Role of sister chromatid exchanges in chromatid aberration formation

Nature ◽  
1977 ◽  
Vol 268 (5617) ◽  
pp. 235-236 ◽  
Author(s):  
TAKAJI IKUSHIMA
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchanges ◽  
Chromatid Aberration ◽  
Chromatid Exchanges

Saccharomyces cerevisiae rad51 Mutants Are Defective in DNA Damage-Associated Sister Chromatid Exchanges but Exhibit Increased Rates of Homology-Directed Translocations

Genetics ◽  
2001 ◽  
Vol 158 (3) ◽  
pp. 959-972
Author(s):  
Michael Fasullo ◽  
Peter Giallanza ◽  
Zheng Dong ◽  
Cinzia Cera ◽  
Thomas Bennett
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Dna Damage ◽  
Sister Chromatid ◽  
Sister Chromatid Exchanges ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
Dna Damaging Agents ◽  
Break Induced Replication ◽  
Chromatid Exchanges

Abstract Saccharomyces cerevisiae Rad51 is structurally similar to Escherichia coli RecA. We investigated the role of S. cerevisiae RAD51 in DNA damage-associated unequal sister chromatid exchanges (SCEs), translocations, and inversions. The frequency of these rearrangements was measured by monitoring mitotic recombination between two his3 fragments, his3-Δ5′ and his3-Δ3′::HOcs, when positioned on different chromosomes or in tandem and oriented in direct or inverted orientation. Recombination was measured after cells were exposed to chemical agents and radiation and after HO endonuclease digestion at his3-Δ3′::HOcs. Wild-type and rad51 mutant strains showed no difference in the rate of spontaneous SCEs; however, the rate of spontaneous inversions was decreased threefold in the rad51 mutant. The rad51 null mutant was defective in DNA damage-associated SCE when cells were exposed to either radiation or chemical DNA-damaging agents or when HO endonuclease-induced double-strand breaks (DSBs) were directly targeted at his3-Δ3′::HOcs. The defect in DNA damage-associated SCEs in rad51 mutants correlated with an eightfold higher spontaneous level of directed translocations in diploid strains and with a higher level of radiation-associated translocations. We suggest that S. cerevisiae RAD51 facilitates genomic stability by reducing nonreciprocal translocations generated by RAD51-independent break-induced replication (BIR) mechanisms.

Additive Action of Vitamins C and E against Hydrocortisone-Induced Genotoxicity in Human Lymphocyte Chromosomes

2002 ◽  
Vol 72 (4) ◽  
pp. 204-209 ◽  
Author(s):  
Sultan Ahmad ◽  
Afsahul Hoda ◽  
Mohammad Afzal
Keyword(s):  
Chromosomal Aberrations ◽  
Human Lymphocyte ◽  
Sister Chromatid ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Sister Chromatid Exchanges ◽  
Additive Action ◽  
Hydrocortisone Administration ◽  
Chromatid Exchanges

In earlier reports, hydrocortisone administration to human lymphocytes in culture was shown to cause chromosomal aberrations and increased sister chromatid exchanges. With a view to study the ameliorative action of some antioxidants against this effect, vitamins C and E were used separately and in combination along with hydrocortisone treatment, at different dosage and for different durations, on human lymphocyte cultures. The levels of chromosomal aberrations and sister chromatid exchanges were lowered, suggesting a protective role of vitamins against genotoxic damage. Administration of vitamins C and E combined appeared to be more effective in preventing chromosomal damage than separate administration, demonstrating the additive action of these vitamins against steroid-induced genotoxicity.

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.

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