Divergent effects of climatic factors on termite body size: alate versus worker castes.

Body size is an important functional trait to animals. Caste division of eusocial insects can exert a profound influence on their interactions with environment. We investigate the intra-specific variation of body size between caste within Odontotermes formosanus (Shiraki) (Blattodea: Termitidae), the most common and widely distributed termite species in Taiwan Island. By utilizing specimens from the NCHU Termite Collection and WorldClim data, we describe the body size distribution pattern of O. formosanus on two castes, worker and alate, and relationship with climatic factors is examined. The body size of workers is positively correlated with latitude and elevation. The body size of alates does not correlate with latitude but is positively correlated with elevation. Temperature factors negatively affect the body size of both castes. Precipitation has a positive effect on the body size of alates and no effect on workers. Additionally, humidity and temperature fluctuations over time have divergent effects on the body size of alates and workers. The results provide evidence of trait evolution decoupling at the intraspecific level, which may be shaped by climatic factors.

A review of porcine skeletal muscle plasticity and implications for genetic improvement of carcass and meat quality.

Skeletal muscle is characterized by a remarkable plasticity to adapt to stimuli such as contractile activity, loading conditions, substrate supply or environmental factors. The existing knowledge of muscle plasticity along with developed genetic and genomic technologies, have enabled creating animal breeding strategies and allowed for implementing agriculturally successful porcine genetic improvement programs. The primary focus of this review paper is on pig skeletal muscle plasticity as it relates to genetic improvement of desirable carcass composition and pork quality traits. Biological constraints between practically realized breeding objectives, pig skeletal muscle biology, and pork quality are also discussed. Future applications of genetic and genomic technologies and plausible focus on new breeding objectives enhancing pork production sustainability are proposed as well.

YY1 knockout in pro-B cells impairs lineage commitment, enabling unusual hematopoietic lineage plasticity.

During B-cell development, cells progress through multiple developmental stages, with the pro-B-cell stage defining commitment to the B-cell lineage. YY1 is a ubiquitous transcription factor that is capable of both activation and repression functions. We found here that knockout of YY1 at the pro-B-cell stage eliminates B lineage commitment. YY1 knockout pro-B cells can generate T lineage cells in vitro using the OP9-DL4 feeder system and in vivo after injection into sublethally irradiated Rag1-/- mice. These T lineage-like cells lose their B lineage transcript profile and gain a T-cell lineage profile. Single-cell RNA-seq experiments showed that as YY1 knockout pro-B cells transition into T lineage cells in vitro, various cell clusters adopt transcript profiles representing a multiplicity of hematopoietic lineages, indicating unusual lineage plasticity. In addition, YY1 KO pro-B cells in vivo can give rise to other hematopoietic lineages in vivo. Evaluation of RNA-seq, scRNA-seq, ChIP-seq, and scATAC-seq data indicates that YY1 controls numerous chromatin-modifying proteins leading to increased accessibility of alternative lineage genes in YY1 knockout pro-B cells. Given the ubiquitous nature of YY1 and its dual activation and repression functions, YY1 may regulate commitment in multiple cell lineages.

Investigating the role of HSP90 in cancer cell phenotypic plasticity.

"What are the mechanisms driving tumor evolution under the selective pressure of chemotherapeutics?" The emerging importance of epigenetic gene regulation in cancer progression necessitates not only our understanding of which genes are potential targets but also what mechanisms are employed in targeting those genes. Understanding the mechanisms that promote the evolution of the normal genome and epigenome is central to understanding how cancer cells adapt to chemotherapy. Our previous investigations have shown that heat shock protein 90 (HSP90) has a critical role in epigenetic gene regulation through histone acetylation and phenotypic plasticity. We recently extended these results in an A549 lung cancer model to test the role of HSP90 in the plasticity of cells regarding multi-drug resistance and epithelial-to-mesenchymal transition phenotypes. HSP90 is over-expressed in multiple cancers with poor prognosis. We propose that inhibition of HSP90 results in lower phenotypic plasticity of cancer cells making them more susceptible to chemotherapeutic intervention. Here we review the context of our results in the broader field of evolution of these phenotypes.

Treatment-induced stemness and lineage plasticity in driving prostate cancer therapy resistance.

Most human cancers are heterogeneous consisting of cancer cells at different epigenetic and transcriptional states and with distinct phenotypes, functions, and drug sensitivities. This inherent cancer cell heterogeneity contributes to tumor resistance to clinical treatment, especially the molecularly targeted therapies such as tyrosine kinase inhibitors (TKIs) and androgen receptor signaling inhibitors (ARSIs). Therapeutic interventions, in turn, induce lineage plasticity (also called lineage infidelity) in cancer cells that also drives therapy resistance. In this Perspective, we focus our discussions on cancer cell lineage plasticity manifested as treatment-induced switching of epithelial cancer cells to basal/stem-like, mesenchymal, and neural lineages. We employ prostate cancer (PCa) as the prime example to highlight ARSI-induced lineage plasticity during and towards development of castration-resistant PCa (CRPC). We further discuss how the tumor microenvironment (TME) influences therapy-induced lineage plasticity. Finally, we offer an updated summary on the regulators and mechanisms driving cancer cell lineage infidelity, which should be therapeutically targeted to extend the therapeutic window and improve patients' survival.

Sex differences in glutamate transmission and plasticity in reward related regions.

Disruptions in glutamate homeostasis within the mesolimbic reward circuitry may play a role in the pathophysiology of various reward related disorders such as major depressive disorders, anxiety, and substance use disorders. Clear sex differences have emerged in the rates and symptom severity of these disorders which may result from differing underlying mechanisms of glutamatergic signaling. Indeed, preclinical models have begun to uncover baseline sex differences throughout the brain in glutamate transmission and synaptic plasticity. Glutamatergic synaptic strength can be assessed by looking at morphological features of glutamatergic neurons including spine size, spine density, and dendritic branching. Likewise, electrophysiology studies evaluate properties of glutamatergic neurons to provide information of their functional capacity. In combination with measures of glutamatergic transmission, synaptic plasticity can be evaluated using protocols that induce long-term potentiation or long-term depression. This review will consider preclinical rodent literature directly comparing glutamatergic transmission and plasticity in reward related regions of males and females. Additionally, we will suggest which regions are exhibiting evidence for sexually dimorphic mechanisms, convergent mechanisms, or no sex differences in glutamatergic transmission and plasticity and highlight gaps in the literature for future investigation.

Neural correlates of motor learning: Network communication versus local oscillations.

Learning new motor skills through training, also termed motor learning, is central for everyday life. Current training strategies recommend intensive task-repetitions aimed at inducing local activation of motor areas, associated with changes in oscillation amplitudes ("event-related power") during training. More recently, another neural mechanism was suggested to influence motor learning: modulation of functional connectivity (FC), that is, how much spatially separated brain regions communicate with each other before and during training. The goal of the present study was to compare the impact of these two neural processing types on motor learning. We measured EEG before, during, and after a finger-tapping task (FTT) in 20 healthy subjects. The results showed that training gain, long-term expertise (i.e., average motor performance), and consolidation were all predicted by whole-brain alpha- and beta-band FC at motor areas, striatum, and mediotemporal lobe (MTL). Local power changes during training did not predict any dependent variable. Thus, network dynamics seem more crucial than local activity for motor sequence learning, and training techniques should attempt to facilitate network interactions rather than local cortical activation.

Both, local and network processing mechanisms support motor sequence learning. The aim of the present study was to compare the impact of these two processing types on motor learning. We measured EEG before, during, and after a finger-tapping task (FTT) in 20 healthy subjects. The results showed that only network dynamics, measured with functional connectivity, could predict learning, long-term expertise, and consolidation. Conversely, local activity, measured with event-related power decrease, did not predict any dependent measure. Specifically, network interactions of the primary motor area, the striatum, and the medial temporal lobe correlated with learning performance. Therefore, network dynamics seem more crucial than local activity for motor sequence learning and training techniques should facilitate network interactions rather than local cortical activation.

Unlocking Choline's Potential in Alzheimer's Disease: A Narrative Review exploring the Neuroprotective and Neurotrophic role of Phosphatidylcholine and assessing its Impact on Memory and Learning.

BACKGROUND AND AIMS: Growing evidence suggests nutritional intervention may influence the development and progression of Alzheimer's Disease (AD). Choline, an essential dietary nutrient plays a critical role in neurological development and brain function, however, its effects on AD in humans is unclear. The research aims to investigate mechanistic links between dietary choline intake and cognitive functioning, focusing on the role of phosphatidylcholine (PC) in neuroplasticity and its interaction with amyloid beta (Aß) peptides in neuron membranes. Additionally, human evidence on potential benefits of PC interventions on AD, cognition and proposed mechanisms are evaluated. METHODS: A reproducible systematic literature search was performed using a three-tranche strategy, consisting of a review, mechanism and intervention search. Using PubMed as the main database, 1254 titles and abstracts were screened, 149 papers were read in full and 65 peer-reviewed papers were accepted, critically appraised and analysed in a narrative review. RESULTS: Predominantly preclinical evidence demonstrated that PC enhances neuroplasticity, a key biological substrate for cognition, by activating intracellular neuronal signalling pathways or through neuron membrane function. Molecular dynamic simulation methods provided mechanistic understanding of the interconnection between neuronal PC content and the potential behaviour and trajectory of Aß peptide aggregation. The results indicate that the neuronal membrane composition of PC is critical to inhibiting Aß aggregation and neuronal damage, protecting the neuron from Aß toxicity. This might provide a foundation for optimising cellular PC which may prove beneficial in the treatment or prevention of neurodegenerative disease. Altered PC metabolism in AD was evidenced in observational studies; however, whether this relationship represents a cause or consequence of AD remains to be determined. Human intervention studies did not produce conclusive evidence supporting its effectiveness in enhancing cognitive function. This lack of consistency primarily stems from methodological constraints within the conducted studies. Human observational research provided the most compelling evidence linking a higher dietary PC intake to reduced risk of dementia and significant improvements in cognitive testing. CONCLUSION: Despite the lack of randomised control trials (RCTs) assessing the efficacy of lecithin/PC to improve cognition in AD patients, there exists promising evidence supporting its neuroprotective and neurotrophic role. This review establishes an evidence-based framework through chains of mechanistic evidence, that may provide potential strategies for enhanced neuroprotection and reduced neurodegeneration caused by AD. Considering the escalating global burden of AD and the current shortcomings in effective treatments, this review together with the limitations and gaps identified in the existing research present valuable insights that emphasise the urgency of more comprehensive research into the relationship between PC and AD.

Divergent Flowering Time Responses to Increasing Temperatures Are Associated With Transcriptome Plasticity and Epigenetic Modification Differences at FLC Promoter Region of Arabidopsis thaliana.

Understanding the genetic, and transcriptomic changes that drive the phenotypic plasticity of fitness traits is a central question in evolutionary biology. In this study, we utilised 152 natural Swedish Arabidopsis thaliana accessions with re-sequenced genomes, transcriptomes and methylomes and measured flowering times (FTs) under two temperature conditions (10°C and 16°C) to address this question. We revealed that the northern accessions exhibited advanced flowering in response to decreased temperature, whereas the southern accessions delayed their flowering, indicating a divergent flowering response. This contrast in flowering responses was associated with the isothermality of their native ranges, which potentially enables the northern accessions to complete their life cycle more rapidly in years with shorter growth seasons. At the transcriptome level, we observed extensive rewiring of gene co-expression networks, with the expression of 25 core genes being associated with the mean FT and its plastic variation. Notably, variations in FLC expression sensitivity between northern and southern accessions were found to be associated with the divergence FT response. Further analysis suggests that FLC expression sensitivity is associated with differences in CG, CHG and CHH methylation at the promoter region. Overall, our study revealed the association between transcriptome plasticity and flowering time plasticity among different accessions, providing evidence for its relevance in ecological adaptation. These findings offer deeper insights into the genetics of rapid responses to environmental changes and ecological adaptation.

The apparent seasonal biphenism in Drosophila suzukii stems in reality from continuous reaction norms.

The spotted wing drosophila (SWD) is supposed to show only two distinct seasonal phenotypes: the dark, diapausing winter morph (WM) and the light, reproductively active summer morph (SM). It is unclear if these phenotypes result from a true developmental switch or from the expression of extreme phenotypes of continuous thermal reaction norms. This study aims to investigate this question by examining traits across a range of temperatures. Using 12 developmental temperatures (8 to 30 °C), we assessed traits including viability, growth, morphology, cold tolerance, metabolic rate, and ovarian maturation. Gradual increases in temperature induced gradual changes in all these traits, indicating classical nonlinear thermal reaction norms. Low temperatures (14 °C and below) produced flies with extended development, dark color, larger size, increased cold tolerance, reduced metabolism, and delayed oogenesis, characteristic of the WM. Given the months required for emergence and egg maturation at cold, distinct generations of SWD may develop in discrete environments resulting in an apparent biphenism. What appears to be distinct phenotypes (WM and SM) may actually result from continuous thermal reaction norms. This implies the need for precise terminology in SWD. We recommend using terms like 'winter-acclimated' or 'winter phenotype' rather than 'winter morph'. © 2024 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Midkine is upregulated in the hippocampus following both spatial and olfactory reward association learning and enhances memory.

Hippocampal neuronal plasticity is a fundamental process underpinning learning and memory formation and requiring elaborate molecular mechanisms that result in the dynamic remodelling of synaptic connectivity. The neurotrophic properties of midkine (Mdk) have been implicated in the development and repair of the nervous system, while Mdk knockout resulted in deficits in the formation of certain types of memory. The role of Mdk in the process of memory-associated neuronal plasticity, however, remains poorly understood. We investigated the learning-induced regulation of Mdk in spatial navigation and association learning using the water maze and the odour reward association learning paradigms, characterising a temporal profile of Mdk protein expression post-learning. Both learning events revealed similar patterns of upregulation of expression of the protein in the rat hippocampal dentate gyrus, which were rapid and transient. Moreover, administration of recombinant Mdk during the endogenous Mdk upregulation following learning enhanced memory in the water maze task revealing a pro-cognitive action of Mdk. We further show that, within the adult hippocampus, Mdk mRNA is predominantly expressed in granular and pyramidal neurons and that hippocampal neuronal Mdk expression is regulated by the canonical plasticity-associated neurotransmitter glutamate. Finally, we confirm that the positive action of Mdk on neurite outgrowth previously noted in cortical and cerebellar neurons extends to hippocampal neurons. Together, our findings suggest a role for Mdk in glutamate-mediated hippocampal neuronal plasticity important for long-term memory consolidation.

Rapid and local neuroestrogen synthesis supports long-term potentiation of hippocampal Schaffer collaterals-cornu ammonis 1 synapse in ovariectomized mice.

In aging women, cognitive decline and increased risk of dementia have been associated with the cessation of ovarian hormones production at menopause. In the brain, presence of the key enzyme aromatase required for the synthesis of 17-ß-estradiol (E2) allows for local production of E2 in absence of functional ovaries. Understanding how aromatase activity is regulated could help alleviate the cognitive symptoms. In female rodents, genetic or pharmacological reduction of aromatase activity over extended periods of time impair memory formation, decreases spine density, and hinders long-term potentiation (LTP) in the hippocampus. Conversely, increased excitatory neurotransmission resulting in rapid N-methyl-d-aspartic acid (NMDA) receptor activation rapidly promotes neuroestrogen synthesis. This rapid modulation of aromatase activity led us to address the hypothesis that acute neuroestrogens synthesis is necessary for LTP at the Schaffer collateral-cornu ammonis 1 (CA1) synapse in absence of circulating ovarian estrogens. To test this hypothesis, we did electrophysiological recordings of field excitatory postsynaptic potential (fEPSPs) in hippocampal slices obtained from ovariectomized mice. To assess the impact of neuroestrogens synthesis on LTP, we applied the specific aromatase inhibitor, letrozole, before the induction of LTP with a theta burst stimulation protocol. We found that blocking aromatase activity prevented LTP. Interestingly, exogenous E2 application, while blocking aromatase activity, was not sufficient to recover LTP in our model. Our results indicate the critical importance of rapid, activity-dependent local neuroestrogens synthesis, independent of circulating hormones for hippocampal synaptic plasticity in female rodents.

Scale-dependence in elk habitat selection for a reintroduced population in Wisconsin, USA.

Habitat selection is a critical aspect of a species' ecology, requiring complex decision-making that is both hierarchical and scale-dependent, since factors that influence selection may be nested or unequal across scales. Elk (Cervus canadensis) ranged widely across diverse ecoregions in North America prior to European settlement and subsequent eastern extirpation. Most habitat selection studies have occurred within their contemporary western range, even after eastern reintroductions began. As habitat selection can vary by geographic location, available cover, season, and diel period, it is important to understand how a non-migratory, reintroduced population in northern Wisconsin, USA, is limited by the lack of variation in topography, elevation, and vegetation. We tested scale-dependent habitat selection on 79 adult elk from 2017 to 2020 using resource selection functions across temporal (i.e., seasonal) and spatial scales (i.e., landscape and home range). We found that selection varied both spatially and temporally, and elk selected areas with the greatest potential to influence fitness at larger scales, meaning elk selected areas closer to escape cover and further from "risky" features (e.g., annual wolf territory centers, county roads, and highways). We found stronger avoidance of annual wolf territory centers during spring, suggesting elk were selecting safer habitats during calving season. Elk selected habitats with less canopy cover across both spatial scales and all seasons, suggesting that elk selected areas with better access to forage as early seral stage stands have greater forage biomass than closed-canopy forests and direct solar radiation to provide warmth in the cooler seasons. This study provides insight into the complexity of hierarchical decision-making, such as how risky habitat features and land cover type influence habitat selection differently across seasons and spatial scales, influencing the decision-making of elk. Scale-dependent behavior is crucial to understand within specific geographic regions, as these decisions scale up to influence population dynamics.

Local adaptation, plasticity, and evolved resistance to hypoxic cold stress in high-altitude deer mice.

A fundamental question in evolutionary biology concerns the relative contributions of phenotypic plasticity vs. local adaptation (genotypic specialization) in enabling wide-ranging species to inhabit diverse environmental conditions. Here, we conduct a long-term hypoxia acclimation experiment to assess the relative roles of local adaptation and plasticity in enabling highland and lowland deer mice (Peromyscus maniculatus) to sustain aerobic thermogenesis at progressively increasing elevations. We assessed the relative physiological performance capacities of highland and lowland natives as they were exposed to progressive, stepwise increases in hypoxia, simulating the gradual ascent from sea level to an elevation of 6,000 m. The final elevation of 6,000 m far exceeds the highest attainable elevations within the species' range, and therefore tests the animals' ability to tolerate levels of hypoxia that surpass the prevailing conditions within their current distributional limits. Our results demonstrate that highland natives exhibit superior thermogenic capacities at the most severe levels of hypoxia, suggesting that the species' broad fundamental niche and its ability to inhabit such a broad range of elevational zones is attributable to genetically based local adaptation, including evolved changes in plasticity. Transcriptomic and physiological measurements identify evolved changes in the acclimation response to hypoxia that contribute to the enhanced thermogenic capacity of highland natives.

The ivory lncRNA regulates seasonal color patterns in buckeye butterflies.

Long noncoding RNAs (lncRNAs) are transcribed elements increasingly recognized for their roles in regulating gene expression. Thus far, however, we have little understanding of how lncRNAs contribute to evolution and adaptation. Here, we show that a conserved lncRNA, ivory, is an important color patterning gene in the buckeye butterfly Junonia coenia. ivory overlaps with cortex, a locus linked to multiple cases of crypsis and mimicry in Lepidoptera. Along with a companion paper by Livraghi et al., we argue that ivory, not cortex, is the color pattern gene of interest at this locus. In J. coenia, a cluster of cis-regulatory elements (CREs) in the first intron of ivory are genetically associated with natural variation in seasonal color pattern plasticity, and targeted deletions of these CREs phenocopy seasonal phenotypes. Deletions of different ivory CREs produce other distinct phenotypes as well, including loss of melanic eyespot rings, and positive and negative changes in overall wing pigmentation. We show that the color pattern transcription factors Spineless, Bric-a-brac, and Ftz-f1 bind to the ivory promoter during wing pattern development, suggesting that they directly regulate ivory. This case study demonstrates how cis-regulation of a single noncoding RNA can exert diverse and nuanced effects on the evolution and development of color patterns, including modulating seasonally plastic color patterns.

Nerve injury augments Cacna2d1 transcription via CK2-mediated phosphorylation of the histone deacetylase HDAC2 in dorsal root ganglia.

Development of chronic neuropathic pain involves complex synaptic and epigenetic mechanisms. Nerve injury causes sustained upregulation of α2δ-1 (encoded by the Cacna2d1 gene) in the dorsal root ganglion (DRG), contributing to pain hypersensitivity by directly interacting with and augmenting presynaptic NMDA receptor activity in the spinal dorsal horn. Under normal conditions, histone deacetylase 2 (HDAC2) is highly enriched at the Cacna2d1 gene promoter in the DRG, which constitutively suppresses Cacna2d1 transcription. However, nerve injury leads to HDAC2 dissociation from the Cacna2d1 promoter, promoting the enrichment of active histone marks and Cacna2d1 transcription in primary sensory neurons. In this study, we determined the mechanism by which nerve injury diminishes HDAC2 occupancy at the Cacna2d1 promoter in the DRG. Spinal nerve injury in rats increased serine-394 phosphorylation of HDAC2 in the DRG. Coimmunoprecipitation showed that nerve injury enhanced the physical interaction between HDAC2 and casein kinase II (CK2) in the DRG. Furthermore, repeated intrathecal treatment with CX-4945, a potent and specific CK2 inhibitor, markedly reversed nerve injury-induced pain hypersensitivity, HDAC2 phosphorylation, and α2δ-1 expression levels in the DRG. In addition, treatment with CX-4945 largely restored HDAC2 enrichment at the Cacna2d1 promoter and reduced the elevated levels of acetylated H3 and H4 histones, particularly H3K9ac and H4K5ac, at the Cacna2d1 promoter in the injured DRG. These findings suggest that nerve injury increases CK2 activity and CK2-HDAC2 interactions, which enhance HDAC2 phosphorylation in the DRG. This, in turn, diminishes HDAC2 enrichment at the Cacna2d1 promoter, thereby promoting Cacna2d1 transcription.

Glial Control of Cortical Neuronal Circuit Maturation and Plasticity.

The brain is a highly adaptable organ that is molded by experience throughout life. Although the field of neuroscience has historically focused on intrinsic neuronal mechanisms of plasticity, there is growing evidence that multiple glial populations regulate the timing and extent of neuronal plasticity, particularly over the course of development. This review highlights recent discoveries on the role of glial cells in the establishment of cortical circuits and the regulation of experience-dependent neuronal plasticity during critical periods of neurodevelopment. These studies provide strong evidence that neuronal circuit maturation and plasticity are non-cell autonomous processes that require both glial-neuronal and glial-glial cross talk to proceed. We conclude by discussing open questions that will continue to guide research in this nascent field.

Highly plastic Zn-0.3Ca alloy for guided bone regeneration membrane: Breaking the trade-off between antibacterial ability and biocompatibility.

A common problem for Zn alloys is the trade-off between antibacterial ability and biocompatibility. This paper proposes a strategy to solve this problem by increasing release ratio of Ca2+ ions, which is realized by significant refinement of CaZn13 particles through bottom circulating water-cooled casting (BCWC) and rolling. Compared with conventionally fabricated Zn-0.3Ca alloy, the BCWC-rolled alloy shows higher antibacterial abilities against E. coli and S. aureus, meanwhile much less toxicity to MC3T3-E1 cells. Additionally, plasticity, degradation uniformity, and ability to induce osteogenic differentiation in vitro of the alloy are improved. The elongation up to 49 %, which is the highest among Zn alloys with Ca, and is achieved since the sizes of CaZn13 particles and Zn grains are small and close. As a result, the long-standing problem of low formability of Zn alloys containing Ca has also been solved due to the elimination of large CaZn13 particles. The BCWC-rolled alloy is a promising candidate of making GBR membrane.

Memory-efficient neurons and synapses for spike-timing-dependent-plasticity in large-scale spiking networks.

This paper addresses the challenges posed by frequent memory access during simulations of large-scale spiking neural networks involving synaptic plasticity. We focus on the memory accesses performed during a common synaptic plasticity rule since this can be a significant factor limiting the efficiency of the simulations. We propose neuron models that are represented by only three state variables, which are engineered to enforce the appropriate neuronal dynamics. Additionally, memory retrieval is executed solely by fetching postsynaptic variables, promoting a contiguous memory storage and leveraging the capabilities of burst mode operations to reduce the overhead associated with each access. Different plasticity rules could be implemented despite the adopted simplifications, each leading to a distinct synaptic weight distribution (i.e., unimodal and bimodal). Moreover, our method requires fewer average memory accesses compared to a naive approach. We argue that the strategy described can speed up memory transactions and reduce latencies while maintaining a small memory footprint.

Applicability of metabolomics to improve sustainable grapevine production.

Metabolites represent the end product of gene expression, protein interaction and other regulatory mechanisms. The metabolome reflects a biological system's response to genetic and environmental changes, providing a more accurate description of plants' phenotype than the transcriptome or the proteome. Grapevine (Vitis vinifera L.), established for the production of wine grapes, table grapes, and raisins, holds immense agronomical and economic significance not only in the Mediterranean region but worldwide. As all plants, grapevines face the adverse impact of biotic and abiotic stresses that negatively affect multiple stages of grape and wine industry, including plant and berry development pre- and post-harvest, fresh grapes processing and consequently wine quality. In the present review we highlight the applicability of metabolome analysis in the understanding of the mechanisms involved in grapevine response and acclimatization upon the main biotic and abiotic constrains. The metabolome of induced morphogenic processes such as adventitious rooting and somatic embryogenesis is also explored, as it adds knowledge on the physiological and molecular phenomena occurring in the explants used, and on the successfully propagation of grapevines with desired traits. Finally, the microbiome-induced metabolites in grapevine are discussed in view of beneficial applications derived from the plant symbioses.