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Predator-secreted sulfolipids induce fear-like defense responses in C. elegans

Animals respond to predators by altering their behavior and physiological states, but the underlying signaling mechanisms are poorly understood. Using the interactions between Caenorhabditis elegans and its predator, Pristionchus pacificus, we show that neuronal perception by C. elegans of a predator-specific molecular signature induces instantaneous escape behavior and a prolonged reduction in oviposition. Chemical analysis revealed this predator-specific signature to consist of a class of sulfolipids, produced by a biochemical pathway required for developing predacious behavior and specifically induced by starvation. These sulfolipids are detected by four pairs of C. elegans amphid sensory neurons that act redundantly and recruit cyclic nucleotide-gated (CNG) or transient receptor potential (TRP) channels to drive both escape and reduced oviposition. Specific abolishment of predator-evoked C. elegans responses by the anti-anxiety drug sertraline as well as functional homology of the delineated signaling pathways suggests a conserved or convergent strategy for managing predator threats.

neuroscience

Cyclic electron flow in Chlamydomonas reinhardtii

Cyclic electron flow (CEF), one of the major alternative electron transport pathways to the primary linear electron flow (LEF) in chloroplasts has been discovered in the middle of the last century. It is defined as a return of the reductants from the acceptor side of the Photosystem I (PSI) to the pool of its donors via the cytochrome b6f, and has proven essential for photosynthesis. However, despite many efforts aimed at its characterisation, the pathway and regulation of CEF remain equivocal, and its physiological significance remains to be properly defined. Here we use novel spectroscopic approaches to measure CEF in transitory conditions in the green alga Chlamydomonas reinhardtii. We show that CEF operates at the same maximal rate regardless of the oxygen concentration, and that the latter influences LEF, rather than CEF in vivo, which questions the recent hypotheses about the CEF supercomplex formation. We further reveal that the pathways proposed for CEF in the literature are inconsistent with the kinetic information provided by our measurements. We finally provide cues on the regulation of CEF by light.

plant biology

Analysis of hippocampal transcriptomic responses to technical and biological perturbations

Cost-effective next-generation sequencing has made unbiased gene expression analysis possible. Single-neuron gene expression studies may be especially important for understanding nervous system structure and function because of the neuron-specific functionality and plasticity that defines functional neural circuits. Cellular dissociation is a prerequisite technical manipulation for single-cell and single cell-population studies, but the extent to which the cellular dissociation process cells affects neural gene expression has not been determined, nor has it been determined how gene expression is altered by the stress that accompanies many of the behavioral manipulations that are required to study learning and memory and other cognitive functions. Here, we determined to which extent cellular dissociation-induced changes in hippocampal gene expression might confound studies on the behavioral and physiological functions of the hippocampus. We processed tissue punch samples from the dentate gyrus (DG), CA3, and CA1 hippocampus subfields using either a tissue homogenization protocol or a cellular dissociation protocol in preparation for RNA sequencing analysis to evaluate the impact of the tissue preparation. Then, we evaluated the effect of stressful experience and cognitive training on hippocampus subfield specific gene expression and determined to which extent these response overlap with the cellular dissociation response. Finally, we assessed the extent to which the subfield-specific gene expression patterns are consistent with those identified in a recently published hippocampus subfield-specific gene expression database. We report substantial differences in baseline subfield-specific gene expression, that 1% of the hippocampal transcriptome is altered by the process of cellular dissociation, that an even weaker alteration is detected 24 h after stressful experience, and that while these alterations are largely distinct from the subfield specific response of the hippocampus transcriptome to cognitive training, there is nonetheless some important confounding overlap. These findings of the concordant and discordant effects of technical and behavioral manipulations should inform the design of future neural transcriptome studies and thus facilitate a more comprehensive understanding of hippocampal function.

neuroscience

Elevated ozone reduces photosynthetic carbon gain by accelerating leaf senescence of inbred and hybrid maize in a genotype-specific manner

Exposure to elevated tropospheric ozone concentration ([O3]) accelerates leaf senescence in many C3 crops. However, the effects of elevated [O3] on C4 crops including maize (Zea mays L.) are poorly understood in terms of physiological mechanism and genetic variation in sensitivity. Using Free Air gas Concentration Enrichment (FACE), we investigated the photosynthetic response of 18 diverse maize inbred and hybrid lines to season-long exposure to elevated [O3] (~100 nL L-1) in the field. Gas exchange was measured on the leaf subtending the ear throughout the grain filling period. On average over the lifetime of the leaf, elevated [O3] led to reductions in photosynthetic CO2 assimilation of both inbred (-22%) and hybrid (-33%) genotypes. There was significant variation among both inbred and hybrid lines in the sensitivity of photosynthesis to elevated [O3], with some lines showing no change in photosynthesis at elevated [O3]. Based on analysis of inbred line B73, the reduced CO2 assimilation at elevated [O3] was associated with accelerated senescence decreasing photosynthetic capacity, and not altered stomatal limitation. These findings across diverse maize genotypes could advance the development of more ozone tolerant maize, and provide experimental data for parameterization and validation of studies modeling how O3 impacts crop performance.

plant biology

Interplay between mitochondria and diet mediates pathogen and stress resistance in C. elegans

Diet is a crucial determinant of organismal biology. Here we demonstrate the dramatic impact of a subtle shift in diet on the ability of Caenorhabditis elegans to survive pathogenic or abiotic stress. Interestingly, this shift occurs independently of canonical host defense pathways, arising instead from improvements in mitochondrial health. Using a variety of assays, we reveal that the most common C. elegans food source (E. coli OP50) results in a vitamin B12 deficiency that compromises mitochondrial homeostasis. Increasing B12 supply by feeding on E. coli HT115 or by supplementing bacterial media with methylcobalamin restored mitochondrial function, even if the bacteria were dead. B12 supplementation also efficiently increased host health without adversely affecting lifespan. Our study forges a molecular link between a dietary deficiency (nutrition/microbiota) and a physiological consequence (host sensitivity), using the host-microbiota-diet framework. The ubiquity of B12 deficiency (~10-40% of US adults) highlights the importance of our findings.

molecular biology

A convergent depression vulnerability pathway encoded by emergent spatiotemporal dynamics

Fluctuations in brain local field potential (LFP) oscillations reflect emergent network-level signals that mediate behavior. Cracking the code whereby these LFP oscillations coordinate in time and space (spatiotemporal dynamics) to represent complex behaviors would provide fundamental insights into how the brain signals emotional processes at the network level. Here we use machine learning to integrate LFP activity acquired concurrently from seven cortical and subcortical brain regions into an analytical model that predicts the emergence of depression-related behavioral dysfunction across individual mice subjected to chronic social defeat stress. We uncover a spatiotemporal dynamic network in which activity originates in prefrontal cortex (PFC) and nucleus accumbens (NAc, ventral striatum), relays through amygdala and ventral tegmental area (VTA), and converges in ventral hippocampus (VHip). The activity of this network correlates with acute threat responses and brain-wide cellular firing, and it is enhanced in three independent molecular-, physiological-, and behavioral-based models of depression vulnerability. Finally, we use two antidepressant manipulations to demonstrate that this vulnerability network is biologically distinct from the networks that signal behavioral dysfunction after stress. Thus, corticostriatal to VHip-directed spatiotemporal dynamics organized at the network level are a novel convergent depression vulnerability pathway.

neuroscience

SWELL1 is a glucose sensor required for β-cell excitability and insulin secretion

Insulin secretion from the pancreatic {beta}-cell initiated by activation of voltage-gated Ca2+ channels (VGCC) to trigger Ca2+-mediated insulin vesicle fusion with the {beta}-cell plasma membrane. The firing of VGCC depends on the {beta}-cell membrane potential, which is in turn mediated by the balance of depolarizing (excitatory) and hyperpolarizing (inhibitory) ionic currents1-3. While much attention has focused on inhibitory potassium currents4-10 there is little knowledge about the excitatory currents required to depolarize the {beta}-cell, including the molecular identity of these excitatory currents3. Here we show that SWELL1 (LRRC8a) mediates a swell-activated, depolarizing chloride current (ICl,SWELL) in {beta}-cells. Hypotonic and glucose-stimulated {beta}-cell swelling activates SWELL1-mediated ICl,SWELL and this is required for both glucose-stimulated and hypotonic swell-mediated activation of VGCC-dependent intracellular calcium signaling in {beta}-cells. SWELL1 KO MIN6 cells and {beta}-cell targeted SWELL1 KO murine islets exhibit significantly impaired glucose-stimulated insulin secretion, with preserved insulin content in vitro. Tamoxifen-inducible {beta}-cell targeted SWELL1 KO mice have normal fasting insulin levels but display markedly impaired glucose-stimulated insulin secretion. Our results reveal a physiological role for SWELL1 as a glucose sensor - linking glucose-mediated {beta}-cell swelling to SWELL1-dependent activation of VGCC-triggered calcium signaling, and highlights SWELL1-mediated \"swell-secretion\" coupling as required for glucose-stimulated insulin secretion.

cell biology

High-quality genome assemblies uncover caste-specific long non-coding RNAs in ants

Ants are an emerging model system for neuroepigenetics, as embryos with virtually identical genomes develop into different adult castes that display strikingly different physiology, morphology, and behavior. Although a number of ant genomes have been sequenced to date, their draft quality is an obstacle to sophisticated analyses of epigenetic gene regulation. Using long reads generated with Pacific Biosystem single molecule real time sequencing, we have reassembled de novo high-quality genomes for two ant species: Camponotus floridanus and Harpegnathos saltator. The long reads allowed us to span large repetitive regions and join sequences previously found in separate scaffolds, leading to comprehensive and accurate protein-coding annotations that facilitated the identification of a Gp-9-like gene as differentially expressed in Harpegnathos castes. The new assemblies also enabled us to annotate long non-coding RNAs for the first time in ants, revealing several that were specifically expressed during Harpegnathos development and in the brains of different castes. These upgraded genomes, along with the new coding and non-coding annotations, will aid future efforts to identify epigenetic mechanisms of phenotypic and behavioral plasticity in ants.

genomics

A cerebellar mechanism for learning prior distributions of time intervals

Knowledge about the statistical regularities of the world is essential for cognitive and sensorimotor function. In the domain of timing, prior statistics are crucial for optimal prediction, adaptation and planning. Where and how the nervous system encodes temporal statistics, however, is not known. Deriving from physiological and anatomical evidence for cerebellar learning, we develop a computational model that demonstrates how the cerebellum could learn prior distributions of time intervals and support Bayesian temporal estimation. The model shows that salient features observed in human Bayesian time interval estimates can be readily captured by learning in the cerebellar cortex and circuit level computations in the cerebellar deep nuclei.

neuroscience

Systematic identification of novel regulatory interactions controlling biofilm formation in the bacterium Escherichia coli

Here, we investigated novel interactions of three global regulators of the network that controls biofilm formation in the model bacterium Escherichia coli using computational network analysis, an in vivo reporter assay and physiological validation experiments. We were able to map critical nodes that govern planktonic to biofilm transition and identify 8 new regulatory interactions for CRP, IHF or Fis responsible for the control of the promoters of rpoS, rpoE, flhD, fliA, csgD and yeaJ. Additionally, an in vivo promoter reporter assay and motility analysis revealed a key role for IHF as a repressor of cell motility through the control of FliA sigma factor expression. This investigation of first stage and mature biofilm formation indicates that biofilm structure is strongly affected by IHF and Fis, while CRP seems to provide a fine-tuning mechanism. Taken together, the analysis presented here shows the utility of combining computational and experimental approaches to generate a deeper understanding of the biofilm formation process in bacteria.

microbiology

Activation of Somatostatin Inhibitory Neurons by Lypd6-nAChRα2 System Restores Juvenile-like Plasticity in Adult Visual Cortex

The limitation of plasticity in the adult brain impedes functional recovery later in life from brain injury or disease. This pressing clinical issue may be resolved by enhancing plasticity in the adult brain. One strategy for triggering robust plasticity in adulthood is to reproduce one of the hallmark physiological events of experience-dependent plasticity observed during the juvenile critical period - rapidly reduce the activity of parvalbumin (PV)-expressing interneurons and disinhibit local excitatory neurons. This may be achieved through enhancement of local inhibitory inputs, particularly those of somatostatin (SST)-expressing interneurons. However, to date the means for manipulating SST interneurons for enhancing cortical plasticity in the adult brain are not known. We show that SST interneuron-selective overexpression of Lypd6, an endogenous nicotinic signaling modulator, enhances ocular dominance plasticity in the adult primary visual cortex (V1). Lypd6 overexpression mediates a rapid experience-dependent increase in the visually evoked activity of SST interneurons as well as a simultaneous reduction in PV interneuron activity and disinhibition of excitatory neurons. Recapitulating this transient activation of SST interneurons using chemogenetics similarly enhanced V1 plasticity. Notably, we show that SST-selective Lypd6 overexpression restores visual acuity in amblyopic mice that underwent early long-term monocular deprivation. Our data in both male and female mice reveal selective modulation of SST interneurons and a putative downstream circuit mechanism as an effective method for enhancing experience-dependent cortical plasticity as well as functional recovery in adulthood. Significance StatementThe decline of cortical plasticity after closure of juvenile critical period consolidates neural circuits and behavior, but this limits functional recovery from brain diseases and dysfunctions in later life. Here we show that activation of cortical SST interneurons by Lypd6, an endogenous modulator of nicotinic acetylcholine receptors (nAChRs), enhances experience-dependent plasticity and recovery from amblyopia in adulthood. This manipulation triggers rapid reduction of PV interneuron activity and disinhibition of excitatory neurons, which are known hallmarks of cortical plasticity during juvenile critical periods. Our study demonstrates modulation of SST interneurons by Lypd6 to achieve robust levels of cortical plasticity in the adult brain and may provide promising targets for restoring brain function in the event of brain trauma or disease.

neuroscience

Cofilin Drives Rapid Turnover and Fluidization of Entangled F-actin

The shape of most animal cells is controlled by the actin cortex, a thin, isotropic network of dynamic actin filaments (F-actin) situated just beneath the plasma membrane. The cortex is held far from equilibrium by both active stresses and turnover: Myosin-II molecular motors drive deformations required for cell division, migration, and tissue morphogenesis, while turnover of the molecular components of the actin cortex relax stress and facilitate network reorganization. While many aspects of F-actin network viscoelasticity are well-characterized in the presence and absence of motor activity, a mechanistic understanding of how non-equilibrium actin turnover contributes to stress relaxation is still lacking. To address this, we developed a reconstituted in vitro system wherein the steady-state length and turnover rate of F-actin in entangled solutions are controlled by the actin regulatory proteins cofilin, profilin, and formin, which sever, recycle, and nucleate filaments, respectively. Cofilin-mediated severing accelerates the turnover and spatial reorganization of F-actin, without significant changes to filament length. Microrheology measurements demonstrate that cofilin-mediated severing is a single-timescale mode of stress relaxation that tunes the low-frequency viscosity over two orders of magnitude. These findings serve as the foundation for understanding the mechanics of more physiological F-actin networks with turnover, and inform an updated microscopic model of single-filament turnover. They also demonstrate that polymer activity, in the form of ATP hydrolysis on F-actin coupled to nucleotide-dependent cofilin binding, is sufficient to generate a form of active matter wherein asymmetric filament disassembly preserves filament number in spite of sustained severing.\n\nSignificance StatementWhen an animal cell moves or divides, a disordered network of actin filaments (F-actin) plays a central role in controlling the resulting changes in cell shape. While it is known that continual turnover of F-actin by cofilin-mediated severing aids in reorganization of the cellular cytoskeleton, it is unclear how the turnover of structural elements alters the mechanical properties of the network. Here we show that severing of F-actin by cofilin results in a stress relaxation mechanism in entangled solutions characterized by a single-timescale set by the severing rate. Additionally, we identify ATP hydrolysis and nucleotide-dependent cofilin binding as sufficient ingredients to generate a non-equilibrium steady-state in which asymmetric F-actin disassembly preserves filament number in spite of sustained severing.

biophysics

Voltage-gating of mechanosensitive PIEZO channels

Mechanosensitive PIEZO ion channels are evolutionarily conserved proteins whose presence is critical for normal physiology in multicellular organisms. Here we show that, in addition to mechanical stimuli, PIEZO channels are also powerfully modulated by voltage and can even switch to a purely voltage gated mode. Mutations that cause human diseases such as Xerocytosis profoundly shift voltage sensitivity of PIEZO1 channels towards the resting membrane potential and strongly promote pure voltage gating. Our data may be explained by the presence of an inactivation gate in the pore, the opening of which is promoted by outward permeation. Invertebrate (fly) and vertebrate (fish) PIEZO proteins are also voltage sensitive but voltage gating is a much more prominent feature of these older channels. We propose that the voltage sensitivity of PIEZO channels is a deep property co-opted to add a regulatory mechanism for PIEZO activation in widely different cellular contexts.

neuroscience

Neural Responses to Heartbeats of Physically Trained and Sedentary Young Adults

Regular physical exercise has a positive impact on brain function and cognitive performance. However, it is not yet clear whether the physiological and behavioral benefits associated to physical exercise are caused exclusively by changes in cardiovascular fitness. Here, we explore the relation between regular physical exercise and transient electroencephalographic responses to afferent cardiac signals. We find differences in the neural processing of heartbeats between individuals who exercise regularly and their sedentary counterparts. These differences, localised at two distinct spatio-temporal clusters, occur before the presentation of a target stimulus and correlate with behavioral performance only in the high-fit group. We hypothesise that the different neural processing of afferent cardiac activity by physically trained individuals reflects enhanced interoceptive sensitivity, which contributes to improved sustained attention. Our results are in line with recent research highlighting the role of neural monitoring of visceral signals in perceptual processing and even the generation of the sense of self.

neuroscience

Partial Unwinding of Transmembrane Helices Facilitates Alternating Access in the Neurotransmitter:Sodium Symporter LeuT

The prokaryotic neurotransmitter:sodium symporter (NSS) LeuT from Aquifex aeolicus is an established structural model for mammalian NSS counterparts. Here, we investigate the substrate translocation mechanism of LeuT by measuring the solution-phase structural dynamics of the transporter in distinct functional states by hydrogen/deuterium exchange mass spectrometry (HDX-MS). Our HDX-MS data pinpoint LeuT segments involved in substrate transport and reveal for the first time a comprehensive and detailed view of the solution-phase dynamics associated with transition of the transporter between outward- and inwardfacing configurations in a Na+- as well as K+-dependent manner. The results suggest that partial unwinding of transmembrane helices 1/5/6/7 drive LeuT from a substrate-bound, outward-facing occluded conformation towards an inward-facing open state. We thereby envisage that substrate release is facilitated by formation of two distinct solvent pathways, which mediate access to the Na+ and substrate binding sites.\n\nThe neurotransmitter:sodium symporter (NSS) family includes prokaryotic and eukaryotic integral membrane proteins that harness the energy stored in the Na+ concentration gradient to transport solutes across the cell membrane (1, 2). Mammalian NSS proteins play an important role in terminating the neurotransmission in the central nervous system by rapid uptake of neurotransmitters against their concentration gradient into the presynaptic neuron or neighboring glial cells (3-5). Numerous neuropsychiatric conditions are associated with altered function of NSS transporters or low neurotransmitter concentrations in the synaptic cleft (2). Many NSS proteins therefore represent favorable targets for therapeutic drugs that act as potent transport inhibitors to increase neurotransmitter levels at the synaptic junction (2, 6). Despite the importance of mammalian NSS proteins in neurobiology and pharmacology, the molecular mechanisms underlying the transport function of mammalian NSS family members have proven difficult to elucidate by traditional methods as the target proteins are unstable in detergent-solubilized form (7) and difficult to purify in required quantity and purity.\n\nThe prokaryotic NSS protein LeuT from Aquifex aeolicus has emerged as an important structural model to investigate the structure-function relationship of mammalian NSS counterparts (7-9). High-resolution crystal structures of LeuT in distinct functional states (10-13) have established a structural framework and given rise to mechanistic models depicting the substrate transport mechanism (14, 15). LeuT comprises 12 transmembrane segments (TMs) that are interconnected by relatively short extracellular (EL) and intracellular (IL) loops. The first TMs 1-5 share a similar structural repeat with the following TMs 6-10 but are inverted in the membrane plane (10). The specific arrangement of TM domains, also referred to as the 5+5 or LeuT fold (10), has been observed in other NSS proteins (16-18), but also in transporters without sequence homology to LeuT (19, 20), suggesting the possibility of a conserved structural scaffold for many secondary active transporters (8). The primary binding site for the substrate (S1) and residues involved in coordination of two sodium ions (Na1 and Na2) are located approximately halfway across the membrane bilayer in the core of the transporter (10). The characteristic unwound regions of TMs 1 and 6 (providing both TMs with an a- and a b-section) fulfill a dual role in coordinating the sodium ions and forming interactions with the substrate molecule. Individual amino acid residues of TMs 3 and 8 as well as the sodium occupancy in the Na1 site complete the S1 binding pocket.\n\nAccording to the widely embraced alternating access model (21, 22), secondary active transporters isomerize between distinct functional states in a substrate-dependent manner. That is, the substrate binding site is alternatively exposed to either the intracellular or extracellular aqueous environment. X-ray crystallography provided structures of LeuT in outward-facing open (11, 12), outward-facing occluded (10), and inwardfacing open (11) conformations and led to the identification of external and internal gating residues in LeuT and related transporters (23-26). Based on these structural snapshots, it has been hypothesized that local and large-scale structural rearrangements are required to regulate the molecular gates and the outward-to-inward transition of the transporter, respectively (11). Combined evidence from crystallographic, functional, and simulation studies suggest that the underlying allosteric couplings are essential for LeuT to function as a symporter (27). Several key aspects of the transport cycle, in particular the molecular mechanism related to the transition of LeuT to the inward-facing open state, have remained controversial and are the subject of extensive debate (8, 28-30).\n\nHere, we have studied the substrate translocation mechanism of LeuT by measuring the structural dynamics of the protein in solution as a function of time and substrate/ion composition (e.g. leucine, Na+, K+, and Cs+) by local hydrogen/deuterium exchange mass spectrometry (HDX-MS). The exchange of hydrogen to deuterium (HDX) of backbone amides in a protein is dependent on the presence and stability of hydrogen bonds and thus provides a sensitive probe for higher-order structure and dynamics of the target protein in solution (31, 32). HDX-MS is a non-perturbing technique that allows the collection of structural dynamics data along the entire protein backbone in a coherent manner without the need for sequence alterations or changes to the covalent structure of the protein for labeling (33). Briefly, the target protein is diluted into deuterated buffer and labeled for various time intervals. The isotopic exchange reaction is quenched by lowering pH and temperature to approximately 2.5 and 0 {degrees}C, respectively, and the protein subsequently digested using an acid-stable protease (e.g. pepsin). Chromatographic separation and mass analysis of these peptides, in turn, reveal the shift in mass over time (i.e., deuterium uptake) of individual regions of the target protein, which is commonly referred to as local HDX analysis. A more detailed background on the HDX-MS technique and its applications in protein science can be found in several reviews (34-37).\n\nOur HDX-MS measurements provide a detailed map of LeuT regions involved in conformational changes during substrate transport (TMs 1a/1b/2/5/6a/6b/7 and interconnecting loops IL1/EL2/EL3/EL4b) and allow for the first time an unperturbed global view on the structural dynamics associated with the outward-to-inward transition of the wild-type transporter in solution. Of special interest, our acquired HDX data suggest that several helices (TMs 1a/5/6/7 and EL4b) are partially unwound in the course of substrate transport and that these unfolding events are dynamically coupled between individual helices that form the substrate binding site and the cytoplasmic gate. Addition of Na+ or the combination of Na+ and leucine destabilized discrete structural motifs on the extracellular side, stabilized the inner gate of LeuT, and substantially reduced the rate of unfolding in individual TM helices relative to the K+-bound state. We envisage that partial unwinding of TM helices accompanies the outward-to-inward isomerization in LeuT and that the same concept might be relevant to related transporters bearing the LeuT fold, hence extending the general model of NSS transport mechanism. Moreover, we provide additional experimental evidence for a potential role of K+ in the transport cycle as K+ selectively shifted the conformational equilibrium of LeuT in a dose-dependent manner towards an inwardfacing state under physiologically relevant concentrations.

biophysics

Transcriptomic Resilience of a Coral Holobiont to Low pH

Ocean acidification is considered as one of the major threats for coral reefs at a global scale. Marine calcifying organisms, including stony corals, are expected to be the most affected by the predicted decrease of the surface water pH at the end of the century. The severity of the impacts on coral reefs remains as matter of controversy. Although previous studies have explored the physiological response of stony corals to changes in pH, the response of the holobiont (i.e. the coral itself plus its symbionts) remains largely unexplored. In the present study, we assessed the changes in overall gene expression of the coral Montipora digitata and its microalgal symbionts after a short (three days) and a longer (42 days) exposure to low pH (7.6). The short-term exposure to low pH caused small differences in the expression level of the host, impacting mostly genes associated with stress response in other scleractinians. Resilience to Acidification of a Coral Holobiont Longer exposure to low pH resulted in no significant changes in gene expression of the coral host. Gene expression in the eukaryotic symbionts remained unaltered at both exposure times. Our findings suggest resilience, in terms of gene expression, of the Montipora digitata holobiont to pH decrease, as well as capability to acclimatize to extended periods of exposure to low pH.

ecology

Systems Therapeutics for Axonal Regeneration in the Central Nervous System

There are no known drugs or drug combinations that promote substantial central nervous system axonal regeneration after injury. We used systems pharmacology approaches to model pathways underlying axonal growth and identify a four-drug combination that regulates multiple subcellular processes in the cell body and axon using the optic nerve crush model in rats. We intravitreally injected agonists HU-210 (cannabinoid receptor-1) and IL-6 (interleukin 6 receptor) to stimulate retinal ganglion cells for axonal growth. We applied, in gel foam at the site of nerve injury, Taxol to stabilize growing microtubules, and activated protein C to clear the debris field since computational models predicted that this drug combination regulating two subcellular processes at the growth cone produces synergistic growth. Morphology experiments show that the four-drug combination promotes axonal regrowth to the optic chiasm and beyond. Physiologically, drug treatment restored pattern electroretinograms and some of the animals had detectable visual evoked potentials in the brain and behavioral optokinetic responses. We conclude that spatially targeted drug treatment can promote robust axonal regeneration and can restore limited functional recovery.

neuroscience

Hypoosmolar dose-dependent swelling occurs in both pyramidal neurons and astrocytes in acute hippocampal slices

Normal nervous system function is critically dependent on the balance of water and ions in the extracellular space. Pathological reduction in brain interstitial osmolarity results in osmotically-driven flux of water into cells, causing cellular edema which reduces the extracellular space and increases neuronal excitability and risk of seizures. Astrocytes are widely considered to be particularly susceptible to cellular edema due to selective expression of the water channel aquaporin-4 (AQP4). The apparent resistance of pyramidal neurons to osmotic swelling has been attributed to lack of functional water channels. In this study we report rapid volume changes in CA1 pyramidal cells in hypoosmolar ACSF (hACSF) that are equivalent to volume changes in astrocytes across a variety of conditions. Astrocyte and neuronal swelling was significant within 1 minute of exposure to 17 or 40% hACSF, was rapidly reversible upon return to normosmolar ACSF, and repeatable upon re-exposure to hACSF. Neuronal swelling was not an artifact of patch clamp, occurred deep in tissue, was similar at physiological vs. room temperature, and occurred in both juvenile and adult hippocampal slices. Neuronal swelling was neither inhibited by TTX, nor by antagonists of NMDA or AMPA receptors, suggesting that it was not occurring as a result of excitotoxicity. Surprisingly, genetic deletion of AQP4 did not inhibit, but rather augmented, astrocyte swelling in severe hypoosmolar conditions. Taken together, our results indicate that neurons are not osmoresistant as previously reported, and that osmotic swelling is driven by an AQP4-independent mechanism.

neuroscience