Changing capacity for DNA excision repair in mouse embryonic cells in vitro

Peleg, Leah; Raz, Eyal; Ben-Ishai, R.

doi:10.1016/0014-4827(77)90095-7

Cited by 90 publications

(21 citation statements)

References 12 publications

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“…6B). This lineage had a mean of 9 grains/nucleus (37% of foreskin fibroblasts), representing a level of UDS that was 3-fold higher than the next highest level of UDS documented [17,18] namely that of the primary fetal skin fibroblasts (12.5% FF) (Fig. 6A).…”

Section: Resultsmentioning

confidence: 95%

“…Human foreskin fibroblast (ff) cells were included in all experiments to serve as a standard for comparison for all of the mouse cell lineages. Adult mouse skin was also included in these studies to serve as a reference point for a level of UDS that has been previously documented in murine skin fibroblasts [17,18,32,33].…”

Section: Resultsmentioning

confidence: 99%

“…In addition Peleg et al [18] have shown that later gestation (13-15 dg) embryonic fibroblasts have a greater capacity to perform excision repair than adult mouse skin. These results raise the issue of stage-specificity or differentiative status as a factor in excision repair within mammalian cells.…”

Section: Discussionmentioning

confidence: 99%

“…The pattern or role of NER has never been defined in specific lineages during mammalian development, despite the fact that several human DNA repair deficiency syndromes manifest developmental abnormalities [16]. Studies of NER in mixed lineages during development using the functional assay for NER, UDS, have shown that in contrast to established mouse cell lines, primary murine embryonic fibroblasts excise dimers at a greater rate [17,18] and perform higher levels of repair synthesis [19]. Early passages of mixed embryonic fibroblasts have been shown to manifest higher levels of excision repair than later passages [17].…”

Section: Introductionmentioning

confidence: 99%

“…Early passages of mixed embryonic fibroblasts have been shown to manifest higher levels of excision repair than later passages [17]. Peleg et al [18] have since shown that the capacity for excision repair of UV radiation damage in passaged embryonic fibroblasts from mouse is dependent upon the gestational stage and the duration of in vitro growth. This study was performed on repeatedly passaged mixed primary embryo fibroblasts at 13-15 or 17-19 days gestation (dg).…”

Section: Introductionmentioning

confidence: 99%

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Elevated DNA Excision Repair Capacity in the Extraembryonic Mesoderm of the Midgestation Mouse Embryo

Latimer

Hultner

Cleaver

et al. 1996

Experimental Cell Research

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In order to determine whether there is differential cell-type-specific DNA repair we measured the nucleotide excision repair capacity of the four distinct cell lineages that comprise the extraembryonic yolk sac using the unscheduled DNA synthesis assay. Yolk sacs from mouse embryos at 11.5-12.5 days gestation were microdissected to yield purified trophoblast, parietal endoderm, mesoderm, and visceral endoderm, as well as fetal skin fibroblasts which were then grown as primary explants. At this midgestational stage of development, the yolk sac provides essential functions for the sustenance of the embryo while the complex process of organogenesis is proceeding in the liver, kidney, and gut. Trophoblast giant cells, parietal endoderm, and visceral endoderm all demonstrated low levels of unscheduled DNA synthesis consistent with levels measured in adult mouse skin fibroblasts. As has previously been documented, embryonic mouse skin fibroblasts were reproducibly 2-to 3-fold higher than adult mouse skin fibroblasts in levels of DNA excision repair. The extraembryonic mesoderm, however, displayed a statistically significant level of unscheduled DNA synthesis 10-fold higher than adult mouse skin fibroblasts or the other lineages of the midgestation yolk sac. Further, the S-indexes of these lineages were also determined to assess the possible relevance of differential repair to the proliferative status of the cells. These data demonstrate that DNA excision repair capacity is lineage-specific during embryogenesis in the mouse. These studies may begin to provide a context for understanding the perplexing developmental aspects such as the characteristic congenital abnormalities associated with the human heritable DNA repair deficiency diseases.

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Elevated DNA Excision Repair Capacity in the Extraembryonic Mesoderm of the Midgestation Mouse Embryo

Latimer

Hultner

Cleaver

et al. 1996

Experimental Cell Research

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The regulation of DNA repair during development

Mitchell

Hartman

1990

BioEssays

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DNA repair is important in such phenomena as carcinogenesis and aging. While much is known about DNA repair in single-cell systems such as bacteria, yeast, and cultured mammalian cells, it is necessary to examine DNA repair in a developmental context in order to completely understand its processes in complex metazoa such as man. We present data to support the notion that proliferating cells from organ systems, tumors, and embryos have a greater DNA repair capacity than terminally differentiated, nonproliferating cells. Differential expression of repair genes and accessibility of chromatin to repair enzymes are considered as determinants in the developmental regulation of DNA repair.

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Revisiting the rodent repairadox

Hanawalt

2001

Environ and Mol Mutagen

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Cultured rodent and human cells typically display similar clonal survival characteristics following exposure to ultraviolet light (UV). However, compared to human cells, cultured cells from mice, rats, and hamsters are generally deficient in excision repair of the most prominent DNA lesion produced by UV, the cyclobutane pyrimidine dimer. In light of recent studies on the control of nucleotide excision repair, we are beginning to understand the basis for this so-called "repairadox." The resolution of this issue is important because rodents are so widely employed as surrogates for humans in genetic toxicology. This article will review the evolution in our understanding of rodent DNA repair and will also "revisit" my early association with my graduate mentor and esteemed colleague, Dick Setlow, in his honor upon the attainment of his 80th birthday.

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Changing capacity for DNA excision repair in mouse embryonic cells in vitro

Cited by 90 publications

References 12 publications

Elevated DNA Excision Repair Capacity in the Extraembryonic Mesoderm of the Midgestation Mouse Embryo

Elevated DNA Excision Repair Capacity in the Extraembryonic Mesoderm of the Midgestation Mouse Embryo

The regulation of DNA repair during development

Revisiting the rodent repairadox

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