Understanding the drivers of species coexistence is essential in ecology. Niche and fitness differences (i.e. how species limit themselves compared to others and species' differences in competitive ability, respectively) permit studying the consequences of species interactions. Yet, the multitude of methods to compute niche and fitness differences hampers cross‐community comparisons. Such shortcoming leaves a gap in our understanding of the natural drivers of species coexistence and whether niche or/and fitness differences capture them. Here, we standardised niche and fitness differences across 953 species pairs to investigate species coexistence across ecological groups and methodological settings (experimental setup, natural co‐occurrence, population model used and growth method). Using data gathered from 29 empirical papers, we asked whether large niche differences, small fitness differences or both explain predicted coexistence. Moreover, we performed an automated clustering algorithm to understand whether different underlying mechanisms drive species interactions. Finally, we tested whether any ecological or/and methodological settings drive these clusters. Species pairs predicted to coexist have larger niche differences but not smaller fitness differences than species pairs predicted not to coexist. Also, species pairs group into two clear clusters along the niche difference axis: those predicted to coexist and those that are not. Surprisingly, ecological or methodological settings do not drive these clusters. Synthesis. Overall, our results show that species coexistence is mainly influenced by mechanisms acting on niche differences, highlighting the importance of sustaining mechanisms that promote niche differences to maintain species coexistence. In addition, our results provide evidence that communities predicted to coexist differ from those that are not in ways that transcend their ecological grouping.
Single-stranded DNA-binding proteins (SSBs) play a key role in genome maintenance, binding and organizing single-stranded DNA (ssDNA) intermediates. Multimeric SSBs, such as the human mitochondrial SSB (HmtSSB), present multiple sites to interact with ssDNA, which has been shown in vitro to enable them to bind a variable number of single-stranded nucleotides depending on the salt and protein concentration. It has long been suggested that different binding modes might be used selectively for different functions. To study this possibility, we used optical tweezers to determine and compare the structure and energetics of long, individual HmtSSB–DNA complexes assembled on preformed ssDNA and on ssDNA generated gradually during ‘in situ’ DNA synthesis. We show that HmtSSB binds to preformed ssDNA in two major modes, depending on salt and protein concentration. However, when protein binding was coupled to strand-displacement DNA synthesis, only one of the two binding modes was observed under all experimental conditions. Our results reveal a key role for the gradual generation of ssDNA in modulating the binding mode of a multimeric SSB protein and consequently, in generating the appropriate nucleoprotein structure for DNA synthetic reactions required for genome maintenance.
1 February 2015 in Journal of Cosmology and Astroparticle Physics
Many species show synchronous fluctuations in population size over large geographical areas, which are likely to increase their regional extinction risk. Here we examine how the degree of spatial synchrony in population dynamics is affected by trophic interactions using a two-species predator-prey model with spatially correlated environmental noise. We show that the predator has a larger spatial scale of population synchrony than the prey if the population fluctuations of both species are mainly determined by the direct effect of stochastic environmental variations in the prey. This result implies that in ecosystems regulated from the bottom up, the spatial scale of synchrony of the predator population increases beyond the scale of the spatial autocorrelation in the environmental noise and in the prey fluctuations. Harvesting the prey increases the spatial scale of population synchrony of the predator, while harvesting the predator reduces the spatial scale of the population fluctuations of its prey. Hence, the development of sustainable harvesting strategies should also consider the impact on unharvested species at other trophic levels as well as human perturbations of ecosystems, whether the result of exploitation or an effect on dispersal processes, as they can affect food web structures and trophic interactions over large geographical areas.
Ligands binding to polymers regulate polymer functions by changing their physical and chemical properties. This ligand regulation plays a key role in many biological processes. We propose here a model to explain the mechanical, thermodynamic, and kinetic properties of the process of binding of small ligands to long biopolymers. These properties can now be measured at the single molecule level using force spectroscopy techniques. Our model performs an effective decomposition of the ligand-polymer system on its covered and uncovered regions, showing that the elastic properties of the ligand-polymer depend explicitly on the ligand coverage of the polymer (i.e., the fraction of the polymer covered by the ligand). The equilibrium coverage that minimizes the free energy of the ligand-polymer system is computed as a function of the applied force. We show how ligands tune the mechanical properties of a polymer, in particular its length and stiffness, in a force dependent manner. In addition, it is shown how ligand binding can be regulated applying mechanical tension on the polymer. Moreover, the binding kinetics study shows that, in the case where the ligand binds and organizes the polymer in different modes, the binding process can present transient shortening or lengthening of the polymer, caused by changes in the relative coverage by the different ligand modes. Our model will be useful to understand ligand-binding regulation of biological processes, such as the metabolism of nucleic acid. In particular, this model allows estimating the coverage fraction and the ligand mode characteristics from the force extension curves of a ligand-polymer system.