Laboratory-scale evidence for lightning-mediated gene transfer in soil.

Electrical fields and current can permeabilize bacterial membranes, allowing for the penetration of naked DNA. Given that the environment is subjected to regular thunderstorms and lightning discharges that induce enormous electrical perturbations, the possibility of natural electrotransformation of bacteria was investigated. We demonstrated with soil microcosm experiments that the transformation of added bacteria could be increased locally via lightning-mediated current injection. The incorporation of three genes coding for antibiotic resistance (plasmid pBR328) into the Escherichia coli strain DH10B recipient previously added to soil was observed only after the soil had been subjected to laboratory-scale lightning. Laboratory-scale lightning had an electrical field gradient (700 versus 600 kV m(-1)) and current density (2.5 versus 12.6 kA m(-2)) similar to those of full-scale lightning. Controls handled identically except for not being subjected to lightning produced no detectable antibiotic-resistant clones. In addition, simulated storm cloud electrical fields (in the absence of current) did not produce detectable clones (transformation detection limit, 10(-9)). Natural electrotransformation might be a mechanism involved in bacterial evolution.

Binding of the phytotoxin zinniol stimulates the entry of calcium into plant protoplasts.

Zinniol [1,2-bis(hydroxymethyl)-3-methoxy-4-methyl-5-(3-methyl-2-butenyloxy)benzene], a toxin produced by fungi of the Alternaria group, causes symptoms in plants that resemble those induced by the fungi. The phytotoxin binds to carrot protoplasts and isolated membranes in a saturable and reversible manner. Receptor occupancy stimulates entry of calcium into protoplasts. Zinniol can partially reverse the effects and binding of the calcium-channel blockers desmethoxyverapamil and bepridil. Selected cell lines that are insensitive to zinniol lose part of their binding capacity and sensitivity to the action of the agonist-like compound but are still able to bind calcium-channel blockers. We conclude that zinniol acts on calcium entry but that the targets of the toxin and of calcium-channel blockers are dissimilar, suggesting the occurrence of sites affected both by zinniol and by channel blockers and of sites affected only by zinniol.

Radioimmunoassay of the phytotoxic compound zinniol.

The phytotoxic compound zinniol, produced by phytopathogenic fungi such as Alternaria spp. and Phoma macdonaldii was conjugated to bovine serum albumine by the mixed anhydride method. Antiserum against zinniol was obtained by injection at multiple intradermal sites of rabbits. Sensitivity of the R.I.A. was 0.14 ng/tube, the within and between-assay coefficient of variation were less than 10 and 14% respectively. Negligible binding occurred when analogs of zinniol were tested for cross reactivity. The excellent accuracy of this R.I.A., applied to ethanolic extracts of plants, might allow to determine the production of toxin by the parasite during the infection process.

Rhynchosporoside, a host-selective toxin produced by Rhynchosporium secalis, the causal agent of scald disease of barley.

Rhynchosporoside, a phytotoxic compound, has been isolated from cultures of Rhynchosporium secalis, the causal agent of scald disease of barley. The toxin is a cello-bioside of 1,2-propanediol. The compound may play some role in symptom expression because it was isolated from diseased plants in concentrations similar to those that could cause symptoms in toxin-treated plants. The toxin causes leaf tip and marginal necrosis and subsequent chlorosis of the entire leaf. The toxin affects only certain cultivars and lines of barley and rye; however, it also affects certain nonhosts of R. secalis. The genetic factor controlling host resistance to the fungus is not identical to that controlling insensitivity to the toxin.