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PubMed1975

Genetic control of radiation sensitivity in Schizosaccharomyces pombe.

Genetic analysis of a large number of radiation-sensitive mutants of S. pombe, isolated in different laboratories, showed that these isolates represent 22 non-allelic loci. The mutants were shown to fall into three distinct classes concerning response to UV and ionizing radiation, including two mutants which are primarily sensitive to ionizing radiation but not to UV. Single-gene mutants were crossed to obtain supersensitive double mutants. Such double mutants showed a marked increase in sensitivty to a variety of inactivating agents as compared to the parental strains. The isolation of three classes of radiation-sensitive mutants and the construction of double mutants implies the presence of multiple pathways in S. pombe for repair of radiation-induced damage. The bearing of these data on cellular repair mechanisms in eukaryotes is discussed.

Alleles↗
PubMed1987

[Comparative effectiveness of different types of radiation in the induction of gene mutations: basic and applied aspects].

Large-scale radiation-genetic studies on bacterial cells (E. coli) and Drosophila (D. melanogaster) using methods like an analysis of mutations of some structural genes and assessment of the frequency of mutations with relation to survival have shown for the first time that the efficacy of neutrons (E = 0.85 MeV) in the induction of gene mutations in Pro- and Eukaryotae is much lower than that of weak ionizing radiation with the same survival. Some features of radiation mutagenesis in a Drosophila mutant c(3)G defective in genetic recombination were described. A low level of the frequency of radiation-induced mutations typical of this mutant was also characteristic for some E. coli rec--mutants. A fact earlier reported for bacteria consisting in a higher (than one could expect extrapolation of lethal-sublethal irradiation doses to small ones) frequency of gene mutations in the range of relatively small absorbed doses of gamma-irradiation (the survival rate being not lower than 80%) was also first established for Drosophila. The importance of these entirely new facts for the theory of mutations in radiation genetics are briefly discussed.

Animals↗
PubMed2003

Tissue-specific p53 responses to ionizing radiation and their genetic modification: the key to tissue-specific tumour susceptibility?

Although little is understood of the underlying mechanisms, there are tissue-specific responses to tumourigenic and therapeutic agents and these responses are influenced by genetic factors. Ionizing radiation is an important tumourigenic and therapeutic agent for which there is substantial evidence for such tissue-dependent and genotype-dependent responses. Because the p53 tumour suppressor protein is a major determinant of cellular responses to radiation, the present study has investigated whether modification of the p53 pathway contributes to tissue-dependent and genotype-dependent responses using inbred strains of mice. Comparison of responses in haemopoietic and epithelial cells in irradiated C57BL/6 and DBA/2 mice revealed significant differences in p53 and apoptotic responses in different cell types and in different cells of the same type, reflecting the complexity of damage responses operating in the whole organism. The data suggest that p53-mediated up-regulation of Bax is a major determinant of apoptosis in the spleen, but not in the intestine, whereas p53-mediated induction of p21(waf1) plays an anti-apoptotic role in the spleen, but not in the intestine. It is also shown that p53 stabilization and differential transactivational activities towards Bax or p21(waf1) are influenced by genetic factors that act in a tissue-specific manner. Analysis of ATM, a potential mediator of differential p53 activation, indicates that this key regulator of radiation responses is preferentially induced in epithelial cells, but is unlikely to account for genetic modification of p53 or apoptotic responses in the mouse strains studied. Polymorphisms in the p53 or DNA-PKcs genes are also unlikely to account for the genetic modifications that are reported here. There are numerous further potential modifiers of the p53 pathway, but analysis of backcross and inter-cross mice demonstrates that genes responsible for the complex modification of these in vivo responses can be identified by linkage analysis. This approach has the potential to reveal new or unexpected interactions involving the p53 pathway that determine both short-term and long-term effects of radiation exposure and the basis of tissue-specific responses and tumour susceptibility.

Animals↗
PubMed1982

Mutation frequencies in male mice and the estimation of genetic hazards of radiation in men.

Estimation of the genetic hazards of ionizing radiation in men is based largely on the frequency of transmitted specific-locus mutations induced in mouse spermatogonial stem cells at low radiation dose rates. The publication of new data on this subject has permitted a fresh review of all the information available. The data continue to show no discrepancy from the interpretation that, although mutation frequency decreases markedly as dose rate is decreased from 90 to 0.8 R/min (1 R = 2.6 x 10(-4) coulombs/kg) there seems to be no further change below 0.8 R/min over the range from that dose rate of 0.0007 R/min. Simple mathematical models are used to compute: (a) a maximum likelihood estimate of the induced mutation frequency at the low dose rates, and (b) a maximum likelihood estimate of the ratio of this to the mutation frequency at high dose rates in the range of 72 to 90 R/min. In the application of these results to the estimation of genetic hazards of radiation in man, the former value can be used to calculate a doubling dose--i.e, the dose of radiation that induces a mutation frequency equal to the spontaneous frequency. The doubling dose based on the low-dose-rate data compiled here is 110 R. The ratio of the mutation frequency at low dose rate to that at high dose rate is useful when it becomes necessary to extrapolate from experimental determinations, or from human data, at high dose rates to the expected risk at low dose rates. The ratio derived from the present analysis is 0.33.

Animals↗
PubMed1989

Increased cancer risk as a genetic effect of ionizing radiation.

The well known genetic effects of ionizing radiation include severe developmental disorders in the progeny of irradiated parents resulting in embryonic death, stillbirth and early postnatal mortality, congenital abnormalities, malformations and fertility disturbances in live-born organisms. These effects are considered to be due to gross mutations (genomic, chromosomal and those of essential genes). Physiological inferiority and an increased cancer risk in phenotypically normal offspring of irradiated parents appear to be two further types of genetic effect of radiation. The genetic background of these effects is suggested to be induced recessive polygene mutations and regulatory DNA alterations, which may lead to instability of the hereditary apparatus of cells, activation of protooncogenes and other inducible processes. A comparison of somatic and genetic effects of radiation shows certain similarities, not only in phenomenology, but probably also in pathogenetic mechanisms.

Animals↗
PubMed1998

Genetics of adaptive radiation in Hawaiian and Cook Islands species of Tetramolopium (Asteraceae). II. Genetic linkage map and its implications for interspecific breeding barriers.

In a study of the genetic mechanisms associated with adaptive radiation in Hawaiian Tetramolopium, a genetic linkage map was constructed in an interspecific cross. A total of 125 RFLP and RAPD markers were mapped into 117 different loci on nine linkage groups for a map length of 665.7 cM. Segregation distortion occurred in 49% of the mapped probes, located primarily in four linkage groups. High percentages of one parental species genotype (Tetramolopium rockii) were recovered in three of these blocks and the second parental species (T. humile) in the remaining block. The high degree of distorted segregation suggests the buildup of internal crossing barriers, even though island plant species are typically characterized as highly cross compatible with few to no internal crossing barriers. This work and a review of previous crossing studies in island plants show that internal (postmating) crossing barriers do exist. The weak crossing barriers have likely been overlooked because the main focus has been on diversification and speciation through adaptation to extremely diverse environments.

Adaptation, Biological↗
PubMedDate not supplied

[The role of reaper-dependent apoptosis in radiation-induced life-span alterations in Drosophila melanogaster].

This is the result of studying on a problem of radio-induced ageing. From the point of view of radiation genetics it is perspective to investigate influence of low doze irradiation on individuals with the mutant phenotypes that allows to assume a role of separate genes and mechanisms controllable by them in determination of life span and ageing. The role of a reaper-dependent way of apoptosis regulation in the induced change of life span is shown. The assumption is put forward that apoptosis has the important role during ageing an animal organism.

Aging↗
PubMed1977

The role of mammals in the future of chemical mutagenesis research.

Radiation genetics has demonstrated that mutagenesis is a complex process affected by many factors. The ABCW hypothesis, that mutation frequency per rad over a wide range of organisms, from microbes to man, is linearly related to DNA content, ignores the fact that, within the mouse alone, different cell stages exhibit a range of mutation rates greater than that listed for the whole evolutionary tree. Also ignored are the findings that the important effects of dose rate and some other factors in the mouse were not predictable even from Drosophila. A much greater maze of complexities has already been found in chemical mutagenesis. This is illustrated even by the results obtained from testing of a single drug. Thus, it is clear that the attempt to extend the ABCW hypothesis to chemicals will be of little, if any, predictive value. Similarly, such concepts as the REC (roentgen-equivalent-chemical), designed to express the mutagenic risk from a chemical by a single unit quantitatively related to radiation damage, are defeated by the extreme qualitative differences in response. Unifying theories and simple non-mammalian tests that reliably predict the results in mammals cannot be expected to materialize until much more information has been collected on transmitted mutations induced in mammalian germ cells.

Alkylating Agents↗