Dialysis-Related Genotoxicity: Sister Chromatid Exchanges and DNA Lesions in T and B Lymphocytes of Uremic Patients. Genomic Damage in Patients on Hemodiafiltration

2006 ◽  
Vol 24 (5-6) ◽  
pp. 569-574 ◽  
Author(s):  
M. Buemi ◽  
F. Floccari ◽  
C. Costa ◽  
C. Caccamo ◽  
N. Belghity ◽  
...  
Keyword(s):  
B Lymphocytes ◽  
Sister Chromatid ◽  
Sister Chromatid Exchanges ◽  
Dna Lesions ◽  
T And B Lymphocytes ◽  
Genomic Damage ◽  
Uremic Patients ◽  
Chromatid Exchanges

Persistence of DNA lesions and the cytological cancellation of sister chromatid exchanges

Chromosoma ◽  
1985 ◽  
Vol 92 (1) ◽  
pp. 7-10 ◽  
Author(s):  
J. B. Schvartzman ◽  
V. J. Goyanes ◽  
A. Campos ◽  
A. M. Lage ◽  
C. Veiras ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchanges ◽  
Dna Lesions ◽  
Chromatid Exchanges ◽  
Persistence Of Dna

scholarly journals Sister chromatid exchanges induced by perturbed replication are formed independently of homologous recombination factors

2021 ◽  
Author(s):  
Anne Margriet Heijink ◽  
Colin Stok ◽  
David Porubsky ◽  
Eleni M. Manolika ◽  
Yannick P. Kok ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Sister Chromatid ◽  
Parp Inhibitor ◽  
Sister Chromatid Exchanges ◽  
Fragile Sites ◽  
Dna Lesions ◽  
Parp Inhibition ◽  
Dna Breaks ◽  
Brca1 Brca2 ◽  
Chromatid Exchanges

SummarySister chromatid exchanges (SCEs) are products of joint DNA molecule resolution, and are considered to form through homologous recombination (HR). Indeed, upon generation of irradiation-induced DNA breaks, SCE induction was compromised in cells deficient for canonical HR factors BRCA1, BRCA2 and RAD51. Contrarily, replication-blocking agents, including PARP inhibitors, induced SCEs independently of BRCA1, BRCA2 and RAD51. PARP inhibitor-induced SCEs were enriched at common fragile sites (CFSs), and were accompanied by post-replicative single-stranded DNA (ssDNA) gaps. Moreover, PARP inhibitor-induced replication lesions were transmitted into mitosis, suggesting that SCEs originate from mitotic processing of under-replicated DNA. We found that DNA polymerase theta (POLQ) was recruited to mitotic DNA lesions, and loss of POLQ resulted in reduced SCE numbers and severe chromosome fragmentation upon PARP inhibition in HR-deficient cells. Combined, our data show that PARP inhibition generates under-replicated DNA, which is transferred into mitosis and processed into SCEs, independently of canonical HR factors.

scholarly journals Sister Chromatid Exchanges Are Mediated by Homologous Recombination in Vertebrate Cells

1999 ◽  
Vol 19 (7) ◽  
pp. 5166-5169 ◽  
Author(s):  
Eiichiro Sonoda ◽  
Masao S. Sasaki ◽  
Ciaran Morrison ◽  
Yuko Yamaguchi-Iwai ◽  
Minoru Takata ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Sister Chromatid ◽  
Sister Chromatid Exchanges ◽  
Dna Lesions ◽  
End Joining ◽  
Chromosomal Stability ◽  
Tumorigenic Potential ◽  
Associated Proteins ◽  
Chromatid Exchanges

ABSTRACT Sister chromatid exchange (SCE) frequency is a commonly used index of chromosomal stability in response to environmental or genetic mutagens. However, the mechanism generating cytologically detectable SCEs and, therefore, their prognostic value for chromosomal stability in mitotic cells remain unclear. We examined the role of the highly conserved homologous recombination (HR) pathway in SCE by measuring SCE levels in HR-defective vertebrate cells. Spontaneous and mitomycin C-induced SCE levels were significantly reduced for chicken DT40 B cells lacking the key HR genes RAD51 and RAD54but not for nonhomologous DNA end-joining (NHEJ)-defectiveKU70 −/− cells. As measured by targeted integration efficiency, reconstitution of HR activity by expression of a human RAD51 transgene restored SCE levels to normal, confirming that HR is the mechanism responsible for SCE. Our findings show that HR uses the nascent sister chromatid to repair potentially lethal DNA lesions accompanying replication, which might explain the lethality or tumorigenic potential associated with defects in HR or HR-associated proteins.

Diagnostic Ultrasound and Sister Chromatid Exchanges

1985 ◽  
Vol 40 (9) ◽  
pp. 589-590
Author(s):  
V. CIARAVINO ◽  
A. BRULFERT ◽  
M. W. MILLER ◽  
D. JACOBSON-KRAM ◽  
W. F. MORGAN
Keyword(s):  
Sister Chromatid ◽  
Diagnostic Ultrasound ◽  
Sister Chromatid Exchanges ◽  
Chromatid Exchanges

scholarly journals PRESENCE OF A BASE LINE LEVEL OF SISTER CHROMATID EXCHANGES IN SOMATIC CELLS OF DROSOPHILA MELANOGASTER IN VIVO AND IN VITRO

Genetics ◽  
1982 ◽  
Vol 100 (2) ◽  
pp. 259-278
Author(s):  
Hideo Tsuji
Keyword(s):  
Drosophila Melanogaster ◽  
Sister Chromatid ◽  
Ganglion Cells ◽  
Sister Chromatid Exchanges ◽  
Base Line ◽  
Cell Cycles ◽  
Chromatid Exchanges ◽  
Third Instar Larvae

ABSTRACT Sister chromatid exchanges (SCEs) under in vivo and in vitro conditions were examined in ganglion cells of third-instar larvae of Drosophila melanogaster (Oregon-R). In the in vivo experiment, third-instar larvae were fed on synthetic media containing 5-bromo-2′-deoxyuridine (BrdUrd). After two cell cycles, ganglia were dissected and treated with colchicine. In the in vitro experiment, the ganglia were also incubated in media containing BrdUrd for two cell cycles, and treated with colchicine. SCEs were scored in metaphase stained with Hoechst 33258 plus Giemsa. The frequencies of SCEs stayed constant in the range of 25-150 vg/ml and 0.25-2.5 vg/ml of BrdUrd in vivo and in vitro, respectively. SCEs gradually increased at higher concentrations, strongly suggesting that at least a fraction of the detected SCEs are spontaneous. The constant levels of SCE frequency were estimated, on the average, at 0.103 per cell per two cell cycles for females and 0.101 for males in vivo and at 0.096 for females and 0.091 for males in vitro. No difference was found in the SCE frequency between sexes at any of the BrdUrd concentrations. The analysis for the distribution of SCEs within chromosomes revealed an extraordinarily high proportion of the SCEs at the junctions between euchromatin and heterochromatin; the remaining SCEs were preferentially localized in the euchromatic regions of the chromosomes and in the heterochromatic Y chromosome. These results were largely inconsistent with those of Gatti et al. (1979).

scholarly journals Sister chromatid exchanges and structural chromosome aberrations in relation to smoking in 91 individuals

Hereditas ◽  
2008 ◽  
Vol 98 (1) ◽  
pp. 77-81 ◽  
Author(s):  
K. HEDNER ◽  
B. HÖGSTEDT ◽  
A.-M. KOLNIG ◽  
E. MARK-VENDEL ◽  
B. STRÖMBECK ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Chromosome Aberrations ◽  
Sister Chromatid Exchanges ◽  
Structural Chromosome ◽  
Chromatid Exchanges
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