The human cytidine-5'-triphosphate synthetase (CTPS) gene was mapped by a direct mapping system combined with fluorescence in situ hybridization and replicated prometaphase R-bands. By high-resolution banding analysis, the signals were localized to band 34.1-34.3 of the short arm of chromosome 1; 1p34.1-p34.3. Simple procedures for the detection of R-bands are described.

In order to clarify the relationship between polyploidization and the capability of phenotypic switching in the imperfect yeast Candida albicans, two types of variants were isolated as segregants from a fusant, which produced a proportion of the cell population with a higher ploidy than the rest, either in a temperaturedependent or -independent manner, when incubated at low (28°C) and high (37°C) temperatures. In the case of the temperature-dependent type of variants, high-ploidy cells appeared at 37°C but rarely at 28°C. This phenotype was named Pldts (temperature-sensitive polyploidization), and the temperature-independent phenotype was called Pld-. The appearance of high-ploidy cells in the culture of the Pldts strain at 37°C was accompanied by a significant increase in the frequency of auxotrophic variants; these variants probably occur as a result of segregation of auxotrophic markers from the heterozygous to the homozygous state. Both Pldts and Pld-phenotypes were recessive in a fusion with a Pld+ parent. An adenine auxotrophic marker (adel) was introduced into a Pldts strain in a heterozygous state, and the individual high-ploidy cells of this strain, grown at 37°C, were micromanipulated to form colonies, which consisted of red and white sectors appearing at high frequency on a pink background. When the adel auxotrophy was introduced into Pld-strains, frequently sectored colonies were produced. These results suggested an increased level of chromosome missegregation in both types of Pld mutants. Analyses by pulsed-field gel electrophoresis of Ade-segregants, derived from a micromanipulated high-ploidy cell of a Pldts strain, suggested the occurrence of nonreciprocal recombination, some of which includes chromosome loss.The dimorphic and pathogenic yeast Candida albicans is diploid as commonly isolated (17), and no sexual cycle has been observed for it (23). Diploidy seems to endow this organism with genetic stability in the short run, since a recessive mutation cannot be expressed until it exists in a homozyogous state after the occurrence of mitotic recombination. However, in the long run, the organism is postulated to accumulate recessive mutations and chromosome rearrangement. Some phenotypic variation (often called phenotypic instability or switching) has been reported to occur in this organism: Slutsky et al. (25) showed that the colony phenotype of azparticular strain, 3153A, changed at a frequency of 10-2 to 10-, which is too high to be a result of mutation. Later, the same laboratory reported a second form of colony morphology variation, smooth-opaque (4, 26). Suzuki et al. (28) albicans was assumed to be coupled to chromosomal rearrangements by Suzuki et al. (28).In this article, two types of variation (Pld-and Pldts) are shown to occur; these cause the phenotype of polyploidy in a temperature-independent or -dependent manner, respectively. Chromosome instability is shown to exist in both Pld-and Pldts strains through the demonstration of segregation of auxotrophic markers including adel. Direc...

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Somaclonal variation is a possible source of variation in plant breeding. To apply this approach to eggplant breeding, somaclonal variations were observed among plants regenerated through somatic embryogenesis induced by 1-naphthaleneacetic acid (NAA) or 2,4-dichlorophenoxyacetic acid (2,4-D). Variations including leaf shape, plant height, flower number per cluster, fruit shape, anther number per flower and pollen fertility were compared among ss300 plants (Ro). Although these variations were confirmed among plants regenerated using both auxins, the frequencies of somaclonal variations in leaf shape, plant height, fruit shape and pollen fertihty in the NAA experiment were higher than those in the 2,4-D experiment. Variations in flower number and anther number were also confirmed among plants from both experiments, although no significant differences in their frequency were observed. Subsequently, the inheritance of variations (leaf shape, fruit shape, and flower number) observed in RQ was investigated from generation to generation (R,). Variations in leaf shape and fruit shape were inherited while those in flower number were not. From these results we concluded that, although a high frequency of somaclonal variations were observed among plants from both methods, embryogenesis with NAA was more efficient than 2,4-D in eggplant.

Expression of distamycin A-inducible rare fragile sites by AT-specific DNA-ligands was examined in lymphoblastoid cell lines derived from heterozygous carriers for the fra(8)(q24), fra(16)(p12), and fra(16)(q22) sites. The sensitivity of fragile site expression to the inducers was different at these fragile sites. The expression of fra(8)(q24) was induced markedly by Hoechst 33258, but not by distamycin A or berenil. An increased expression of fra(16)(p12) was found following treatment with Hoechst 33258 or berenil, but not with distamycin A. At fra(16)(q22), distamycin A markedly induced the fragile site, but Hoechst 33258 and berenil did not. Since their response to the different inducers was similar to that found in cultured lymphocytes, lymphoblastoid cell lines appear to retain their inherent properties. Although BrdUrd alone did not induce any fragile sites, concomitant treatment with BrdUrd plus the inducer was synergistically effective in inducing all the fragile sites. An increased frequency of sister chromatid exchanges was observed at fra(16)(p12) following simultaneous treatment with BrdUrd and berenil, mainly when the site was expressed as an isochromatid gap. Thus, the induced fra(16)(p12) site is a hot spot for the formation of sister chromatid exchanges, as found in other reported fragile sites.