Effect of TPA on the mutagenicity of caffeine in the soybean mutation test

12-O-Tetradecanoylphorbol-13-acetate (TPA) is a well-known tumor promoter in mouse-skin carcinogenesis. Its effects on mutagenesis in a soybean test system were examined, and the effects were judged from the appearance of spots of various colors on the leaves. When soybean seeds were treated with TPA plus 0.03% caffeine, the frequency of spots per leaf decreased significantly and in proportion to the concentration of TPA. TPA alone at concentrations of 1–20 μg/ml did not induce any mutations. Mutations induced by γ-rays were not affected by administration of TPA either before or after exposure to γ-rays. The mechanism of suppression by TPA of mutations induced by caffeine is discussed.     

Protection of mouse spermatogonia against x-ray induced translocations

Adult male C57BL mice were exposed to 75, 150, 300 or 450 R X-rays with or without pre-treatment with Adeturon (S-2-aminoethyl-isothiuronium bromide hydrobromide (AET) adenosine triphosphate, 500 mg/kg b.w.). Twelve weeks later, primary spermatocytes were examined cytologically at diakinesis-metaphase I for persisting chromosomal translocations, namely multivalents in the form of rings or chains.For the dose range studied, regression analysis indicated that the data were best fitted to the equation Y = aD + bD² with coefficients for translocated-cell and translocations-per-cell yields, respectively, a = 1.57·10^?2 and 1.59·10^?2 and b = ?2.29·10^?5 and ?2.09·10^?5, for Adeturon protected irradiated animals vs.a = 1.80·10^?2 and 2.05·10^?2, and b = ?0.94·10^?5 and ?1.19·10^?5, in non-protected irradiated animals.Adeturon protection of heritable structures in mouse germ cells showed a dose reduction factor of about 2.     

Ultraviolet light sensitive mutants of Coprinus lagopus. I. Isolation and characterization

4UV-sensitive mutants have been isolated from the wild type strain BC9/66 of Coprinus lagopus by following a new replica plating technique. Complementation and recombination studies between these mutants suggest 3 gene loci uvs1, uvs2 and uvs3, two of the mutants being allelic (uvs3-1 and uvs3-2). The mutants uvs2, uvs3-1 and uvs3-2 show photoreactivation whereas the mutant uvs1 appears to be deficient in this respect. None of the mutants of the wild type showed significant recovery after dark holding.     

Tyrosine kinase and cooperative TGFbeta signaling in the reproductive organs of Schistosoma mansoni

Drug-induced suppression of female schistosome sexual maturation is an auspicious strategy to combat schistosomiasis since the eggs are the causative agent. The establishment of drug targets requires knowledge about the molecular mechanisms that regulate the development of the female reproductive organs, which include vitellarium and ovary. This review summarizes recent studies suggesting tyrosine kinases as important factors for the regulation of female gonad development. In this context, especially cytoplasmatic tyrosine kinases of the Src class seem to play dominant roles. Moreover, experimental data and theoretical concepts are provided supporting a crosstalk between tyrosine kinase and TGFbeta signaling in the production of vitellocytes. Finally, we take advantage from the schistosome genome project to propose a model for the regulation of vitelline-cell production and differentiation.     

Repair mechanisms involved in prophage reactivation and UV reactivation of UV-irradiated phage lambda

Survival of UV-irradiated phage λ is increased when the host is lysogenic for a homologous heteroimmune prophage such as λimm434 (prophage reactivation). Survival can also be increased by UV-irradiating slightly the non-lysogenic host (UV reactivation).Experiments on prophage reactivation were aimed at evaluating, in this recombination process, the respective roles of phage and bacterial genes as well as that of the extent of homology between phage and prophage.To test whether UV reactivation was dependent upon recombination between the UV-damaged phage and cellular DNAs, lysogenic host cells were employed. Such hosts had thus as much DNA homologous to the infecting phage as can be attained. Therefore, if recombination between phage and host DNAs was involved in this repair process, it could clearly be evidenced.By using unexposed or UV-exposed host cells of the same type, prophage reactivation and UV reactivation could be compared in the same genetic background.The following results were obtained: (1) Prophage reactivation is strongly decreased in a host carrying recA mutations but quite unaffected by mutation lex-I known to prevent UV reactivation; (2) In the absence of the recA⁺ function, the red⁺ but not the int⁺ function can substitute for recA⁺ to produce prophage reactivation, although less efficiently; (3) Prophage reactivation is dependent upon the number of prophages in the cell and upon their degree of homology to the infecting phage. The presence in a recA host of two prophages either in cis (on the chromosome) or in trans (on the chromosome and on an episome) increases the efficiency of prophage reactivation; (4) Upon prophage reactivation there is a high rate of recombination between phage and prophage but no phage mutagenesis; (5) The rate of recombination between phage and prophage decreases if the host has been UV-irradiated whereas the overall efficiency of repair is increased. Under these conditions UV reactivation of the phage occurs as in a non-lysogen, as attested by the high rate of mutagenesis of the restored phage.These results demonstrate that UV reactivation is certainty not dependent upon recombination between two pre-existing DNA duplexes. The hypothesis is offered that UV reactivation involves a repair mechanism different from excision and recombination repair processes.