Toxicological and behavioral analyses indicates the safety of a biofertilizer in the non-target D. melanogaster.

The demand for food to feed the growing world population has been promoting the indiscriminate use of chemical fertilizers, which can be detrimental to the environment. In order to maintain high crop productivity without damaging the ecosystem, biofertilizers have emerged as alternative to reduce the use of chemical fertilizers. So, environmentally safer biofertilizer can replace the exploitation of more toxic chemical fertilizer. Here, the fly Drosophila melanogaster was used to study the potential toxicity of the biofertilizer Beifort®. Flies were exposed to high concentrations of Beifort® in the diet (1.8 mL/L, 9.0 mL/L and 18 mL/L), and morphological and behavioral endpoints of toxicity were analyzed (development from egg to adult age, flies longevity, climbing performance, memory and learning of an associative learning, larvae digestive tract damage and plasmid DNA break). Beifort® did not modify flies development, survival, digestive track cell damage, locomotor activity or memory. Beifort® did not induce DNA breakage in vitro and had no toxicity to the non-target D. melanogaster after in vivo exposure. Thus, in addition of promoting the sustainable use of agricultural wastes, the exploitation of Beifort® can contribute to decrease the use of chemical fertilizers.

A genetic cluster of patients with variant xeroderma pigmentosum with two different founder mutations.

BACKGROUND: Xeroderma pigmentosum (XP) is a rare human syndrome associated with hypersensitivity to sunlight and a high frequency of skin tumours at an early age. We identified a community in the state of Goias (central Brazil), a sunny and tropical region, with a high incidence of XP (17 patients among approximately 1000 inhabitants). OBJECTIVES: To identify gene mutations in the affected community and map the distribution of the affected alleles, correlating the mutations with clinical phenotypes. METHODS: Functional analyses of DNA repair capacity and cell-cycle responses after ultraviolet exposure were investigated in cells from local patients with XP, allowing the identification of the mutated gene, which was then sequenced to locate the mutations. A specific assay was designed for mapping the distribution of these mutations in the community. RESULTS: Skin primary fibroblasts showed normal DNA damage removal but abnormal DNA synthesis after ultraviolet irradiation and deficient expression of the Polη protein, which is encoded by POLH. We detected two different POLH mutations: one at the splice donor site of intron 6 (c.764 +1 G>A), and the other in exon 8 (c.907 C>T, p.Arg303X). The mutation at intron 6 is novel, whereas the mutation at exon 8 has been previously described in Europe. Thus, these mutations were likely brought to the community long ago, suggesting two founder effects for this rare disease. CONCLUSIONS: This work describes a genetic cluster involving POLH, and, particularly unexpected, with two independent founder mutations, including one that likely originated in Europe.