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Gamma radiation, known to produce genetic damage in both somatic and germ cells of experimental animals and man, can also block thromboxane A2 (TXA2) and prostaglandin E1 (PGE1) synthesis. In this communication evidence is presented that colchicine, a known TXA2 and PGE1 synthesis stimulator, can suppress the genetic damage induced in the germ cells of mice by gamma radiation. This evidence lends support to the hypothesis that an altered PG system could be responsible for mutagenesis and carcinogenesis.
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Analysis of adaptive radiation has had a central role in the development of evolutionary theory, but it is not clear why some groups radiate and others do not. Two recent papers by Albertson and colleagues on the genetic architecture of East African cichlid fishes implicate hybridization, transgressive segregation and genetic covariation in the early stages of adaptive radiation. Transgressive segregation and genetic covariation might be key innovations in genetic architecture that favor adaptive radiation.
The identification of breast cancer susceptibility genes, such as BRCA1, BRCA2, ATM, and p53, has been accompanied by the examination of the effects of radiation in combination with genetic mutations at these loci. Women at high risk for developing breast cancer may respond differently than the general population to low- and high-dose radiation exposures associated with screening and treatment. Epidemiologic studies are being performed to investigate the effects of radiation on subsequent breast cancer development in genetically predisposed individuals. Mouse strains with specific genetic modifications are being created to study the consequence of both inherited mutations and radiation on mammary gland carcinogenesis. Finally, studies investigating DNA damage-response pathways after radiation exposure are being performed. Recent work on the effects of several known or suspected breast cancer susceptibility genes, alone or in combination with radiation, is presented here, and directions for future research are considered.
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Estimates of the genetic damage from radiation exposures of human populations are needed in order to set reasonable limits for future exposures. In addition to the three rads per generation received by the gonads from natural sources, a similar amount is currently contributed by medical radiology and a further five rads per generation has been suggested as an upper limit for exposures from the future peaceful uses of atomic energy. Two methods of estimating the genetic damage from such an increase suggest that there might be in the vicinity of 250 to 800 severely affected individuals per year in a population of 20 million people, or within an order of magnitude of the current highway fatality rate for Canada of about 4000 per year. Although the true value may be less, or greater, by as much as tenfold, the effect is in any case large enough to justify continued scrutiny.
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A map has been assembled that extends from the XY homology region in Xq21.3 to proximal Xq24, approximately 20 Mb, formatted with 200 STSs that include 25 dinucleotide repeat polymorphic markers and more than 80 expressed sequences including 30 genes. New genes HTRP5, CAPN6, STPK, 14-3-3PKR, and CALM1 and previously known genes including BTK, DDP, GLA, PLP, COL4A5, COL4A6, PAK3, and DCX are localized; candidate loci for other disorders for which genes have not yet been identified, including DFN-2, POF, megalocornea, and syndromic and nonsyndromic mental retardation, are also mapped in the region. The telomeric end of the contig overlaps a yeast artificial chromosome (YAC) contig from Xq24-q26 and with other previously published contigs provides complete sequence-tagged site (STS)/YAC-based coverage of the long arm of the X chromosome. The order of published landmark loci in genetic and radiation hybrid maps is in general agreement. Combined with high-density STS landmarks, the multiple YAC clone coverage and integrated genetic, radiation hybrid, and transcript map provide resources to further disease gene searches and sequencing.
An albino mutant of Blepharisma intermedium is much more sensitive (on the basis of time to regeneration of transected cells) to short-wavelength ultraviolet radiation than the wild type (containing a reddish pigment) from which the mutant derived. In the wild type, absorption of ultraviolet light by the pigment present in the outer surface of the cell presumably reduces the intensity of the radiation impinging on the vulnerable interior.
Genetic diversity may buffer amphibian populations against environmental vicissitudes. We hypothesized that wood frogs (Rana sylvatica)from populations with lower genetic diversity are more susceptible to ultraviolet-B (UV-B) radiation than those from populations with higher diversity. We used RAPD markers to obtain genetic diversity estimates for 12 wood frog populations. We reared larval wood frogs from these populations and exposed experimental groups of eggs and larvae to one of three treatments: unfiltered sunlight, sunlight filtered through a UM-B-blocking filter (Mylar), and sunlight filtered through a UV-B-transmitting filter (acetate). In groups exposed to UVB, larval mortality and deformity rates increased significantly, but egg mortality did not. We found a significant negative relationship between genetic diversity and egg mortality, larval mortality, and deformity rates. Furthermore, the interaction between UV-B treatment and genetic diversity significantly affected larval mortality. Populations with low genetic diversity experienced higher larval mortality rates when exposed to UVB than did populations with high genetic diversity. This is the first time an interaction between genetic diversity and an environmental stressor has been documented in amphibians. Differences in genetic diversity among populations, coupled with environmental stressors, may help explain patterns of amphibian decline.
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