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PubMed2000

Genetics of adaptive radiation in Hawaiian species of Tetramolopium (Asteraceae). III. Evolutionary genetics of sex expression.

Despite numerous studies of speciation on oceanic islands, few insights exist on the genetic changes involved in the origin and diversification of island taxa. Here we report a genetic analysis of the evolutionary change in sex expression in Hawaiian Tetramolopium. The most diverse clade in the genus is characterized by a monoecious breeding system. The breeding system resulted from a change in sex expression in disc florets from the ancestral hermaphroditic condition to the derived male state. Analysis of an F2 population from a cross between the two forms of sex expression indicates two regions of the Tetramolopium linkage map are associated with the loss of female function in disc florets. Quantitative trait locus mapping of the two linkage groups confirms that two loci control 56% of the phenotypic variation of the trait in the F2 population. Additive and dominance effects are apparent but no statistical evidence of epistasis was found. Several related reproductive traits also have few genetic associations on the linkage map, but are generally distinct from the control of sex expression. Although modifier loci are likely to be involved, the apparent simple genetic change underlying sex expression parallels a major evolutionary diversification in Hawaiian Tetramolopium and may have initiated the divergence of this novel clade.

Adaptation, Biological↗
PubMed1981

The impact of random and lineal fission of the genetic divergence of small human groups: a case study among the Yanomama.

Most of the genetic divergence that currently separates populations of Homo sapiens must have arisen during that long period when the local village (or band) was the basic unit of biological evolution. Studies of tribally intact Amerindian groups exhibiting such small-group organization have demonstrated marked genetic divergence between nearby villages. Some of this genetic radiation can be attributed to the effects of random genetic drift over time within these small demes. Some of it, however, might be better ascribed to the consequences of nonrandom genetic assortment at the time of village fission, a recurring event for such groups. Even random genetic assortment at the time of fission would lead to some genetic divergence, due to the finite size of the parent gene pool. We term the genetic consequences of random assortment the random fission effect. Routinely, village fission occurs along family lines, leading to even greater genetic divergence between the daughter villages. We use the term lineal fission effect to describe the genetic consequences of nonrandom assortment and contrast these results with those derived from random assortment--A formal treatment of random and lineal fission effects is developed, first for the single-locus case, then for the multiple-locus extension. Using this formulation, three Yanomama fission events were examined. Fission in the Yanomama often involves a great deal of mutual hostility between the two factions, so that subsequent gene flow between the two daughter villages is minimal. The first two examples are typical of the Yanomama behavior norm, and are accompanied by a minimum of subsequent gene flow between the daughter villages. In these two cases, the observed divergence values are very large and are also very unlikely under random fission. The lineal fission effect is pronounced. The net impact of lineal fission is to reduce the effective size of the village at the time of fission by a factor of four, relative to expectation from random fission. The third example, however, involved an unusually amicable split of a village, followed by free genetic exchange between the fission products. This "friendly fission" yields an observed divergence value not much in excess of the expectation from random fission.--The long-term consequences of such fission bottlenecks in effective population size are discussed for both intra- and inter-tribal genetic diversity. It appears that the rate of genetic divergence for tribal and subtribal groups may have been somewhat greater than would be expected from classical drift arguments.

Female↗
PubMed1994

Genetic susceptibility to radiation and chemotherapy injury: diagnosis and management.

Over 5% of the cancer patient population may be radiation sensitive due to genetics, and the sensitive patients may be greatly overrepresented among patients with cancer therapy complications. These individuals include not only rare ataxia telangiectasia (AT) homozygotes with up to three-fold normal radiation sensitivity, but also far more numerous patients with slight radiosensitivity conjectured to be carriers of AT or to have another inherited mutagen sensitivity. Procedures may eventually be used to reliably determine patient tolerance for radiation and antineoplastic agents before initiation or completion of therapy, to have the therapy approach but not exceed the radiation tolerance of the individual patient's irradiated normal tissue. Such procedures could include study of patient's cultured normal cells (e.g., fibroblasts, marrow cells, or lymphocytes) in much the same way that patients' cultured tumor cells may eventually be widely used in the human tumor stem cell assay to predict which course of radiotherapy or chemotherapy should be most useful for treating a cancer. Studies with the normal cells could include cytotoxicity assays, serially determined accumulated genetic damage over the course of therapy, or Southern blot analysis to identify carriers of DNA repair mutations. Such studies could permit more aggressive radiotherapy of most patients due to the noninclusion of a sensitive subpopulation of patients, with less radiotherapy of the relatively few radiation sensitive patients. The patient's tumor cells should have inherited any radiation (or chemotherapy) sensitivity mutations present in the patient's normal cells, so reducing the radiotherapy dose to compensate for the more radiosensitive patients' sensitivity will not necessarily result in undertreatment of the tumor.

Antineoplastic Agents↗
PubMed1992

Workshop on DNA repair.

A workshop on DNA repair with emphasis on eukaryotic systems was held, under the auspices of the EC Concerted Action on DNA Repair and Cancer, at Noordwijkerhout (The Netherlands) 14-19 April 1991. The local organization of the meeting was done under the auspices of the Medical Genetic Centre South-West, The Netherlands (MGC), c/o Department of Radiation Genetics and Chemical Mutagenesis, University of Leiden (The Netherlands). Local organizers were: D. Bootsma (chairman), W. Ferro, J.H.J. Hoeijmakers, A.R. Lehmann, P.H.M. Lohman, L. Mullenders, and A.A. van Zeeland (secretarial assistance: Mrs. C. Escher-van Heerden and Mrs. R. Bontre). Over 190 scientists participated, and the format of the meeting followed that of the 1987 workshop on the 'Molecular Aspects of DNA Repair' (Friedberg et al., 1987). Plenary review talks in the mornings were followed, in the afternoon, by poster viewing in three or four parallel sessions. Groups of 15-20 posters were discussed in detail, and later on, in plenary sessions, chairpersons of the poster discussions reviewed the afternoons' posters. The principal themes of the meeting were the isolation and characterisation of repair genes and proteins, repair in specific sequences, consequences of defective DNA repair, and new methods for detecting DNA damage and repair. Remarkable progress has been made recently in all of these areas, and many exciting new results were presented. It is impossible to summarize all contributions to this (intensive) one-week meeting. Therefore, and for the sake of coherence, presentations that did not fit easily into any of the general themes of the meetings have not been included.

Animals↗
PubMed2001

Risk of stillbirth in offspring of men exposed to ionising radiation.

Radiation genetic risk models are employed to predict the frequency of radiation-related stillbirths to partners of occupationally exposed male workers, using the incidence data recently reported by Parker et al from an epidemiological study of Cumbrian births. Expanding on previously developed conservative risk estimates suggests that, of the 130 observed stillbirths to partners of male radiation workers, 0.3 cases would be attributable to paternal preconceptional irradiation, in contrast to the 17.5 (95% confidence interval: 3.1 to 31.9) cases predicted by Parker et al from their preferred dose-response model. The incompatibility of the results reported by Parker et al with those from other investigations, both epidemiological and experimental, and the inability of the study to consider a number of factors which might affect stillbirth rates, particularly those relating to the mother, make it difficult to accept that paternal irradiation received occupationally could have contributed to a detectable increase in stillbirths.

Abnormalities, Radiation-Induced↗
PubMed1977

Genetic damage from diagnostic radiation.

Using the data from the Tri-State Leukemia Survey and a mathematical model, the hypothesis that low levels of diagnostic radiation produce severe genetic damage that is expressed in the child of the exposed person as leukemia and other diseases is tested. It is estimated that for about 1% of the exposed persons who are affected by radiation, there is a 50-fold increase in the risk of leukemia and a five-fold increase in certain other diseases.

Adolescent↗
PubMed1983

[Radiation exposure during digital subtraction angiography (DSA) of the kidney and aortic arch].

The somatic and genetic radiation dose from DSA and conventional film angiography were compared, using an Anderson-Rando phantom. The dose is greatly influenced by the method of examination; for the examination of the aortic arch in a male, DSA reduces it by a factor of 4 as compared with conventional angiography, in a female by a factor of 11. For renal DSA (PA) somatic dose for a man is 25 times greater, and for a woman 18 times greater, than with conventional angiography (AP). Renal DSA should therefore be carried out in an AP projection in order to reduce the bone marrow dose in the lumbar spine.

Angiography↗
PubMed1979

[Radiation dose in abdominal examinations with whole body computer tomography (author's transl)].

The somatic and genetic radiation exposure in abdominal CT examinations with Delta 50 and Delta 50 fast was measured via thermoluminescent dosimeters and compared with the exposure in conventional methods of x-ray diagnosis. With Delta 50 fast, the dose surface product for on examination of the pancreas is about 2900 Rcm2, and for an examination of the kidneys about 3400 Rcm2. It is thus comparable with a gastrointestinal examination or a urogram. The gonadal doses determined for CT are lower than those received from standard x-ray examination.

Gonads↗
PubMed2005

Inhibition of protein-tyrosine phosphatases by mild oxidative stresses is dependent on S-nitrosylation.

Previous studies have shown that a Ca(2+)-dependent nitric-oxide synthase (NOS) is activated as part of a cellular response to low doses of ionizing radiation. Genetic and pharmacological inhibitor studies linked this NO signaling to the radiation-induced activation of ERK1/2. Herein, a mechanism for the radiation-induced activation of Tyr phosphorylation-dependent pathways (e.g. ERK1/2) involving the inhibition of protein-Tyr phosphatases (PTPs) by S-nitrosylation is tested. The basis for this mechanism resides in the redox-sensitive active site Cys in PTPs. These studies also examined oxidative stress induced by low concentrations of H(2)O(2). S-Nitrosylation of total cellular PTP and immunopurified SHP-1 and SHP-2 was detected as protection of PTP enzymatic activity from alkylation by N-ethylmaleimide and reversal by ascorbate. Both radiation and H(2)O(2) protected PTP activity from alkylation by a mechanism reversible by ascorbate and inhibited by NOS inhibitors or expression of a dominant negative mutant of NOS-1. Radiation and H(2)O(2) stimulated a transient increase in cytoplasmic free [Ca(2+)]. Radiation, H(2)O(2), and the Ca(2+) ionophore, ionomycin, also stimulated NOS activity, and this was associated with an enhanced S-nitrosylation of the active site Cys(453) determined by isolation of S-nitrosylated wild type but not active site Cys(453) --> Ser SHP-1 mutant by the "biotin-switch" method. Thus, one consequence of oxidative stimulation of NO generation is S-nitrosylation and inhibition of PTPs critical in cellular signal transduction pathways. These results support the conclusion that a mild oxidative signal is converted to a nitrosative one due to the better redox signaling properties of NO.

Animals↗
PubMedDate not supplied

[Nikolaĭ Vladimirovich Timofeev-Resovskiĭ (1900-1981). (Essay on his life and works)].

The article contains a brief review of the basic works (1925-1981) written by Nikolay V. Timofeeff-Ressovsky--one of the famous geneticist of the elapsing century, the founder of radiobiology and radiation genetics, biocenology and radioecology, a prominent evolutionary biologist. In genetics, his name is associated with the development of fundamental problems of population genetics, phenogenetics, gene interaction and investigations of the role of environmental and genetic factors in expression of different characters. Timofeeff-Ressovsky classical works on mutagenesis process and especially, radiation mutagenesis, promoted penetration of methods and approaches applied in molecular physics and chemistry, into genetic analysis, and accelerated forming of the modern molecular genetics. A special place in the development of population genetics is occupied by the hypothesis of microevolutionary process developed by Nikolay V. Timofeeff-Ressovsky along with other famous biologists in the end of the 30-ies. This hypothesis connected Darwin's evolutionary theory with rapidly developing concepts of genetics. In the last years of his life, Timofeeff-Ressovsky was especially interested in a global problem which was called by him "The Biosphere and Humanity". Here was especially strikingly shown the broadness of his approach to the analysis of the biosphere phenomena in the best traditions of the Russian natural science. In the course of time, the wealth of Nikolay V. Timofeeff-Ressovsky's scientific heritage not only remains valuable, but also takes on more profundity and value.

History, 20th Century↗