Fifteen important questions in the spatial ecology of diatoms

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Trophic interactions and abiotic factors drive functional and phylogenetic structure of vertebrate herbivore communities across the Arctic tundra biome

Communities are assembled from species that evolve or colonise a given geographic region, and persist in the face of abiotic conditions and interactions with other species. The evolutionary and colonisation histories of communities are characterised by phylogenetic diversity, while functional diversity is indicative of abiotic and biotic conditions. The relationship between functional and phylogenetic diversity infers whether species functional traits are divergent (differing between related species) or convergent (similar among distantly related species). Biotic interactions and abiotic conditions are known to influence macroecological patterns in species richness, but how functional and phylogenetic diversity of guilds vary with biotic factors, and the relative importance of biotic drivers in relation to geographic and abiotic drivers is unknown. In this study, we test whether geographic, abiotic or biotic factors drive biome‐scale spatial patterns of functional and phylogenetic diversity and functional convergence in vertebrate herbivores across the Arctic tundra biome. We found that functional and phylogenetic diversity both peaked in the western North American Arctic, and that spatial patterns in both were best predicted by trophic interactions, namely vegetation productivity and predator diversity, as well as climatic severity. Our results show that both bottom–up and top–down trophic interactions, as well as winter temperatures, drive the functional and phylogenetic structure of Arctic vertebrate herbivore assemblages. This has implications for changing Arctic ecosystems; under future warming and northward movement of predators potential increases in phylogenetic and functional diversity in vertebrate herbivores may occur. Our study thus demonstrates that trophic interactions can determine large‐scale functional and phylogenetic diversity just as strongly as abiotic conditions.     

Mitochondrial DNA polymorphisms as risk factors for Parkinson’s disease and Parkinson’s disease dementia

The activity of complex I of the mitochondrial respiratory chain has been found to be decreased in patients with Parkinsons disease (PD), but no mutations have been identified in genes encoding complex I subunits. Recent studies have suggested that polymorphisms in mitochondrial DNA (mtDNA)-encoded complex I genes (MTND) modify susceptibility to PD. We hypothesize that the risk of PD is conveyed by the total number of nonsynonymous substitutions in the MTND genes in various mtDNA lineages rather than by single mutations. To test this possibility, we determined the number of nonsynonymous substitutions of the seven MTND genes from 183 Finns. The differences in the total number of nonsynonymous substitutions and the nonsynonymous to synonymous substitution rate ratio (K_a/K_s) of MTND genes between the European mtDNA haplogroup clusters (HV, JT, KU, IWX) were analysed by using a statistical approach. Patients with PD (n=238) underwent clinical examination together with mtDNA haplogroup analysis and the clinical features between patient groups defined by the number of nonsynonymous substitutions were compared. Our analysis revealed that the haplogroup clusters HV and KU had a lower average number of amino acid replacements and a lower K_a/K_s ratio in the MTND genes than clusters JT and IWX. Supercluster JTIWX with the highest number of amino acid replacements was more frequent among PD patients and even more frequent among patients with PD who developed dementia. Our results suggest that a relative excess of nonsynonymous mutations in MTND genes in supercluster JTWIX is associated with an increased risk of PD and the disease progression to dementia.     

Deletion of the Laminin α4 Chain Leads to Impaired Microvessel Maturation

The laminin alpha4 chain, a component of laminin-8 and -9, is expressed in basement membranes, such as those beneath endothelia, the perineurium of peripheral nerves, and around developing muscle fibers. Laminin alpha4-null mice presented with hemorrhages during the embryonic and neonatal period and had extensive bleeding and deterioration of microvessel growth in experimental angiogenesis, as well as mild locomotion defects. Histological examination of newborn mice revealed delayed deposition of type IV collagen and nidogen into capillary basement membranes, and electron microscopy showed discontinuities in the lamina densa. The results demonstrate a central role for the laminin alpha4 chain in microvessel growth and, in the absence of other laminin alpha chains, in the composition of endothelial basement membranes.     

Characterization of systemic metabolic phenotypes associated with subclinical atherosclerosis

Detailed molecular phenotyping gives insight into disease mechanisms and can individualize medical practice for improved risk assessment and treatment. We show in an epidemiological study (n = 4309) that the multi-metabolic profiles obtained by serum NMR metabonomics inherently associate with the extent of atherosclerosis already in preclinical stages. Data-driven analysis of the spectral profiles of healthy, young adults revealed three distinct metabolic phenotypes associated with high carotid intima-media thickness (IMT), a surrogate marker of cardiovascular disease. The phenotypes were characterized by varying combinations of well-known metabolic disturbances like elevated VLDL and LDL and low HDL levels. Low IMT was also associated with distinct metabolic phenotypes with lipoprotein as well as other biochemical characteristics partly opposing those found for the high IMT phenotypes. Profiles of low-molecular-weight metabolites quantified from the experimentation were also characteristic for the metabolic phenotypes and substantiate developments toward the use of multi-metabolic risk phenotypes. The methodology can be taken as a direct extension for the routine analytics used for the risk assessment of atherosclerosis; quantification of metabolites will complement and might even replace conventional lipid measurements. Serum NMR metabonomics is therefore anticipated as a rational option for comprehensive cardiovascular risk assessment.     

Down-regulation of Seladin-1 Increases BACE1 Levels and Activity through Enhanced GGA3 Depletion during Apoptosis

Seladin-1 is a neuroprotective protein selectively down-regulated in brain regions affected in Alzheimer disease (AD). Seladin-1 protects cells against β-amyloid (Aβ) peptide 42- and oxidative stress-induced apoptosis activated by caspase-3, a key mediator of apoptosis. Here, we have employed RNA interference to assess the molecular effects of seladin-1 down-regulation on the β-secretase (BACE1) function and β-amyloid precursor protein (APP) processing in SH-SY5Y human neuroblastoma cells in both normal and apoptotic conditions. Our results show that ∼60% reduction in seladin-1 protein levels, resembling the decrease observed in AD brain, did not significantly affect APP processing or Aβ secretion in normal growth conditions. However, under apoptosis, seladin-1 small interfering RNA (siRNA)-transfected cells showed increased caspase-3 activity on average by 2-fold when compared with control siRNA-transfected cells. Increased caspase-3 activity coincided with a significant depletion of the BACE1-sorting protein, GGA3 (Golgi-localized γ-ear-containing ADP-ribosylation factor-binding protein), and subsequently augmented BACE1 protein levels and activity. Augmented BACE1 activity in turn correlated with the enhanced β-amyloidogenic processing of APP and ultimately increased Aβ production. These adverse changes associated with decreased cell viability in seladin-1 siRNA-transfected cells under apoptosis. No changes in GGA3 or BACE1 levels were found after seladin-1 knockdown in normal growth conditions. Collectively, our results suggest that under stress conditions, reduced seladin-1 expression results in enhanced GGA3 depletion, which further leads to augmented post-translational stabilization of BACE1 and increased β-amyloidogenic processing of APP. These mechanistic findings related to seladin-1 down-regulation are important in the context of AD as the oxidative stress-induced apoptosis plays a key role in the disease pathogenesis.     

Elements of metacommunity structure and community‐environment relationships in stream organisms

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AMP-activated protein kinase: a potential player in Alzheimer's disease

AMP-activated protein kinase (AMPK) stimulates energy production via glucose and lipid metabolism, whereas it inhibits energy consuming functions, such as protein and cholesterol synthesis. Increased cytoplasmic AMP and Ca(2+) levels are the major activators of neuronal AMPK signaling. Interestingly, Alzheimer's disease (AD) is associated with several abnormalities in neuronal energy metabolism, for example, decline in glucose uptake, mitochondrial dysfunctions and defects in cholesterol metabolism, and in addition, with problems in maintaining Ca(2+) homeostasis. Epidemiological studies have also revealed that many metabolic and cardiovascular diseases are risk factors for cognitive impairment and sporadic AD. Emerging studies indicate that AMPK signaling can regulate tau protein phosphorylation and amyloidogenesis, the major hallmarks of AD. AMPK is also a potent activator of autophagic degradation which seems to be suppressed in AD. All these observations imply that AMPK is involved in the pathogenesis of AD. However, the responses of AMPK activation are dependent on stimulation and the extent of activating stress. Evidently, AMPK signaling can repress and delay the appearance of AD pathology but later on, with increasing neuronal stress, it can trigger detrimental effects that augment AD pathogenesis. We will outline the potential role of AMPK function in respect to various aspects affecting AD pathogenesis.