Habitat fragmentation and large-scale conservation: what do we know for sure?

We review the ecological effects of habitat fragmentation, comparing the theoretical approaches that have been taken to understanding it with the existing evidence from empirical studies. Theory has emphasized the spatial aspects of fragmentation and the role of dispersal among patches, and has generated interesting predictions such as a nonlinear relationship between the amount of remaining habitat and the probability of species persistence. However, while the few available large-scale empirical studies of fragmentation all tend to show that it has major effects, these documented effects tend to be relatively simple ones such as the degradation of habitat quality within fragments. There is good reason to be cautious of any claim that corridors or the spatial configuration of remaining habitat can compensate for the overall loss of habitat.
This is an invited Minireview on the occasion of the 50th anniversary of the Nordic Ecological Society Oikos.     

Insights into the oligomerization process of the C-terminal domain of human plasma membrane Ca²+-ATPase

Plasma membrane calcium pumps (PMCAs) sustain a primary transport system for the specific removal of cytosolic calcium ions from eukaryotic cells. PMCAs are characterized by the presence of a C-terminal domain referred to as a regulatory domain. This domain is target of several regulatory mechanisms: activation by Ca2+-calmodulin complex and acidic phospholipids, phosphorylation by kinase A and C, proteolysis by calpain and oligomerization. As far as oligomerization is concerned, the C-terminal domain seems to be crucial for this process. We have cloned the C-terminal domain of the human PMCA isoform 1b, and characterized its properties in solution. The expressed protein maintains its tendency to oligomerize in aqueous solutions, but it is dissociated by amphipathic molecules such as diacylglycerol and sodium dodecyl sulphate. The presence of sodium dodecyl sulphate stabilizes the domain as a compact structure in monomeric form retaining the secondary structure elements, as shown by small angle neutron scattering and circular dichroism measurements. The importance of oligomerization for the regulation of PMCA activity and intracellular calcium concentration is discussed.     

Respiratory chain defects: what do we know for sure about their consequences in vivo?

The function and the structure of mitochondria have been the subject of intensive research since the discovery of these organelles. Yet, the investigation of patients with mitochondrial disease reveals that we do not understand a large part of the underlying pathogenic processes. This has disastrous consequences in terms of the therapy possibly proposed to the patients and their family. An attempt is made in this short review to question our present ideas on the potential consequences of mitochondrial dysfunctions and to enlighten new observations which might be valuable in the understanding of the physiopathology of these diseases.     

Does plasma membrane H+-ATPase activation by fusicoccin involve protein kinase?

Sugar beet ( Beta vulgaris L.) root suspension-cultured cells were converted to protoplasts which responded to fusicoccin (FC) by a rise in cytoplasmic pH (pH_cyt) averaging 0.25 units in the fluorimetric assay. This effect was blocked by erythrosin B, a specific inhibitor of the plasma membrane H₊-ATPase. A protein kinase inhibitor, staurosporine also caused cytosolic alkalinization that was sensitive to H⁺-ATPase inhibitors. Most strikingly, the effect of staurosporine was suppressed by fusicoccin and vice versa. Addition of okadaic acid, entailing overall protein phosphorylation, also led to H⁺-ATPase activation, whereupon fusicoccin lost its effect on proton transport. In parallel, kinetic and inhibitor analyses demonstrated that FC binding to the protoplast plasma membrane involved two sites with dissociation constants of 1 n M and 0.2 μ M and was indifferent to phosphorylation and dephosphorylation inhibitors. Thus, it could be concluded that (1) the effect of FC on cytoplasmic pH probably depends on the phosphorylation state of plasma membrane proteins and may have either sign; (2) the activation of H⁺-ATPase by FC most likely proceeds directly through conformational receptor-enzyme interaction.     

Host cell invasion by apicomplexans: what do we know?

Apicomplexan zoites enter host cells by forming and actively moving through a tight junction (TJ) formed between the parasite and host cell surfaces. Although the TJ was first described decades ago, its molecular characterization has proved difficult mainly because of its transient existence during an internalization process that lasts only seconds. In the past 7 years, work has led to a model of the TJ in which the association between AMA1 and RON proteins structures the TJ and bridges the cytoskeletons of the two cells. However, more recent work questions this view. Here, we critically discuss the current model and speculate on alternative models of the AMA1-RON association and of the apicomplexan TJ.     

Spatial dynamics in model plant communities: what do we really know?

A variety of models have shown that spatial dynamics and small-scale endogenous heterogeneity (e.g., forest gaps or local resource depletion zones) can change the rate and outcome of competition in communities of plants or other sessile organisms. However, the theory appears complicated and hard to connect to real systems. We synthesize results from three different kinds of models: interacting particle systems, moment equations for spatial point processes, and metapopulation or patch models. Studies using all three frameworks agree that spatial dynamics need not enhance coexistence nor slow down dynamics; their effects depend on the underlying competitive interactions in the community. When similar species would coexist in a nonspatial habitat, endogenous spatial structure inhibits coexistence and slows dynamics. When a dominant species disperses poorly and the weaker species has higher fecundity or better dispersal, competition-colonization trade-offs enhance coexistence. Even when species have equal dispersal and per-generation fecundity, spatial successional niches where the weaker and faster-growing species can rapidly exploit ephemeral local resources can enhance coexistence. When interspecific competition is strong, spatial dynamics reduce founder control at large scales and short dispersal becomes advantageous. We describe a series of empirical tests to detect and distinguish among the suggested scenarios.     

Clonal mobility and its implications for spatio‐temporal patterns of plant communities: what do we need to know next?

Patterns of clonal growth and their controls on the level of individuals have been studied thoroughly, but little is known about the actual clonal mobility of plant individuals in vegetation and about its role in generating vegetation patterns and influencing species coexistence. Current evidence shows that communities are composed of spatially nonmobile ‘matrix‐forming species’ and mobile ‘inter‐matrix’ species, while local between‐species variation in clonal mobility has been shown to be positively correlated to small‐scale richness. We identify two major gaps in the knowledge. (1) Clonal mobility has a strong species‐specific component, but the existing information is mainly qualitative and describes the potential mobility of species the best. Also, species may respond by their clonal growth in a plastic way to some environmental stimuli, such as neighbors or abiotic environment, but this data comes almost exclusively from artificial conditions. We know very little of the actual spatial mobility of clonal plant individuals in the field and of the factors that determine it. (2) Theoretical research indicates that localized dispersal plays prime role in determination of community structure. While clonal mobility shares many important features with the seed dispersal, it also shows important differences to it, such as in dispersal kernel (non‐monotonic in clonal dispersal), role of microsite limitation, and role of plasticity. We have little information how systematic are these differences, and whether these differences in dispersal can play any role in shaping community dynamics. We conclude that clonal mobility has an important role in structuring plant communities in a small scale and propose further studies to address specific mechanisms, as well as community context of evolution of clonality.     

Mechanisms of tolerance to herbivore damage:what do we know?

Identifying mechanisms of tolerance to herbivore damage will facilitate attempts to understand the role of tolerance in the evolutionary and ecological dynamics of plants and herbivores. Investigations of the physiological and morphological changes that occur in plants in response to herbivore damage have identified several potential mechanisms of tolerance. However, it is unlikely that all physiological changes that occur following damage are tolerance mechanisms. Few studies have made direct comparisons between the expression of tolerance and the relative expression of putative mechanisms. I briefly review empirical evidence for some of the better-studied potential mechanisms, including increased photosynthetic activity, compensatory growth, utilization of stored reserves, and phenological delays. For each of these mechanisms I discuss reasons why the relationship between tolerance and these characters may be more complicated than it first appears. I conclude by discussing several empirical approaches, including herbivore manipulations, quantitative trait loci (QTL) analysis, and selection experiments, that will further our understanding of tolerance mechanisms. This revised version was published online in July 2006 with corrections to the Cover Date.     

Skin and diabetes mellitus: what do we know?

Diabetes mellitus (DM) is becoming increasingly prevalent worldwide. Although major complications of this condition involve kidney, retina and peripheral nerves, the skin of diabetic patients is also frequently injured. Hence, interest is mounting in the definition of the structural and molecular profile of non-complicated diabetic skin, i.e., before injuries occur. Most of the available knowledge in this area has been obtained relatively recently and, in part, derives from various diabetic animal models. These include both insulin-dependent and insulin-resistant models. Structural work in human diabetic skin has also been carried out by means of tissue samples or of non-invasive methods. Indications have indeed been found for molecular/structural changes in diabetic skin. However, the overall picture that emerges is heterogeneous, incomplete and often contradictory and many questions remain unanswered. This review aims to detail, as much as possible, the various pieces of current knowledge in a systematic and synoptic manner. This should aid the identification of areas in which key questions are still open and more research is needed. A comprehensive understanding of this field could help in determining molecular targets for the prevention and treatment of skin injuries in DM and markers for the monitoring of cutaneous and systemic aspects of the disease. Additionally, with the increasing development of non-invasive optics-based deep-tissue-imaging diagnostic technologies, precise knowledge of cutaneous texture and molecular structure becomes an important pre-requisite for the use of such methods in diabetic patients.     

Regulation of the Na+/K+-ATPase by insulin: Why and how?

The sodium-potassium ATPase (Na⁺/K⁺-ATPase or Na⁺/K⁺-pump) is an enzyme present at the surface of all eukaryotic cells, which actively extrudes Na⁺ from cells in exchange for K⁺ at a ratio of 3:2, respectively. Its activity also provides the driving force for secondary active transport of solutes such as amino acids, phosphate, vitamins and, in epithelial cells, glucose. The enzyme consists of two subunits ( and ) each expressed in several isoforms. Many hormones regulate Na⁺/K⁺ -ATPase activity and in this review we will focus on the effects of insulin. The possible mechanisms whereby insulin controls Na⁺/K⁺-ATPase activity are discussed. These are tissue- and isoform-specific, and include reversible covalent modification of catalytic subunits, activation by a rise in intracellular Na⁺ concentration, altered Na⁺ sensitivity and changes in subunit gene or protein expression. Given the recent escalation in knowledge of insulin-stimulated signal transduction systems, it is pertinent to ask which intracellular signalling pathways are utilized by insulin in controlling Na⁺/K⁺-ATPase activity. Evidence for and against a role for the phosphatidylinositol-3-kinase and mitogen activated protein kinase arms of the insulin-stimulated intracellular signalling networks is suggested. Finally, the clinical relevance of Na⁺/K⁺-ATPase control by insulin in diabetes and related disorders is addressed.     

UV radiation: what we know and do we protect ourselves adequately?

Chronic sun exposure causes degenerative changes in the skin that are recognized as photoaging, immunosuppression and photocarcinogenesis. Sun is necessary for life, so total sun avoidance is impossible. Sun exposure during the first 15 years of life and blistering sunburns before age 20 have been linked to an increased risk of melanoma. Individuals who have outdoor lifestyles, live in sunny climates, and are lightly pigmented will experience the greatest degree of photoaging. In our study, performed four years ago, we have shown the knowledge of more than 4000 people about the effects of UV rays on the skin. The results show us that sun exposure is still exaggerated and uncontrolled due to the lack of knowledge about this topic. Encouraging photoprotection and improving the awareness of the general public about the harmful effects of too much sun exposure must be the leading preventative health strategy.     

Regulation of the Ca2+-ATPase by cholesterol: A specific or non-specific effect?

Abstract

Like other integral membrane proteins, the activity of the Sarco/Endoplasmic Reticulum Ca²⁺-ATPase (SERCA) is regulated by the membrane environment. Cholesterol is present in the endoplasmic reticulum membrane at low levels, and it has the potential to affect SERCA activity both through direct, specific interaction with the protein or through indirect interaction through changes of the overall membrane properties. There are experimental data arguing for both modes of action for a cholesterol-mediated regulation of SERCA. In the current study, coarse-grained molecular dynamics simulations are used to address how a mixed lipid-cholesterol membrane interacts with SERCA. Candidates for direct regulatory sites with specific cholesterol binding modes are extracted from the simulations. The binding pocket for thapsigargin, a nanomolar inhibitor of SERCA, has been suggested as a cholesterol binding site. However, the thapsigargin binding pocket displayed very little cholesterol occupation in the simulations. Neither did atomistic simulations of cholesterol in the thapsigargin binding pocket support any specific interaction. The current study points to a non-specific effect of cholesterol on SERCA activity, and offers an alternative interpretation of the experimental results used to argue for a specific effect.