From laboratory to the field: biological control of Fusarium graminearum on infected maize crop residues.

AIM: To evaluate biological control agents (BCAs) against Fusarium graminearum on infected maize stalks as a means to reduce Fusarium head blight (FHB) in subsequently grown wheat. METHODS AND RESULTS: In the laboratory, BCAs were applied against F. graminearum on maize stalk pieces. Clonostachys rosea inhibited the perithecia development and ascospore discharge when applied before, simultaneously with and after the pathogen. In the field, we simulated a system with high disease pressure, that is, a maize-wheat rotation under no-tillage, by preparing maize stalks inoculated with F. graminearum. The infected stalks were treated with formulations of C. rosea selected in vitro or the commercial BCA strain Trichoderma atrobrunneum ITEM908 and exposed to field conditions over winter and spring between winter wheat rows. Monitoring with spore traps and of FHB symptoms, as well as quantification of F. graminearum incidence and DNA in harvested grain revealed significant reductions by C. rosea by up to 85, 91, 69 and 95% compared with an inoculated but untreated positive control, respectively. Deoxynivalenol (DON) and zearalenone (ZEN) contents were reduced by up to 93 and 98%, respectively. Treatments with T. atrobrunneum were inconsistent, with significant reductions of DON and ZEN under warm and wet climatic conditions only. CONCLUSIONS: The findings support the application of C. rosea against F. graminearum on residues of maize to suppress the primary inoculum of FHB. SIGNIFICANCE AND IMPACT OF THE STUDY: As sustainable agriculture requires solutions to control FHB, hence, the application of C. rosea during the mulching of maize crop residues should be evaluated in on-farm experiments.

Genotoxicity testing with the somatic white-ivory system in the eye of Drosophila melanogaster.

The white-ivory test in Drosophila melanogaster is designed to detect chemically induced reversions of the sex-linked, recessive unstable eye-color mutation white-ivory to the wild-type form. After exposure of larvae reversions are detectable as clones of red facets in the eye of newly enclosed adult flies. Tester strains containing a quadruplication of the white-ivory gene on the X-chromosome(s) were used. In a strain with males carrying 4 copies of the gene and females carrying 8 copies of the gene, spontaneous reversions occurred proportional to the gene copy number. In contrast to this, chemically induced reversions occurred only 1.36 times more frequently in females (carrying 8 copies of the gene) than in males (carrying 4 copies). Since chemicals inducing different lesions in DNA (bleomycin, cyclophosphamide, daunomycin, diethyl sulfate and 7,12-dimethylbenz[a]anthracene) did induce statistically significant frequencies of reversions the test appears to be capable of detecting a wide variety of genotoxic chemicals with different modes of action. The recombinogen strychnine did not induce reversions.

Mutagenesis in spermatozoa of Drosophila melanogaster by cross-linking agents depends on the mus(1)101+ gene product in the oocyte.

In Drosophila melanogaster the sex-linked gene must(1)101+ is essential for mutagenesis induced by a cross-linking agent: mature sperm mutagenized by nitrogen mustard (HN2) yield high frequencies of induced sex-linked recessive lethals if tested with wild-type oocytes but practically no recessive lethals if tested with homozygous mus(1)101D1 oocytes. In the absence of mus(1)101+ at least some cross-links act as lethal lesions, whereas in the presence of mus(1)101+ some act as premutational lesions. The lack of delayed mutations in mutant oocytes indicates that the lesions are efficiently eliminated and do not lead to mutagenesis in later post-fertilization nuclear divisions. The mutation mus(1)101D1 is not a null allele because, in tests with heterozygotes, it reduces mutagenesis to a lesser extent than a deletion including the mus(1)101 locus. It is a leaky allele with such a reduced activity that, in homozygous condition, mutagenesis is practically absent. In deletion heterozygotes the mus(1)101+ gene is not dosage-compensated.

Thirty compounds tested in the Drosophila wing spot test.

The Drosophila wing somatic mutation and recombination test (SMART) was evaluated for its suitability in genotoxicity screening by testing 30 chemicals. Of the 2 crosses used, the mwh-flr3 cross turned out to be more convenient than the previously used mwh-flr cross. Based on the experience gained with both acute exposures and chronic exposures of different duration, we suggest that the optimal strategy in genotoxicity screening is to start with chronic exposure of 3-day-old larvae for 48 h (that is, until pupation). Only for unstable compounds and very volatile compounds and gases are acute treatments, including inhalation, recommended. In general, a qualitative evaluation of the genotoxicity of a compound in the wing assay is possible with as few as 1-2 different exposure concentrations. A more quantitative evaluation of genotoxicity, based upon dose-response data, can often be achieved with as few as 3-4 concentrations. The results reported here were obtained in 2 different laboratories, demonstrating that the wing spot test is easily transferable to other laboratories. The experience gained indicates that the assay has now been developed to an extent that a coordinated international comparative validation study is desirable.