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.

During the larval feeding period, the growth of the wing imaginal disks of Lepidoptera is dependent on continuous feeding. Feeding and nutrition exert their effect via the secretion of bombyxin, the lepidopteran insulin-like hormone. When larvae stop feeding and enter the wandering stage in preparation for metamorphosis, the control of imaginal disk growth becomes feeding and nutrition-independent. Growth of the wing imaginal disks of non-feeding wandering stage Manduca sexta can be stopped by removal of the brain, indicating that a brain-derived factor is required for continued disk growth. Isolated wing disk growth in vitro requires both 20-hydroxyecdysone (20E) and either brain extract or bombyxin to achieve normal growth. In vitro, brain extracts and synthetic bombyxin have little or no effect in stimulating disk growth, but they greatly enhance the effect of 20E, indicating that 20E and bombyxin act synergistically to modulate growth of the imaginal disk. Brain extract and bombyxin induce a suite of insulin-response events in cultured wing disks, which indicate that bombyxin and 20E act through separate and synergistic pathways. The dose-response to 20E reaches a plateau at about 0.1 microg/ml. Tracheal differentiation of the wing disks can be induced to initiate in vitro by a low concentration of 20E, whereas higher concentrations of 20E only stimulate growth.

No abstract

No abstract