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Impact of genetically modified crops on soil- and plant-associated microbial communities.

Transgenic or genetically modified plants possess novel genes that impart beneficial characteristics such as herbicide resistance. One of the least understood areas in the environmental risk assessment of genetically modified crops is their impact on soil- and plant-associated microbial communities. The potential for interaction between transgenic plants and plant residues and the soil microbial community is not well understood. The recognition that these interactions could change microbial biodiversity and affect ecosystem functioning has initiated a limited number of studies in the area. At this time, studies have shown the possibility that transgenes can be transferred to native soil microorganisms through horizontal gene transfer, although there is not evidence of this occurring in the soil. Furthermore, novel proteins have been shown to be released from transgenic plants into the soil ecosystem, and their presence can influence the biodiversity of the microbial community by selectively stimulating the growth of organisms that can use them. Microbial diversity can be altered when associated with transgenic plants; however, these effects are both variable and transient. Soil- and plant-associated microbial communities are influenced not only by plant species and transgene insertion but also by environmental factors such as field site and sampling date. Minor alterations in the diversity of the microbial community could affect soil health and ecosystem functioning, and therefore, the impact that plant variety may have on the dynamics of the rhizosphere microbial populations and in turn plant growth and health and ecosystem sustainability, requires further study.

Bacteria↗

Increase in isoleucine accumulation by alpha-aminobutyric acid-resistant mutants of Serratia marcescens.

Several alpha-aminobutyric acid-resistant (Abu-r) mutants of Serratia marcescens were found to be superior to the parent strain in converting d-threonine to l-isoleucine. One of them accumulated 1.5 times more l-isoleucine that the parent strain. The level of acetohydroxy acid (AHA) synthetase in this mutant increased twofold above that of the parent strain. In the parent strain, AHA synthetase was repressed and l-isoleucine accumulation was decreased by either l-valine or l-leucine, whereas in the mutant the AHA synthetase level and l-isoleucine accumulation were not affected by these amino acids. AHA synthetase of the Abu-r mutant was feedback-inhibited by l-valine to the same extent as that of the parent strain. The level of d-threonine dehydratase in both strains was only slightly affected by several amino acids tested. l-Threonine dehydratase of the parent strain and of the mutant was almost completely inhibited by l-isoleucine. These results indicate that the increase in l-isoleucine accumulation by Abu-r mutants is due to the genetic derepression of AHA synthetase.

Aminobutyrates↗

Salmonella abony-Salmonella typhimurium recombinant nonvirulent for the mouse.

A previous genetic investigation involving a mouse-nonvirulent Salmonella abony donor (high frequency of recombination) and a virulent S. typhimurium recipient indicated that two unlinked "low-virulence" loci determined nonvirulence. A nonvirulent recombinant was analyzed to determine the basis for its nonvirulence. The recombinant was smooth (like the parental strains) and prototrophic. The doubling time in mouse serum of the recombinant and the S. abony parent (both streptomycin-resistant) was longer than that of the wild-type streptomycin-sensitive ancestor of the S. typhimurium recipient. The virulent recipient also grew poorly in serum. However, the nonvirulence of the recombinant was probably not due to its inheritance of the streptomycin-resistance allele from the donor, because other recombinants were streptomycin-resistant but still virulent. Unlike the nonvirulent S. abony (but like the S. typhimurium), the recombinant was insusceptible to rapid intravenous clearance in normal mice. It therefore appears that neither of the "low-virulence" loci determine diminished virulence by enhancing phagocytosis. Clearance of the recombinant was enhanced by opsonization with immune serum. Counts of viable bacteria in the blood, liver, and spleen of normal mice after intravenous challenge showed that the recombinant, like the S. abony donor, failed to proliferate in the tissues, whereas the virulent S. typhimurium did so markedly. It is concluded that the nonproliferation of the recombinant was determined by one or both of the "low-virulence" loci from the nonvirulent S. abony donor.

Animals↗

Conditional dihydrostreptomycin resistance in Bacillus subtilis.

Mutants resistant to dihydrostreptomycin were isolated and genetically analyzed in Bacillus subtilis. Two new classes of mutants distinct from the ribosomal strA locus were found. One class, strB, was located between metC3 and ura-1 on the chromosome. The second class, strC, mapped in the spore gene region close to the spoA locus. Both mutant classes were resistant to dihydrostreptomycin during growth but sensitive to the antibiotic during sporulation. Resuspension sporulation experiments with a strB mutant showed that sensitivity to the antibiotic was acquired early in the sporulation process. The germination and outgrowth of strB spores was sensitive to the antibiotic until growth commenced, whereupon the culture was resistant. Thus the mutants are sensitive to dihydrostreptomycin during both sporulation and germination but resistant during the growth phase.

Bacillus subtilis↗

Osmotic-sensitive mutant of Salmonella typhimurium.

A strain (DA82) having peculiar osmotic properties was isolated in Salmonella typhimurium. The mutant shows increased elasticity of its cell wall and makes spherical instead of elongated cells, regardless of the osmolality of the medium. The strain withstands dilution in distilled water without disruption or death and grows normally in 0.1 molal NaCl broth (240 milliosmol), but it dies exponentially in low-osmolality broth (40 milliosmol). Addition of salts or sucrose instantly stops death and allows growth and cell division to proceed. Death is not due to lysis because this appears at later times and at a much lower rate. Osmotic inactivation is temperature-dependent: higher death rates occur at higher incubation temperatures. Inhibition of protein synthesis by chloramphenicol (20 mug/ml) prevents osmotic death. At 37 C and at lower temperatures, the phenomenon of osmotic death is transient. After a variable interval, growth of the osmotic-sensitive strain resumes. It is assumed that the strain's osmotic behavior is due to membrane defectiveness. The membrane disfunction and the wall defect shown by the strain may be consequences of a single genetic alteration or the results of independent mutations.

Antibodies↗