A very energetic supernova associated with the gamma-ray burst of 29 March 2003

Over the past five years evidence has mounted that long-duration (>2 s) gamma-ray bursts (GRBs)-the most luminous of all astronomical explosions-signal the collapse of massive stars in our Universe. This evidence was originally based on the probable association of one unusual GRB with a supernova, but now includes the association of GRBs with regions of massive star formation in distant galaxies, the appearance of supernova-like 'bumps' in the optical afterglow light curves of several bursts and lines of freshly synthesized elements in the spectra of a few X-ray afterglows. These observations support, but do not yet conclusively demonstrate, the idea that long-duration GRBs are associated with the deaths of massive stars, presumably arising from core collapse. Here we report evidence that a very energetic supernova (a hypernova) was temporally and spatially coincident with a GRB at redshift z = 0.1685. The timing of the supernova indicates that it exploded within a few days of the GRB, strongly suggesting that core-collapse events can give rise to GRBs, thereby favouring the 'collapsar' model.     

Reduced antinociception in mice lacking neuronal nicotinic receptor subunits

Nicotine exerts antinociceptive effects by interacting with one or more of the subtypes of nicotinic acetylcholine receptors (nAChRs) that are present throughout the neuronal pathways that respond to pain. To identify the particular subunits involved in this process, we generated mice lacking the alpha4 subunit of the neuronal nAChR by homologous recombination techniques and studied these together with previously generated mutant mice lacking the beta2 nAChR subunit. Here we show that the homozygous alpha4-/- mice no longer express high-affinity [3H]nicotine and [3H]epibatidine binding sites throughout the brain. In addition, both types of mutant mice display a reduced antinociceptive effect of nicotine on the hot-plate test and diminished sensitivity to nicotine in the tail-flick test. Patch-clamp recordings further reveal that raphe magnus and thalamic neurons no longer respond to nicotine. The alpha4 nAChR subunit, possibly associated with the beta2 nAChR subunit, is therefore crucial for nicotine-elicited antinociception.     

Coevolution with viruses drives the evolution of bacterial mutation rates

Bacteria with greatly elevated mutation rates (mutators) are frequently found in natural and laboratory populations, and are often associated with clinical infections. Although mutators may increase adaptability to novel environmental conditions, they are also prone to the accumulation of deleterious mutations. The long-term maintenance of high bacterial mutation rates is therefore likely to be driven by rapidly changing selection pressures, in addition to the possible slow transition rate by point mutation from mutators to non-mutators. One of the most likely causes of rapidly changing selection pressures is antagonistic coevolution with parasites. Here we show whether coevolution with viral parasites could drive the evolution of bacterial mutation rates in laboratory populations of the bacterium Pseudomonas fluorescens. After fewer than 200 bacterial generations, 25% of the populations coevolving with phages had evolved 10- to 100-fold increases in mutation rates owing to mutations in mismatch-repair genes; no populations evolving in the absence of phages showed any significant change in mutation rate. Furthermore, mutator populations had a higher probability of driving their phage populations extinct, strongly suggesting that mutators have an advantage against phages in the coevolutionary arms race. Given their ubiquity, bacteriophages may play an important role in the evolution of bacterial mutation rates.