Topic
Sister chromatid exchange
About: Sister chromatid exchange is a research topic. Over the lifetime, 3187 publications have been published within this topic receiving 90029 citations. The topic is also known as: replication-born DSB repair by SCE & GO:1990414.
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TL;DR: This study examines the chromosome aberration and sister-chromatid exchange frequencies in lymphocytes from a group of 6 pathology workers and 5 unexposed controls and finds no detectable differences could be found between the groups in either chromosomal aberration induction or sister- Chromatid Exchange frequencies.
49 citations
TL;DR: Although baseline levels of SCE appear to be similar in metaphase cells derived from young and old human skin fibroblast cultures, as significant decline in both MMC- and AAAF-induced sister chromatid exchanges was observed in the older cell populations, parallel examination of several cell strains fromYoung and old donors confirmed the decrease in mutagen-induced SCE frequencies in older cell population.
Abstract: Although baseline levels of SCE appear to be similar in metaphase cells derived from young and old human skin fibroblast cultures, a significant decline in both MMC- and AAAF-induced sister chromatid exchanges was observed in the older cell populations. Considerable variation exists in the levels of MMC-induced SCE between individual cell cultures. However, parallel examination of several cell strains from young and old donors confirmed the decrease in mutagen-induced SCE frequencies in older cell populations.
49 citations
TL;DR: Spontaneous and UV induced unequal mitotic sister chromatid recombination was examined in RAD+ and rad52-1 strains carrying the LEU2 gene inserted in the rDNA locus and the rad 52-1 mutation greatly reduces the frequency of UV induced sister chromate recombination.
Abstract: Spontaneous and UV induced unequal mitotic sister chromatid recombination was examined in RAD+ and rad52-1 strains carrying the LEU2 gene inserted in the rDNA locus. The rad52-1 mutation does not affect spontaneous sister chromatid recombination but greatly reduces the frequency of UV induced sister chromatid recombination.
49 citations
TL;DR: The present study revealed that it caused minisatellite mutation (MSM) at a high frequency in NIH 3T3 cells, although no microsatellite mutation was found, and the biological relevance of the induction of MSM in the tumorigenic process by OA is pointed to.
Abstract: Okadaic acid (OA) is a strong tumor promoter of mouse skin carcinogenesis and also a potent inhibitor of serine/threonine protein phosphatases. OA induces various genetic alterations in cultured cells, such as diphtheria-toxin-resistance mutations, sister chromatid exchange, exclusion of exogenous transforming oncogenes, and gene amplification. The present study revealed that it caused minisatellite mutation (MSM) at a high frequency in NIH 3T3 cells, although no microsatellite mutation was found. Nine of 31 clones (29%) exhibited MSM after 6 days of OA treatment, as opposed to only 1 of 30 clones (3%) without OA exposure. Moreover, NIH 3T3 cells treated with OA acquired tumorigenicity in nude mice, giving rise to 7 tumors within 25 weeks in 20 sites where 3 × 106 cells were injected. In contrast, the same numbers of untreated cells gave rise to only one tumor, and the tumor grew much slower. All of three OA-induced tumors examined manifested the MSM. The findings thus point to a molecular mechanism by which OA could function as a tumor promoter, and also the biological relevance of the induction of MSM in the tumorigenic process by OA.
49 citations
Journal Article•
TL;DR: Sensitivity to ultraviolet radiation was studied in lymphoblastoid cell lines derived from 32 members of two families with histories of multiple primary melanomas in several generations, consistent with a dominantly inherited ultraviolet light sensitivity associated with these examples of familial melanoma.
Abstract: Sensitivity to ultraviolet radiation was studied in lymphoblastoid cell lines derived from 32 members of two families with histories of multiple primary melanomas in several generations. As assayed by colony formation in agar or by trypan blue exclusion following irradiation, cellular sensitivity showed a bimodal distribution. All persons with melanoma or multiple moles were in the sensitive group, while some family members exhibited responses similar to those of controls. Cells from four cases of sporadic melanoma showed normal levels of sensitivity. The data are consistent with a dominantly inherited ultraviolet light sensitivity associated with these examples of familial melanoma. Spontaneous and ultraviolet light-induced sister chromatid exchange frequencies were similar to those in control cell lines. No defect in excision repair was detected in any of the above cell lines, but the sensitive group showed postirradiation inhibition of DNA replication intermediate between controls and an excision-deficient xeroderma pigmentosum cell line.
49 citations