Physicochemical structure-activity relationship of DDT congeners and the inhibition of mitochondrial ATPase

Structure-activity relationships were used to determine the physicochemical properties of DDT that are important in the inhibition of oligomycin-sensitive mitochondrial ATPase activity of red coxal muscle tissue homogenates of the American cockroach (Periplaneta americana). The results were compared with structure-activity relationships derived from toxicity values for houseflies (Musca domestica) and blowflies (Phormia regina), reported in the literature. Toxicity was found to be promoted by hydrophobicity and electron donation. Toxicity was concluded to be a route of action process involving the distribution and partitioning of insecticide to active sites and apart from them. Enzyme inhibition, in contrast to factors contributing to toxicity, was determined to be a mode of action process predicted by the lipophilic parameter (π) and the steric constant, van der Waals radii (VWR), and represents action upon a sterically sensitive, hydrophobic site in the membrane sector of mitochondrial ATPase.     

A clamping mechanism involved in SNARE-dependent exocytosis

During neurotransmitter release at the synapse, influx of calcium ions stimulates the release of neurotransmitter. However, the mechanism by which synaptic vesicle fusion is coupled to calcium has been unclear, despite the identification of both the core fusion machinery [soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)] and the principal calcium sensor (synaptotagmin). Here, we describe what may represent a basic principle of the coupling mechanism: a reversible clamping protein (complexin) that can freeze the SNAREpin, an assembled fusion-competent intermediate en route to fusion. When calcium binds to the calcium sensor synaptotagmin, the clamp would then be released. SNARE proteins, and key regulators like synaptotagmin and complexin, can be ectopically expressed on the cell surface. Cells expressing such "flipped" synaptic SNAREs fuse constitutively, but when we coexpressed complexin, fusion was blocked. Adding back calcium triggered fusion from this intermediate in the presence of synaptotagmin.     

Estimating the frequency and extent of bloodworm digging in Maine from aerial photography

The extent and frequency of bloodworm digging in northeast North America has never been investigated, making bloodworm fishery management difficult and an assessment of ecological impact impossible. We examined the spatial and temporal patterns of bloodworm digging by surveying 13 mudflats in mid-coast Maine using monthly aerial photography. We used ArcGIS to “georeference” spatial information into the photographs, allowing us to quantify the area of the mudflat disturbed by digging. Of the 122 ha of flats we monitored, almost 48% was dug in 2006, and 24% was dug in 2007, corresponding to 57.9 ha and 24.8 ha, respectively. Individual flats in this study were dug as much as 155% and as little as 0% annually, but rarely were they dug more than once a year as studies assessing the impact of digging on soft-sediment communities have assumed. Digging activity peaked in early spring with a smaller peak in August. On average, 3% of the visual evidence of digging faded each month. Except for those erased by winter storms and ice scour, no dug strip faded before 5 months of age, therefore flats could be monitored every 4–5 months for an accurate estimate of digging activity. Our results allow us, for the first time, to estimate the impact of digging on the bloodworm resource and to design realistic experiments to measure the impact of digging on the soft-sediment community and non-target species.     

The genomic sequence of the accidental pathogen Legionella pneumophila

We present the genomic sequence of Legionella pneumophila, the bacterial agent of Legionnaires' disease, a potentially fatal pneumonia acquired from aerosolized contaminated fresh water. The genome includes a 45-kilobase pair element that can exist in chromosomal and episomal forms, selective expansions of important gene families, genes for unexpected metabolic pathways, and previously unknown candidate virulence determinants. We highlight the genes that may account for Legionella's ability to survive in protozoa, mammalian macrophages, and inhospitable environmental niches and that may define new therapeutic targets.