Does maternal condition or predation risk influence small mammal population dynamics?

There is strong debate over whether the intrinsic traits of individuals or the extrinsic environment exert the greater influence on small mammal population dynamics. We test the roles of maternal effects (an intrinsic factor) and predation risk (an extrinsic factor) in the population dynamics of wild strain house mice using a 2-factor enclosure experiment. Pre-release supplemental feeding with a high-fat diet created female treatment founders that were 6–10% heavier than controls, a condition that we predicted would be passed on as a maternal effect. Predation risk was enhanced using regular application of predator (red fox Vulpes vulpes ) scats. Founder populations of six females and six males released into eight, 15×15 m enclosures showed near exponential population growth over 17 weeks (maximum 3 generations). But there were no responses to either treatment in terms of survival, inherited body weights, fecundity or population size. We suggest that elevated maternal condition may have only minor and transient intergenerational effects with little long-term consequence. We also suggest that the general significance of predator scats as a cue to predation risk to alter prey behaviour may have been overestimated. Hence our results question the role of either factor in causing long-term responses that influence condition to affect population processes.     

Sulfide induces phosphate release from polyphosphate in cultures of a marine Beggiatoa strain

Sulfur bacteria such as Beggiatoa or Thiomargarita have a particularly high capacity for storage because of their large size. In addition to sulfur and nitrate, these bacteria also store phosphorus in the form of polyphosphate. Thiomargarita namibiensis has been shown to release phosphate from internally stored polyphosphate in pulses creating steep peaks of phosphate in the sediment and thereby inducing the precipitation of phosphorus-rich minerals. Large sulfur bacteria populate sediments at the sites of recent phosphorite formation and are found as fossils in ancient phosphorite deposits. Therefore, it can be assumed that this physiology contributes to the removal of bioavailable phosphorus from the marine system and thus is important for the global phosphorus cycle. We investigated under defined laboratory conditions which parameters stimulate the decomposition of polyphosphate and the release of phosphate in a marine Beggiatoa strain. Initially, we tested phosphate release in response to anoxia and high concentrations of acetate, because acetate is described as the relevant stimulus for phosphate release in activated sludge. To our surprise, the Beggiatoa strain did not release phosphate in response to this treatment. Instead, we could clearly show that increasing sulfide concentrations and anoxia resulted in a decomposition of polyphosphate. This physiological reaction is a yet unknown mode of bacterial polyphosphate usage and provides a new explanation for high phosphate concentrations in sulfidic marine sediments.     

Enhancer of Polycomb is a suppressor of position-effect variegation in Drosophila melanogaster.

Polycomb group (PcG) genes of Drosophila are negative regulators of homeotic gene expression required for maintenance of determination. Sequence similarity between Polycomb and Su(var)205 led to the suggestion that PcG genes and modifiers of position-effect variegation (PEV) might function analogously in the establishment of chromatin structure. If PcG proteins participate directly in the same process that leads to PEV, PcG mutations should suppress PEV. We show that mutations in E(Pc), an unusual member of the PcG, suppress PEV of four variegating rearrangements: In(l)wm4, B(SV), T(2;3)Sb(V) and In(2R)bw(VDe2). Using reversion of a Pelement insertion, deficiency mapping, and recombination mapping as criteria, homeotic effects and suppression of PEV associated with E(Pc) co-map. Asx is an enhancer of PEV, whereas nine other PcG loci do not affect PEV. These results support the conclusion that there are fewer similarities between PcG genes and modifiers of PEV than previously supposed. However, E(Pc) appears to be an important link between the two groups. We discuss why Asx might act as an enhancer of PEV.