimidine dimers, and apurinic-apyrimidinic sites in spore DNA under several UV irradiation conditions by using enzymatic probes and neutral or alkaline agarose gel electrophoresis. DNA from spores irradiated with artificial 254-nm UV-C radiation accumulated single-strand breaks, double-strand breaks, and cyclobutane pyrimidine dimers, while DNA from spores exposed to artificial UV-B radiation (wavelengths, 290 to 310 nm) accumulated only cyclobutane pyrimidine dimers. DNA from spores exposed to full-spectrum sunlight (UV-B and UV-A radiation) accumulated single-strand breaks, double-strand breaks, and cyclobutane pyrimidine dimers, whereas DNA from spores exposed to sunlight from which the UV-B component had been removed with a filter (“UV-A sunlight”) accumulated only single-strand breaks and double-strand breaks. Apurinic-apyrimidinic sites were not detected in spore DNA under any of the irradiation conditions used. Our data indicate that there is a complex spectrum of UV photoproducts in DNA of bacterial spores exposed to solar UV irradiation in the environment.

Transposase promotes double strand breaks and single strand joints at Tn10 termini in vivo

Cell ◽  
1984 ◽  
Vol 39 (1) ◽  
pp. 181-190 ◽  
Author(s):  
Donald Morisato ◽  
Nancy Kleckner
Keyword(s):  
Double Strand Breaks ◽  
Single Strand ◽  
Strand Breaks

scholarly journals Homologous recombination as a resistance mechanism to replication-induced double-strand breaks caused by the antileukemia agent CNDAC

Blood ◽  
2010 ◽  
Vol 116 (10) ◽  
pp. 1737-1746 ◽  
Author(s):  
Xiaojun Liu ◽  
Yaqing Wang ◽  
Sherri Benaissa ◽  
Akira Matsuda ◽  
Hagop Kantarjian ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Cell Survival ◽  
Resistance Mechanism ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Single Strand Break ◽  
Strand Breaks

Abstract The nucleoside analog 2′-C-cyano-2′-deoxy-1-β-D-arabino-pentofuranosyl-cytosine (CNDAC), currently in clinical trials for hematologic malignancies, has a novel action mechanism of causing a single-strand break after its incorporation into DNA. Double-strand breaks (DSBs) are generated thereafter in vivo and, if not repaired, pose lethal impact on cell survival. This study sought to define the mechanisms by which CNDAC-induced DSBs are formed and repaired. We demonstrated that single-strand breaks induced by CNDAC incorporation into DNA were converted to DSBs when cells progressed into the subsequent S-phase. CNDAC-induced DSBs were products of replication, rather than a consequence of apoptosis. ATM, the activator of homologous recombination (HR), was essential for cell survival after CNDAC treatment in cell lines and in primary acute myeloid leukemia samples, as were the HR components, Rad51, Xrcc3, and Brca2. Furthermore, formation of sister chromatid exchanges, a hallmark of HR, increased significantly after CNDAC-treated cells had progressed into a second replication cycle. In contrast, neither the replication stress sensor ATR nor DNA-PK, the initiator of nonhomologous end-joining of DSB, was involved in repair of CNDAC-induced damage. Together, these results indicate that HR, but not nonhomologous end-joining, is the major repair or survival mechanism for DNA damage caused by CNDAC.

scholarly journals Focused Genetic Recombination of Bacteriophage T4 Initiated by Double-Strand Breaks

Genetics ◽  
2002 ◽  
Vol 162 (2) ◽  
pp. 543-556
Author(s):  
Victor Shcherbakov ◽  
Igor Granovsky ◽  
Lidiya Plugina ◽  
Tamara Shcherbakova ◽  
Svetlana Sizova ◽  
...  
Keyword(s):  
Genetic Recombination ◽  
Bacteriophage T4 ◽  
Proximal Part ◽  
Coupling Model ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
The Right ◽  
Frequency Distance

Abstract A model system for studying double-strand-break (DSB)-induced genetic recombination in vivo based on the ets1 segCΔ strain of bacteriophage T4 was developed. The ets1, a 66-bp DNA fragment of phage T2L containing the cleavage site for the T4 SegC site-specific endonuclease, was inserted into the proximal part of the T4 rIIB gene. Under segC+ conditions, the ets1 behaves as a recombination hotspot. Crosses of the ets1 against rII markers located to the left and to the right of ets1 gave similar results, thus demonstrating the equal and symmetrical initiation of recombination by either part of the broken chromosome. Frequency/distance relationships were studied in a series of two- and three-factor crosses with other rIIB and rIIA mutants (all segC+) separated from ets1 by 12-2100 bp. The observed relationships were readily interpretable in terms of the modified splice/patch coupling model. The advantages of this localized or focused recombination over that distributed along the chromosome, as a model for studying the recombination-replication pathway in T4 in vivo, are discussed.

Involvement of Ku80 in microhomology-mediated end joining for DNA double-strand breaks in vivo

DNA Repair ◽  
2007 ◽  
Vol 6 (5) ◽  
pp. 639-648 ◽  
Author(s):  
Yukitaka Katsura ◽  
Shigeru Sasaki ◽  
Masanori Sato ◽  
Kiyoshi Yamaoka ◽  
Kazumi Suzukawa ◽  
...  
Keyword(s):  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
End Joining ◽  
Strand Breaks
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