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Results for “RADIATION GENETICS”

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At least 1,027 records · Page 57Linked to original sources
PubMed2000

A sequence-ready PAC contig of a 550-kb region on rat chromosome 4 including the diabetes susceptibility gene Lyp.

The Lyp locus controls diabetes development in rats. The diabetogenic allele in diabetes-prone BB rats is responsible for T cell lymphopenia characterized by the absence of regulatory T cells. We present refined genetic and radiation hybrid maps of the Lyp region on rat chromosome 4, a single 800-kb rat yeast artificial chromosome and a rat P1-derived artificial chromosome (PAC) contig corresponding to approximately 550 kb, both encompassing the entire candidate region. The contig, consisting of 48 PACs, gives 3- to 12-fold coverage. Genetic, radiation hybrid, and physical data were all in agreement and supported the same marker order. Nine genes and ESTs were identified in the contig in addition to a rat EST from the University of Iowa rat EST database-all possible candidate genes for Lyp. Alignment of our rat PAC contig with sequenced human PAC/BAC contigs confirms the position within the region of 3 of the 10 candidates and identifies an additional 8 genes/ESTs as candidates. These data will facilitate identification of Lyp.

Animals↗
PubMed1992

Historical perspective: a forward look, a backward look.

This paper summarizes how the problems of fallout, genetics, radioactive waste, and regulatory control of radiation were perceived by Dunning, Straub, Taylor, and others in 1955 at the inaugural meeting of the Health Physics Society. It was stated that health physicists had a great opportunity to resolve these problems and to avoid past mistakes. Throughout the 1950s, health physicists made major contributions to elucidating the fallout problem and contributed to its resolution, and it can be considered a success story. Waste disposal is not considered to be a success to date. A major difference has been the lack of political will to grapple with a perceived "no win" situation. The evolution of radiation limits is briefly traced over the past 37 y from voluntary standards to rigorously enforced regulations demanded by society. This paper speculates that the changing international scene makes the United States the pre-eminent nuclear power which will challenge future health physicists to maintain a balance between the control of radioactive material and its peaceful applications.

Health Physics↗
PubMed2005

Comparative landscape genetics and the adaptive radiation of Darwin's finches: the role of peripheral isolation.

We use genetic divergence at 16 microsatellite loci to investigate how geographical features of the Galápagos landscape structure island populations of Darwin's finches. We compare the three most genetically divergent groups of Darwin's finches comprising morphologically and ecologically similar allopatric populations: the cactus finches (Geospiza scandens and Geospiza conirostris), the sharp-beaked ground finches (Geospiza difficilis) and the warbler finches (Certhidea olivacea and Certhidea fusca). Evidence of reduced genetic diversity due to drift was limited to warbler finches on small, peripheral islands. Evidence of low levels of recent interisland migration was widespread throughout all three groups. The hypothesis of distance-limited dispersal received the strongest support in cactus and sharp-beaked ground finches as evidenced by patterns of isolation by distance, while warbler finches showed a weaker relationship. Support for the hypothesis that gene flow constrains morphological divergence was only found in one of eight comparisons within these groups. Among warbler finches, genetic divergence was relatively high while phenotypic divergence was low, implicating stabilizing selection rather than constraint due to gene flow. We conclude that the adaptive radiation of Darwin's finches has occurred in the presence of ongoing but low levels of gene flow caused by distance-dependent interisland dispersal. Gene flow does not constrain phenotypic divergence, but may augment genetic variation and facilitate evolution due to natural selection. Both microsatellites and mtDNA agree in that subsets of peripheral populations of two older groups are genetically more similar to other species that underwent dramatic morphological change. The apparent decoupling of morphological and molecular evolution may be accounted for by a modification of Lack's two-stage model of speciation: relative ecological stasis in allopatry followed by secondary contact, ecological interactions and asymmetric phenotypic divergence.

Adaptation, Biological↗
PubMed2004

Genetic variation in radiation-induced expression phenotypes.

Studies have demonstrated that natural variation in the expression level of genes at baseline is extensive, and the determinants of this variation can be mapped by a genetic-linkage approach. In this study, we used lymphoblastoid cells to explore the variation in radiation-induced transcriptional changes. We found that, among normal individuals, there is extensive variation in transcriptional response to radiation exposure. By studying monozygotic twins, we demonstrated that there is evidence of a heritable component to this variation. The postradiation variation in the expression level of several genes, including the ferredoxin reductase gene (FDXR) and the cyclin-dependent kinase inhibitor 1A gene (CDKN1A), is significantly greater (P<.001) among twin pairs than within twin pairs. The induction of FDXR by radiation showed a bimodal distribution. Our findings have important implications for understanding the genetic basis of radiation response, which has remained largely unknown due to the lack of family material needed for genetic studies. Our approach, which uses expression phenotypes in cell lines, allows us to expose cells from family members to radiation. Similar study design can be applied to dissect the genetic basis of other complex human traits.

Cell Cycle Proteins↗
PubMed2005

Genetic effects of radiofrequency radiation (RFR).

The possible effects of radiofrequency (RF) exposure on the genetic material of cells are considered very important since damage to the DNA of somatic cells can be linked to cancer development or cell death whereas damage to germ cells can lead to genetic damage in next and subsequent generations. This is why the scientific literature reports many investigations on the subject. According to a number of review papers, the conclusion so far is that there is little evidence that RFR is directly mutagenic and that adverse effects that were reported in some of the papers are predominantly the result of hyperthermia. Yet, some subtle indirect effects on DNA replication and/or transcription of genes under relatively restricted exposure conditions cannot be ruled out. Furthermore, the possibility of combined effects of RFR with environmental carcinogens/mutagens merits further attention. The present paper takes into account more recent investigations but the conclusion remains the same. A majority of studies report no increased (cyto)genetic damage but yet, a considerable number of investigations do. However, many studies were not sufficiently characterized, are therefore difficult to replicate and cannot be compared to others. Experimental protocols were very different from one study to another and investigations from a single laboratory were very often limited in the sample size or number of cells investigated, preventing a robust statistical analysis. Subtle, but significant differences between RFR-exposed and sham-exposed cells cannot be found in such conditions. For the above reasons, it was concluded at a workshop in Löwenstein (November 2002) that further investigations by individual laboratories most probably will not add much to the discussion of radiofrequency radiation (RFR) genotoxicity. Large, well coordinated, international collaborative studies involving participation of several experienced scientists are considered an alternative of uttermost importance. One such study is now being planned.

Animals↗
PubMed2003

Genetic interactions between Pten and p53 in radiation-induced lymphoma development.

Genetic analysis of radiation-induced lymphomas from p53 heterozygous or null mice has revealed a high frequency of genetic alterations on mouse chromosome 19. Detailed microsatellite analysis of chromosome 19 deletions identified three independent regions of loss of heterozygosity, one of which was refined to a 0.3 Mb interval that contained the Pten tumor suppressor gene. More than 50% of radiation-induced tumors from p53+/- and p53-/- mice showed heterozygous loss of one Pten allele. In most cases, the remaining allele was wild type and expressed, suggesting that Pten is a haploinsufficient tumor suppressor gene for mouse lymphoma development. This conclusion was supported by the detection of specific intragenic deletions in Pten in tumors that retained one wild-type allele. Pten heterozygous mice were just as sensitive as p53+/- mice to induction of tumors by radiation, and surprisingly, the double p53+/-Pten+/-mice were equivalent to p53 null mice in radiation sensitivity. Despite the fact that Pten appears to be a haploinsufficient tumor suppressor gene, most tumors from both the single and double heterozygous mice had lost the remaining wild-type allele. The mechanism of loss in all cases involved the complete chromosome, suggesting that it is driven by other tumor suppressor genes on this chromosome. This sensitized screen therefore identified complementary roles for Pten and p53 pathways in suppression of tumor development induced by radiation exposure.

Animals↗