No abstract available

[en] The present situation concerning the problem of estimating genetic risks associated with the exposure of living beings, including man, to chemical compounds present in the environment is defined. Since these compounds affect the genetic material of cells by reactions similar to those produced by radiations, attempts have been made to establish rad-equivalences for some of these substances. This idea is discussed through the different publications mentioned

[en] To legislate on mutagenic chemical pollution the problem to be faced is similar to that tackled about 30 years ago regarding pollution by ionizing radiations. It would be useful to benefit from the work of these 30 years by establishing equivalences, if possible, between chemical mutagens and radiations. Inevitable mutagenic pollutions are considered here, especially those associated with fuel based energy production. As with radiations the legislation must derive from a compromise between the harmful and beneficial effects of the polluting system. When deciding on tolerance doses it is necessary to safeguard the biosphere without inflicting excessive restrictions on industry and on the economy. The present article discusses the conditions needed to give meaning to the notion of rad-equivalence. Some examples of already established equivalences are given, together with the first practical consequences which emerge

[en] Current estimates of the genetic risks from exposure to ionizing radiation are based on two kinds of data: a) incidence rates in humans for the genetic diseases that are believed to be present in the population due to mutations of natural origin, and b) radiation induced mutation rates. One necessary prerequisite before any possible increase in genetic load from mutagens can be estimated is baseline information on the magnitude of genetically-caused ill health already present in the population. The present study utilizes the data base of an ongoing population-based Registry with multiple sources of ascertainment to estimate the present population load from genetic disease. It was found that 4.9% of liveborn individuals below 25 can be expected to have genetic or partly genetic diseases. This was composed of single-gene disorders (autosomal dominant, autosomal recessive and X-linked recessive), chromosomal anomalies and multifactorial disorders (including those present at birth and those later in onset). Since previous studies have usually considered all congenital anomalies (ICD 740-759) as part of the genetic load, data are also presented separately for this category to facilitate comparison with earlier studies. These new data should represent a better estimate of the genetic load in the population than previous studies

[en] Auto tetraploid rice has a great genetic potential but low seed setting rate is the major encumbrance in its use. Embryo sac fertility and pollen fertility are the most important factors which affect the seed setting rate in auto tetraploid rice. Whole mount eosin B-staining confocal laser scanning microscopy (WE-CLSM) was used to study the fertility and abnormalities in embryo sacs of diploid and auto tetraploid rice during different seasons. The results indicated that the embryo sac fertility (64.5%) was much low in auto tetraploid than that in diploid rice (86%), and five main types of abnormal embryo sac were found in all 10 auto tetraploid rice. Moreover, some other type abnormal embryo sacs were also observed in auto tetraploid rice. Embryo sac without female germ unit and embryo sac degeneration were the most frequent types of abnormalities in auto tetraploid rice. Embryo sac fertility ranged from 49.3% to 79.3%, pollen fertility ranged from 56.2 to 85.9%, and seed setting rate varied from 12.5 to 69.01% in various genotypes of auto tetraploid rice. Embryo sac and pollen fertility were found to have a significant correlation with seed setting rate. Seasons have significant effect on pollen and embryo sac fertility in both type of rice. All the auto tetraploid lines exhibited different types of embryo sac abnormalities which indicated that these might be related to different genotypes. (author)

[en] 52 SSR primers that gave stable profiles amplified in sample of the Maize inbred line '082' and its 48 mutants were selected from 97 primers, and produced 170 polymorphic amplified fragments. The average number of allele per SSR locus was 3.27 with a range from 2 to 6. The polymorphism information content for the SSR loci varied from 0.039 to 0.715 with an average of 0.327. Genetic similarities among the 49 materials ranged from 0.377 to 1.000 with an average of 0.823. The 49 materials were divided into 6 groups by UPGMA. The results indicated that distinct variation existed among mutants. (authors)

No abstract available

[en] The aim of the present study was to get somaclonal variants and induced mutants of potato for desirable characters with special emphasis on yield and yield components in two cultivars of potato viz., Desiree and Diamant. Inter-nodal explants from both the cultivars were incubated for 14- 20 wks in callus inducing medium comprising MS salts supplemented with NAA (1.0mg/l) and BAP (0.5mg/l) for obtaining somaclonal variants. For mutation induction, 10 week old, well proliferating calli was exposed to 5-50Gy of gamma irradiation. The regenerated plants were analyzed on the basis of morphological characters for variation. The plants were screened on the basis of average shoot height, number of shoots, number of nodes/shoots, average tuber number, tuber size, tuber weight and number of eyes / tuber. Three variant lines (SV1, SV2 and SV3) and 6 gamma mutant lines (GM1, GM2, GM3, GM4 GM5 and GM6) were selected on the basis of better yield and other agronomic characters. The current study demonstrates the production of useful variants both by tissue culture and gamma irradiation in potato. (author)

[en] Vinblastine is shown to induce pronuclear fusion failure in conjugating Tetrahymena thermophila. In this alternate conjugational pathway gametic pronuclei are exchanged between conjugants but do not fuse. Each pronucleus undergoes one mitotic division to produce a new macro- and micronucleus. Genetic consequences of pronuclear fusion failure include the following: (1) the progeny are whole genome homozygotes with nuclei derived from single meiotic products, and (2) half of the progeny are heterokaryons with micro- and macronuclei of different genetic origins. These facts make this process extremely useful in strain construction and mutant isolation. The induction of pronuclear fusion failure by vinblastine suggests that microtubules play an essential role in pronuclear fusion. In this paper the authors present autoradiographic and genetic evidence that vinblastine induces pronuclear fusion failure in T. thermophila

No abstract available