Technology

Identification of a gene associated with Bt resistance in Heliothis virescens. Gahan, L. J. et al. Science 293, 857–860 (2001) [PubMed]

Bt toxin resistance from loss of a putative carbohydrate-modifying enzyme. Griffitts, J. S. et al. Science 293, 860–864 (2001) [PubMed]

The expression of the Bacillus thuringiensis (Bt) toxin in transgenic plants has become an important strategy for pest control in many plant species. However, its use is threatened by the development of pest resistance to Bt toxin. Although resistance is not yet widespread in the field, resistant mutants of several species have been identified in the laboratory. In these two studies, the genetic basis for toxin resistance has been defined in the tobacco mudworm and the nematode Caenorhabditis elegans: mutations in both have been found that could affect the binding and absorption of the toxin in the gut. These mutations provide valuable insight into the mechanisms of Bt toxin resistance and will allow studies of how best to manage the development of toxin resistance in the field.

Evolution

Recent origin of Plasmodium falciparum from a single progenitor. Volkman, S. K. et al. Science 293, 482–484 (2001) [PubMed]

Opinions are divided on the origins of a malaria parasite, Plasmodium falciparum. Abundant genetic variation at certain loci indicates an ancient origin, whereas low variation at silent sites in coding sequences indicates a recent origin. By analysing 25 intron sequences of general metabolic and housekeeping genes, Volkman and colleagues found very few single nucleotide polymorphisms and estimated that P. falciparum originated from 9,500 to 23,000 years ago, consistent with a recent finding that malaria has had a major impact on human evolution only since the introduction of agriculture, ∼10,000 years ago (see In Briefs, August 2001).

Population genetics

Are rare variants responsible for susceptibility to complex diseases? Pritchard, J. K. Am. J. Hum. Genet. 69, 124–137 (2001) [PubMed]

It is assumed that alleles underlying common diseases are old and therefore common in the population (the “common disease, common variant” hypothesis). By incorporating mutation, random genetic drift and purifying selection into a mathematical model for how complex disease loci evolve, this paper shows that, although there might be many susceptibility alleles, there is likely to be extensive allelic heterogeneity at many of these loci. This result has implications, among others, for the effectiveness of association mapping, which depends on rare susceptibility variants.