ALBERT

Notes: Abstract (1) The presence and absence of 22 plant species of various growth forms and habitat associations were analysed in 423 habitat fragments totalling 10.4 km2 in a 268 km2 urban and suburban region, in Birmingham, UK. (2) Multivariate logistic regressions were used to assess the effects of patch geometry and quality on the species distributions. Measures of geometry were area, shape (S-factor), distance from open countryside and various measures of isolation from other patches. Potential habitat for each species was determined quantitatively, and the distribution of each species was considered within a subset of patches containing potentially suitable habitat types. There was found to be a significant positive correlation between the density of patches available to a species and the proportion of these patches which were occupied. (3) Logistic analyses and incidence functions revealed that, for many of the species, occupancy increased with site age, area, habitat number and similarity of adjacent habitats, while increasing distance to the nearest recorded population of the same species decreased the likelihood that a species would be found in a patch. (4) Patterns of occupancy are consistent with increased extinction from small sites, and colonisation of nearby habitats, coupled with an important role for site history. We conclude that spatial dynamics at the scale of the landscape are of importance to the long-term persistence of many plant species in fragmented landscapes, and must be seriously considered in conservation planning and management. These results have direct implications for the siting and connectivity of urban habitat reserves.

Notes: Abstract After discussing approaches to the modelling of mitochondrial regulation in muscle, we describe a model that takes account, in a simplified way, of some aspects of the metabolic and physical structure of the energy production/usage system. In this model, high-energy phosphates (ATP and phosphocreatine) and low energy metabolites (ADP and creatine) diffuse between the mitochondrion and the myofibrillar ATPase, and can be exchanged at any point by creatine kinase. Creatine kinase is not assumed to be at equilibrium, so explicit account can be taken of substantial changes in its activity of the sort that can now be achieved by transgenic technology in vivo. The ATPase rate is the input function. Oxidative ATP synthesis is controlled by juxtamitochondrial ADP concentration. To allow for possible functional ‘coupling’ between the components of creatine kinase associated with the mitochondrial adenine nucleotide translocase and the myofibrillar ATPase, we define parameters ϕ and ψ that set the fraction of the total flux carried by ATP rather than phosphocreatine out of the mitochondrial unit and into the ATPase unit, respectively. This simplification is justified by a detailed analysis of the interplay between the mitochondrial outer membrane porin proteins, mitochondrial creatine kinase and the adenine nucleotide translocase. As both processes of possible ‘coupling’ are incorporated into the model as quantitative parameters, their effect on the energetics of the whole cell model can be explicitly assessed. The main findings are as follows: (1) At high creatine kinase activity, the hyperbolic relationship of oxidative ATP synthesis rate to spatially averaged ADP concentration at steady state implies also a near-linear relationship to creatine concentration, and a sigmoid relation to free energy of ATP hydrolysis. At high creatine kinase activity, the degree of functional coupling at either the mitochondrial or ATPase end has little effect on these relationships. However, lowering the creatine kinase activity raises the mean steady state ADP and creatine concentrations, and this is exaggerated when ϕ or ψ is near unity (i.e. little coupling). (2) At high creatine kinase activity, the fraction of flow at steady state carried in the middle of the model by ATP is small, unaffected by the degree of functional coupling, but increases with ADP concentration and rate of ATP turnover. Lowering the creatine kinase activity raises this fraction, and this is exaggerated when ϕ or ψ is near unity. (3) Both creatine and ADP concentrations show small gradients decreasing towards the mitochondrion (in the direction of their net flux), while ATP and phosphocreatine concentration show small gradients decreasing towards the myosin ATPase. Unless ϕ = ψ ≈ 0 (i.e. complete coupling), there is a gradient of net creatine kinase flux that results from the need to transform some of the ‘adenine nucleotide flux’ at the ends of the model into ‘creatine flux’ in the middle; the overall net flux is small, but only zero if ϕ = ψ. A reduction in cytosolic creatine kinase activity decreases ADP concentration at the mitochondrial end and increases it at the ATPase end. (4) During work-jump transitions, spatial average responses exhibit exponential kinetics similar to those of models of mitochondrial control that assume equilibrium conditions for creatine kinase. (5) In response to a step increase in ATPase activity, concentration changes start at the ATPase end and propagate towards the mitochondrion, damped in time and space. This simplified model embodies many important features of muscle in vivo, and accommodates a range of current theories as special cases. We end by discussing its relationship to other approaches to mitochondrial regulation in muscle, and some possible extensions of the model.