Company matters: The presence of other genotypes alters traits and intraspecific selection in an Arctic diatom under climate change.

Arctic phytoplankton and their response to future conditions shape one of the most rapidly changing ecosystems on the planet. We tested how much the phenotypic responses of strains from the same Arctic diatom population diverge and whether the physiology and intraspecific composition of multistrain populations differs from expectations based on single strain traits. To this end, we conducted incubation experiments with the diatom Thalassiosira hyalina under present-day and future temperature and pCO2 treatments. Six fresh isolates from the same Svalbard population were incubated as mono- and multistrain cultures. For the first time, we were able to closely follow intraspecific selection within an artificial population using microsatellites and allele-specific quantitative PCR. Our results showed not only that there is substantial variation in how strains of the same species cope with the tested environments but also that changes in genotype composition, production rates, and cellular quotas in the multistrain cultures are not predictable from monoculture performance. Nevertheless, the physiological responses as well as strain composition of the artificial populations were highly reproducible within each environment. Interestingly, we only detected significant strain sorting in those populations exposed to the future treatment. This study illustrates that the genetic composition of populations can change on very short timescales through selection from the intraspecific standing stock, indicating the potential for rapid population level adaptation to climate change. We further show that individuals adjust their phenotype not only in response to their physicochemical but also to their biological surroundings. Such intraspecific interactions need to be understood in order to realistically predict ecosystem responses to global change.

An intertidal life: Combined effects of acidification and winter heatwaves on a coralline alga (Ellisolandia elongata) and its associated invertebrate community.

In coastal marine ecosystems coralline algae often create biogenic reefs. These calcareous algal reefs affect their associated invertebrate communities via diurnal oscillations in photosynthesis, respiration and calcification processes. Little is known about how these biogenic reefs function and how they will be affected by climate change. We investigated the winter response of a Mediterranean intertidal biogenic reef, Ellissolandia elongata exposed in the laboratory to reduced pH conditions (i.e. ambient pH - 0.3, RCP 8.5) together with an extreme heatwave event (+1.4 °C for 15 days). Response variables considered both the algal physiology (calcification and photosynthetic rates) and community structure of the associated invertebrates (at taxonomic and functional level). The combination of a reduced pH with a heatwave event caused Ellisolandia elongata to significantly increase photosynthetic activity. The high variability of calcification that occurred during simulated night time conditions, indicates that there is not a simple, linear relationship between these two and may indicate that it will be resilient to future conditions of climate change. In contrast, the associated fauna were particularly negatively affected by the heatwave event, which impoverished the communities as opportunistic taxa became dominant. Local increases in oxygen and pH driven by the algae can buffer the microhabitat in the algal fronds, thus favouring the survival of small invertebrates.

Loss of Myelin Basic Protein Function Triggers Myelin Breakdown in Models of Demyelinating Diseases.

Breakdown of myelin sheaths is a pathological hallmark of several autoimmune diseases of the nervous system. We employed autoantibody-mediated animal models of demyelinating diseases, including a rat model of neuromyelitis optica (NMO), to target myelin and found that myelin lamellae are broken down into vesicular structures at the innermost region of the myelin sheath. We demonstrated that myelin basic proteins (MBP), which form a polymer in between the myelin membrane layers, are targeted in these models. Elevation of intracellular Ca(2+) levels resulted in MBP network disassembly and myelin vesiculation. We propose that the aberrant phase transition of MBP molecules from their cohesive to soluble and non-adhesive state is a mechanism triggering myelin breakdown in NMO and possibly in other demyelinating diseases.

Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model.

Oligodendrocyte damage is a central event in the pathogenesis of the common neuroinflammatory condition, multiple sclerosis (MS). Where and how oligodendrocyte damage is initiated in MS is not completely understood. Here, we use a combination of light and electron microscopy techniques to provide a dynamic and highly resolved view of oligodendrocyte damage in neuroinflammatory lesions. We show that both in MS and in its animal model structural damage is initiated at the myelin sheaths and only later spreads to the oligodendrocyte cell body. Early myelin damage itself is characterized by the formation of local myelin out-foldings-'myelinosomes'-, which are surrounded by phagocyte processes and promoted in their formation by anti-myelin antibodies and complement. The presence of myelinosomes in actively demyelinating MS lesions suggests that oligodendrocyte damage follows a similar pattern in the human disease, where targeting demyelination by therapeutic interventions remains a major open challenge.

Astrocyte Depletion Impairs Redox Homeostasis and Triggers Neuronal Loss in the Adult CNS.

Although the importance of reactive astrocytes during CNS pathology is well established, the function of astroglia in adult CNS homeostasis is less well understood. With the use of conditional, astrocyte-restricted protein synthesis termination, we found that selective paralysis of GFAP(+) astrocytes in vivo led to rapid neuronal cell loss and severe motor deficits. This occurred while structural astroglial support still persisted and in the absence of any major microvascular damage. Whereas loss of astrocyte function did lead to microglial activation, this had no impact on the neuronal loss and clinical decline. Neuronal injury was caused by oxidative stress resulting from the reduced redox scavenging capability of dysfunctional astrocytes and could be prevented by the in vivo treatment with scavengers of reactive oxygen and nitrogen species (ROS/RNS). Our results suggest that the subpopulation of GFAP(+) astrocytes maintain neuronal health by controlling redox homeostasis in the adult CNS.

Cellular, subcellular and functional in vivo labeling of the spinal cord using vital dyes.

Here we provide a protocol for rapidly labeling different cell types, distinct subcellular compartments and key injury mediators in the spinal cord of living mice. This method is based on the application of synthetic vital dyes to the surgically exposed spinal cord. Suitable vital dyes applied in appropriate concentrations lead to reliable in vivo labeling, which can be combined with genetic tags and in many cases preserved for postfixation analysis. In combination with in vivo imaging, this approach allows the direct observation of central nervous system physiology and pathophysiology at the cellular, subcellular and functional level. Surgical exposure and preparation of the spinal cord can be achieved in less than 1 h, and then dyes need to be applied for 30-60 min before the labeled spinal cord can be imaged for several hours.