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Diaz, S.

Publications and source records attributed to Diaz, S..

At least 19 recordsLinked to original sources

Transcriptomics uncovers outer membrane remodeling as conserved strategy for Burkholderia cenocepacia survival in protozoan and macrophage phagosomes

Bacterivorous protists expose bacteria to hostile stress conditions that resemble those encountered within macrophage phagosomes and may therefore act as training grounds for bacterial pathogens. However, the mechanisms enabling bacterial survival within protozoan phagosomes remain poorly understood. Here we characterized the transcriptome of the opportunistic pathogen Burkholderia cenocepacia during transit through phagosomes and expelled food vacuoles of the ubiquitous protozoan ciliate Tetrahymena elliotti. Our data revealed a coordinated response involving bacterial metabolic reprogramming, with the upregulation of NADPH-generating pathways and host nutrient uptake systems, alongside the activation of several stress responses and envelope remodeling to maintain outer membrane barrier function and repair phagosomal damage. Disruption of antioxidant defenses, the RpoE-dependent envelope stress response, the Mla pathway and other proteins required for outer membrane integrity severely impaired intracellular survival in both protozoa and macrophages, revealing conserved mechanisms required for persistence within evolutionarily distant phagocytes. This adaptive response not only contributed to survival but it also primed B. cenocepacia for increased chlorhexidine resistance and adhesion to collagen and human lung epithelial cells. Collectively, our findings reveal that protozoan phagosomes drive physiological adaptations with consequences extending beyond grazing resistance. Protozoa may therefore disseminate stress-adapted bacteria with enhanced resistance and colonization potential, providing a mechanistic link between adaptation to environmental predators and survival in the human host.

microbiology↗

From Atoms to Neuronal Spikes: A Multi-Scale Simulation Framework

Understanding how molecular events in ion channels impact neuronal excitability, as derived from the calculation of the time course of the membrane potentials, can help elucidate the mechanisms of neurological disease-linked mutations and support neuroactive drug design. Here, we propose a multi-scale simulation approach which couples molecular simulations with neuronal simulations to predict the variations in membrane potential and neural spikes. We illustrate this through two examples. First, molecular dynamics simulations predict changes in current and conductance through the AMPAR neuroreceptor when transitioning from the wild-type protein to certain disease-associated variants. The results of these simulations inform morphologically detailed models of cortical pyramidal neurons, which are simulated using the Arbor framework to determine neural spike activity. Based on these multiscale simulations, we suggest that disease associated AMPAR variants may significantly impact neuronal excitability. In the second example, the Arbor model is coupled with coarse-grained Monte Carlo gating simulations of voltage-gated (K+ and Na+) channels. The pre-dicted current from these ion channels altered the membrane potential and, in turn, the excitation state of the neuron was updated in Arbor. The resulting membrane potential was then fed back into the Monte Carlo simulations of the voltage-gated ion channels, resulting in a bidirectional coupling of current and membrane potential. This allowed the transitions of the states of the ion channels to influence the membrane potentials and vice versa. Our simulations also included the crucial -- so far unexplored -- effects of the composition of the lipid membrane embedding the ion channels on the membrane potential and revealed a significant impact of temperature on the neuronal excitability. Our combined approaches predicted membrane potentials consistent with electrophysiological recordings and established a multi-scale framework linking the atomistic perturbations to neuronal excitability.

neuroscience↗

Going green: Recycling transcriptomes to infer evolutionary relationships, gene duplication, gene tree conflict, and patterns of molecular evolution in the Apocynaceae

Background and AimsThe flowering plant family Apocynaceae exhibits diverse adaptations with biological and pharmaceutical significance, many of which have been studied with RNA-seq. However, despite the available transcriptomic data, no focused phylotranscriptomic study has been conducted to characterize the patterns of molecular evolution in this group. In this study, we leverage a dataset composed predominately of publicly available transcriptomes to infer relationships within Apocynaceae and explore the molecular processes that have shaped their divergences. MethodsWe extracted nuclear, chloroplast, and mitochondrial genes from 47 publicly available and one newly sequenced transcriptome to assemble and infer species relationships across Apocynaceae. Leveraging the gene-rich nuclear phylotranscriptomic data, we inferred molecular dates and investigated the complex history of gene tree conflict, molecular rate shifts, and gene duplications. To investigate the genomic basis of adaptations, we analyzed the inferred 14,838 gene duplications at the base of Apocynaceae for shared functional enrichment of genes related to evolutionary innovations. Key ResultsThe Apocynaceae topology inferred from our phylotranscriptomic analysis is highly concordant with the current consensus. Notably, a genome-wide acceleration in molecular rate subtends the Ceropegieae tribe. We observed that a decreased time between divergences is associated with a higher rate of gene tree conflict, a pattern especially prevalent across the Apocynaceaes historically recalcitrant backbone relationships. Furthermore, gene duplications may underlie evolutionary innovations, such as immunity-related gene expansion in the genus Asclepias and duplications associated with trichome modifications in the epiphytic Hoya. Finally, we discuss the contentious history of whole-genome duplication (WGD) within the Apocynaceae and emphasize the need for further investigation into the placement of WGDs. ConclusionsRepurposing transcriptomes is a powerful means of accumulating data for novel insights in plant evolution, especially during uncertain funding and cases where budget restrictions exist. Leveraging this gene-dense dataset, we obtained novel insights into the molecular evolution of Apocynaceae and identified areas for future investigations.

evolutionary biology↗

Higher functional resilience of temperate forests at intermediate latitudes of a large latitudinal gradient in South America

Accurately mapping and assessing plant functional composition across space and time is pivotal for understanding environmental change impacts on the biodiversity and functioning of forests. Here, we test the capabilities of a combination of in-situ and remote sensing approaches to deliver accurate estimates of the functional composition of temperate forest ecosystems considering leaf and stem morphological, nutrient, hydraulic, and photosynthetic traits. We identify hydrological stress, soil, and topography as key drivers of plant functional traits. Further, hydrological stress and soil are key determinants of functional dispersion and redundancy in temperate forests distributed across a large latitudinal (30{degrees}S to 53{degrees}S) gradient in Chile. Functional dispersion peaks across Mediterranean forests, woodlands, and scrub, occupying between 30{degrees}S to 35{degrees}S. Conversely, functional redundancy peaks between 42{degrees}S and 53{degrees}S, corresponding to Magellanic subpolar forests. Although functional dispersion and redundancy peak at different latitudes corresponding to distinct forest types; they are both high at latitudes between 35{degrees}S and 42{degrees}S, coinciding with Valdivian temperate rainforests. Our results highlight areas in temperate forests in South America where both tree functional dispersion and redundancy are high, and hence could potentially be more resilient to environmental changes.

ecology↗

Interplay between homeostatic synaptic scaling and homeostatic structural plasticity maintains the robust firing rate of neural networks

AbstractCritical network states and neural plasticity are essential for flexible behavior in dynamic envi-ronments, allowing for efficient information processing and experience-dependent learning. Synaptic-weight-based Hebbian plasticity and homeostatic synaptic scaling were considered the key mechanisms in enabling memory while stabilizing network dynamics. However, the role of structural plasticity as a homeostatic mechanism is less consistently reported, especially under activity inhibition, leading to an incomplete understanding of its functional impact. In this study, we combined live-cell microscopy of eGPF-labeled neurons in organotypic entorhinal-hippocampal tissue cultures with computational modeling to investigate the response of spine-number-based structural plasticity to activity perturba-tions and its interaction with homeostatic synaptic scaling. Tracking individual dendritic segments, we demonstrated that inhibiting excitatory neurotransmission does not monotonically regulate den-dritic spine density. Specifically, inhibition of AMPA receptors with a low concentration of 2,3-dioxo-6-nitro-7-sulfamoyl-benzo[f]quinoxaline (NBQX, 200 nM) significantly increased spine density, while complete AMPA receptors blockade with 50 {micro}M NBQX reduced spine density. Motivated by these findings, we developed network simulations incorporating a bi-phasic structural plasticity rule governing activity-dependent synapse formation. We showed that this biphasic rule maintained neu-ral activity homeostasis under stimulation and permitted either synapse formation or synapse loss, depending on the degree of activity deprivation. Homeostatic synaptic scaling affected the recurrent connectivity, modulated the network activity, and influenced the outcome of structural plasticity. Specifically, it reduced stimulation-triggered synapse loss by downscaling synaptic weights and res-cued silencing-induced synapse loss by upscaling recurrent inputs, thus reactivating silent neurons. Our interaction between these mechanisms offers an explanation for divergent findings in the existing literature. In summary, calcium-based synaptic scaling and homeostatic structural plasticity rules compete and compensate for one another, ensuring efficient and robust control of firing rate home-ostasis. Significance StatementO_LIThis work combined systematic computer simulations and in vitro experiments to explore the in-terplay between homeostatic structural plasticity and synaptic scaling under conditions of activity deprivation. C_LIO_LIWe identified a non-monotonic relationship between neural activity and spine numbers, where par-tial inhibition of synaptic transmissions increased spine density, while complete inhibition reduced it. C_LIO_LIPartial inhibition led to increased spine sizes across all initial spine sizes, whereas complete inhibition selectively increased the size of relatively large spines. C_LIO_LIA biphasic, spine-number-based homeostatic structural plasticity (HSP) rule reconciled previously divergent experimental findings regarding activity-dependent changes in spine density. C_LIO_LIUsing an engineering and complex systems framework, we proposed that the biphasic HSP rule incorporates a negative feedback mechanism and acts as a redundant and heterogeneous mechanism alongside the synaptic-weight-based homeostatic synaptic scaling (HSS) rule. C_LIO_LIBy comparing simulation and experimental results, we demonstrated the necessity of HSP-HSS interplay in maintaining firing rate homeostasis. C_LIO_LIBoth plasticity rules are driven by intracellular calcium concentration, which reflects cumulative neural activity. Thus, we propose that integral feedback control is critical in firing rate homeostasis. C_LI

neuroscience↗

Potently neutralizing human monoclonal antibodies against the zoonotic pararubulavirus Sosuga virus

Sosuga virus (SOSV) is a recently discovered paramyxovirus with a single known human case of disease. There has been little laboratory research on SOSV pathogenesis or immunity, and no approved therapeutics or vaccines are available. Here, we report the discovery of human monoclonal antibodies (mAbs) from the circulating memory B cells of the only known human case and survivor of SOSV infection. We isolated six mAbs recognizing the functional attachment protein (HN) and 18 mAbs against the fusion (F) protein. The anti-HN mAbs all target the globular head of the HN protein and can be organized into 4 competition-binding groups that exhibit epitope diversity. The anti-F mAbs can be divided into pre- or post-fusion conformation-specific categories and further into 8 competition-binding groups. Generally, pre-fusion conformation-specific anti-F mAbs showed higher potency in neutralization assays than did mAbs only recognizing the post-fusion conformation of F protein. Most of the anti-HN mAbs were more potently neutralizing than the anti-F mAbs, with mAbs in one of the HN competition-binding groups possessing ultra-potent (<1 ng/mL) half maximal inhibitory (IC50) virus neutralization values. These findings provide insight into the molecular basis for human antibody recognition of paramyxovirus surface proteins and the mechanisms of SOSV neutralization.

immunology↗

The evolution of two transmissible leukaemias colonizing the coasts of Europe

Transmissible cancers are malignant cell clones that spread among individuals through transfer of living cancer cells. Several such cancers, collectively known as bivalve transmissible neoplasia (BTN), are known to infect and cause leukaemia in marine bivalve molluscs. This is the case of BTN clones affecting the common cockle, Cerastoderma edule, which inhabits the Atlantic coasts of Europe and north-west Africa. To investigate the origin and evolution of contagious cancers in common cockles, we collected 6,854 C. edule specimens and diagnosed 390 cases of BTN. We then generated a reference genome for the species and assessed genomic variation in the genomes of 61 BTN tumours. Analysis of tumour-specific variants confirmed the existence of two cockle BTN lineages with independent clonal origins, and gene expression patterns supported their status as haemocyte-derived marine leukaemias. Examination of mitochondrial DNA sequences revealed several mitochondrial capture events in BTN, as well as co-infection of cockles by different tumour lineages. Mutational analyses identified two lineage-specific mutational signatures, one of which resembles a signature associated with DNA alkylation. Karyotypic and copy number analyses uncovered genomes marked by pervasive instability and polyploidy. Whole-genome duplication, amplification of oncogenes CCND3 and MDM2, and deletion of the DNA alkylation repair gene MGMT, are likely drivers of BTN evolution. Characterization of satellite DNA identified elements with vast expansions in the cockle germ line, yet absent from BTN tumours, suggesting ancient clonal origins. Our study illuminates the evolution of contagious cancers under the sea, and reveals long-term tolerance of extreme instability in neoplastic genomes.

evolutionary biology↗

Multiscale cosimulation design template implemented for a neuroscience application

Integration of information across heterogeneous sources creates added scientific value. It is, however, a challenge to progress, often a barrier, to interoperate data, tools and models across spatial and temporal scales. Here we present a design template for coupling simulators operating at different scales and enabling co-simulation. We illustrate its functioning along a neuroscience example, in which individual regions of interest are simulated on the cellular level to address mechanistic questions, while the remaining network is efficiently simulated on the population level. A workflow is illustrated for the use case of The Virtual Brain and NEST, in which the cellular-level hippocampus of the mouse is embedded into a full brain network involving micro and macro electrode recordings. This new tool allows integrating knowledge across scales in the same simulation framework and validate them against multiscale experiments, thereby largely widening the explanatory power of computational models.

neuroscience↗

No branch left behind: tracking terrestrial biodiversity from a phylogenetic completeness perspective

Biodiversity, as we see it today, ultimately is the outcome of millions of years of evolution; however, biodiversity in its multiple dimensions is changing rapidly due to increasing human domination of Earth. Here, we present the "phylogenetic completeness" (PC) a concept and methodology that intends to safeguard Earths evolutionary heritage by maintaining all branches of the tree of life. We performed a global evaluation of the PC approach using data from five major terrestrial clades and compared the results to an approach in which species are conserved or lost randomly. We demonstrate that under PC, for a given number of species extinctions, it is possible to maximize the protection of evolutionary innovations in every clade. The PC approach is flexible and can be used to conduct a phylogenetic audit of biodiversity under different conservation scenarios. The PC approach complements existing conservation efforts and is linked to the post-2020 Convention of Biodiversity targets.

ecology↗

The broad shell colour variation in common cockle (Cerastoderma edule) from Northeast Atlantic relies on a major QTL revealed by GWAS using a new high-density genetic map

Shell colour pattern shows broad diversity in molluscs, and both genetic and environmental factors seem to interact to some extent on the final phenotype. Despite information on the genetic component and pathways involved in shell construction and colour has increased in the last decade, more data are needed particularly to understand colour variation and its putative role on adaptation. The European common cockle (Cerastoderma edule) is a valuable species from ecological and commercial perspectives with important variation in colour pattern, but this diversity has never been characterized and the underlying genetic architecture is unknown. In this study, we constructed a high-density genetic map, as an essential tool for genomic screening in common cockle, that was applied to ascertain the genetic basis of colour pattern variation in the species. The consensus map, including 13,874 2b-RAD SNPs, was constituted by the 19 linkage groups (LGs) corresponding to the n = 19 chromosomes of its karyotype and spanned 1,073 cM (730 markers per LG; inter-marker distance of 0.13 cM). Five full-sib families showing segregation for several colour-associated traits were used to perform a GWAS analysis. A major QTL on chromosome 13 explained most of the variation for shell colour patterns. Mining on this genomic region revealed the presence of several candidate genes enriched on Gene Ontology terms such as anatomical structure development, ion transport, membrane transport and cell periphery, closely related to shell architecture, including six chitin-related, one ependymin, several ion binding and transporters, and others related to transit across the cell membrane. Interestingly, this major QTL overlaps with a genomic region previously reported associated with divergent selection in the distribution range of the species, suggesting a putative role on local adaptation.

genomics↗

Assembly of functional diversity in an oceanic island flora

Oceanic island floras are well-known for their morphological peculiarities and exhibit striking examples of trait evolution1,2. These morphological shifts are commonly attributed to insularity and thought to be shaped by biogeographical processes and evolutionary histories of oceanic islands1,3. However, the mechanisms through which biogeography and evolution have shaped the distribution and diversity of plant functional traits remain unclear. Here, we describe the functional trait space of an oceanic island flora (Tenerife, Canary Islands, Spain) using extensive field and laboratory measurements, and relate it to global trade-offs in ecological strategies. We find that the island trait space is concentrated around a functional hotspot dominated by shrubs with a conservative life-history strategy. By dividing the island flora into species groups with distinct biogeographical distributions and diversification histories, our results reveal that long-distance dispersal, and the interplay between inter-island dispersal and archipelago-level speciation processes drive functional divergence and expand trait space. Conversely, speciation via cladogenesis has overall led to functional convergence, densely packing trait space around shrubbiness. Our approach combines ecology, biogeography and evolution and opens avenues for new trait-based insights into how dispersal and speciation shape the assembly of native island floras.

ecology↗

An antibody targeting the N-terminal domain of SARS-CoV-2 disrupts the spike trimer

The protective human antibody response to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus focuses on the spike (S) protein which decorates the virion surface and mediates cell binding and entry. Most SARS-CoV-2 protective antibodies target the receptor- binding domain or a single dominant epitope ( supersite) on the N terminal domain (NTD). Here, using the single B cell technology LIBRA-seq, we isolated a large panel of NTD-reactive and SARS-CoV-2 neutralizing antibodies from an individual who had recovered from COVID-19. We found that neutralizing antibodies to the NTD supersite commonly are encoded by the IGHV1-24 gene, forming a genetic cluster that represents a public B cell clonotype. However, we also discovered a rare human antibody, COV2-3434, that recognizes a site of vulnerability on the SARS-CoV-2 S protein in the trimer interface and possesses a distinct class of functional activity. COV2-3434 disrupted the integrity of S protein trimers, inhibited cell-to-cell spread of virus in culture, and conferred protection in human ACE2 transgenic mice against SARS-CoV-2 challenge. This study provides insight about antibody targeting of the S protein trimer interface region, suggesting this region may be a site of virus vulnerability.

immunology↗

Evolution of Human-specific Alleles Protecting Cognitive Function of Grandmothers

Late-onset Alzheimers Disease (LOAD) pathology is rare in our closest living evolutionary relatives (chimpanzees), which also express much lower microglial levels of CD33(Siglec-3)-a myelomonocytic receptor inhibiting innate immune reactivity by extracellular V-set domain recognition of sialic acid(Sia)-containing "self-associated molecular patterns" (SAMPs). We earlier showed that V-set domain-deficient CD33-variant allele, protective against LOAD, is derived and specific to hominin-lineage. We now report that CD33 also harbors multiple hominin-specific V-set domain mutations and explore selection forces that may have favored such genomic changes. N-glycolylneuraminic acid (Neu5Gc), the preferred Sia-ligand of ancestral CD33 is absent in humans, due to hominin-specific, fixed loss-of-function mutation in CMAH, which generates CMP-Neu5Gc from its precursor, CMP-N-acetylneuraminic acid (Neu5Ac). Extensive mutational analysis and MD-simulations indicate that fixed change in amino acid 21 of hominin V-set domain and conformational changes related to His45 corrected for Neu5Gc-loss by switching to Neu5Ac-recognition. Considering immune-evasive "molecular mimicry" of SAMPs by pathogens, we found that human-specific pathogens Neisseria gonorrhoeae and Group B Streptococcus (affecting fertility and fetuses/neonates respectively) selectively bind huCD33 and this binding is significantly impacted by amino acid 21 modification. Alongside LOAD-protective CD33 alleles, humans harbor additional, derived, population-universal, cognition-protective variants absent in "great ape" genomes. Interestingly, 11 of 13 SNPs in these human genes (including CD33), that protect the cognitive health of elderly populations, are not shared by genomes of archaic hominins: Neanderthals and Denisovans. Finally, we present a plausible evolutionary scenario to compile, correlate and comprehend existing knowledge about huCD33 evolution and suggest that grandmothering emerged in humans.

evolutionary biology↗

Sialoglycan microarray encoding reveals differential sialoglycan binding of phylogenetically-related bacterial AB5 toxin B subunits

Vertebrate sialic acids (Sias) display much diversity in modifications, linkages and underlying glycans. Slide microarrays allow high-throughput explorations of sialoglycan-protein interactions. A microarray presenting [~]150 structurally-defined sialyltrisaccharides with various Sias linkages and modifications still poses challenges in planning, data sorting, visualization and analysis. To address these issues, we devised a simple 9-digit code for sialyltrisaccharides with terminal Sias and underlying two monosaccharides assigned from the non-reducing end, with three digits assigning a monosaccharide, its modifications, and linkage. Calculations based on the encoding system reveals >113,000 likely linear sialyltrisaccharides in nature. Notably a biantennary N-glycan with two terminal sialyltrisaccharides could thus have >1010 potential combinations and a triantennary N-glycan with three terminal sequences, >1015 potential combinations. While all possibilities likely do not exist in nature, sialoglycans encode enormous diversity. While glycomic approaches are used to probe such diverse sialomes, naturally-occurring bacterial AB5 toxin B subunits are simpler tools to track the dynamic sialome in biological systems. Sialoglycan microarray was utilized to compare sialoglycan-recognizing bacterial toxin B subunits. Unlike the poor correlation between B subunits and species phylogeny, there is stronger correlation with Sia-epitope preferences. Further supporting this pattern, we report a B subunit (YenB) from Yersinia enterocolitica (broad host range) recognizing almost all sialoglycans in the microarray, including 4-O-acetylated-Sias not recognized by a Y. pestis orthologue (YpeB). Differential Sia-binding patterns were also observed with phylogenetically-related B subunits from Escherichia coli (SubB), Salmonella Typhi (PltB), S. Typhimurium (ArtB), extra-intestinal E.coli (EcPltB), Vibrio cholera (CtxB), and cholera family homologue of E. coli (EcxB).

molecular biology↗

Development and applications of sialoglycan-recognizing probes (SGRPs) with defined specificities: exploring the dynamic mammalian sialoglycome

Glycans that are abundantly displayed on vertebrate cell surface and secreted molecules are often capped with terminal sialic acids (Sias). These diverse 9-carbon-backbone monosaccharides are involved in numerous intrinsic biological processes. They also interact with commensals and pathogens, while undergoing dynamic changes in time and space, often influenced by environmental conditions. However, most of this sialoglycan complexity and variation remains poorly characterized by conventional techniques, which often tend to destroy or overlook crucial aspects of Sia diversity and/or fail to elucidate native structures in biological systems i.e., in the intact sialome. To date, in situ detection and analysis of sialoglycans has largely relied on the use of plant lectins, sialidases or antibodies, whose preferences (with certain exceptions) are limited and/or uncertain. We took advantage of naturally-evolved microbial molecules (bacterial adhesins, toxin subunits and viral hemagglutinin-esterases) that recognize sialoglycans with defined specificity to delineate 9 classes of Sialoglycan Recognizing Probes (SGRPs: SGRP1-SGRP9) that can be used to explore mammalian sialome changes in a simple and systematic manner, using techniques common in most laboratories. SGRP candidates with specificity defined by sialoglycan microarray studies were engineered as tagged probes, each with a corresponding non-binding mutant probe as a simple and reliable negative control. The optimized panel of SGRPs can be used in methods commonly available in most bioscience labs, such as ELISA, Western Blot, flow cytometry and histochemistry. To demonstrate the utility of this approach, we provide examples of sialoglycome differences in tissues from C57BL/6 wild type mice and human-like Cmah-/- mice.

molecular biology↗

Anti-microbiota vaccines modulate the tick microbiome in a taxon-specific manner

Anti-tick microbiota vaccines have been shown to impact tick feeding but its specificity has not been demonstrated. In this study we aimed to investigate the impact of immune targeting of keystone microbiota bacteria on tick performance, and tick microbiota structure and function. Vaccination against Escherichia coli, the selected keystone taxon, increased tick engorgement weight and reduced bacterial diversity in Ixodes ricinus ticks compared to those that fed on mice immunized against Leuconostoc mesenteroides, a non-keystone taxon or mock-immunized group. The abundance of Escherichia-Shigella, but not Leuconostoc was significantly reduced in ticks fed on E. coli-immunized mice and this reduction was correlated with a significant increase in host antibodies (Abs) of the isotype IgM and IgG specific to E. coli proteins. This negative correlation was not observed between the abundance of Leuconostoc in ticks and anti-L. mesenteroides Abs in mice. We also demonstrated by co-occurrence network analysis, that immunization against the keystone bacterium restructure the hierarchy of the microbial community in ticks and that anti-tick microbiota vaccines reduced the resistance of networks to directed removal of taxa. Functional pathways analysis showed that immunization with a live bacterial vaccine can also induce taxon-specific changes in the abundance of pathways. Our results demonstrated that anti-tick microbiota vaccines can modulate the tick microbiome and that the modification is specific to the taxon chosen for host immunization. These results guide interventions for the control of tick infestations and pathogen infection/transmission.

immunology↗

Global critical natural assets

Sustaining the organisms, ecosystems, and processes that underpin human well-being is necessary to achieve sustainable development. Here we identify critical natural assets, natural and semi-natural ecosystems that provide 90% of the total current magnitude of 14 types of natures contributions to people (NCP). Critical natural assets for maintaining local-scale NCP (12 of the 14 NCP mapped) comprise 30% of total global land area and 24% of national territorial waters, while 44% of land area is required for maintaining all NCP (including those that accrue at the global scale, carbon storage and moisture recycling). At least 87% of the worlds population lives in the areas benefiting from critical natural assets for local-scale NCP, while only 16% lives on the lands containing these assets. Critical natural assets also overlap substantially with areas important for biodiversity (covering area requirements for 73% of birds and 66% of mammals) and cultural diversity (representing 96% of global Indigenous and non-migrant languages). Many of the NCP mapped here are left out of international agreements focused on conserving species or mitigating climate change, yet this analysis shows that explicitly prioritizing critical natural assets for NCP could simultaneously advance development, climate, and conservation goals. Crafting policy and investment strategies that protect critical natural assets is essential for sustaining human well-being and securing Earths life support systems.

ecology↗

Development of mPing-based Activation Tags for Crop Insertional Mutagenesis

Modern plant breeding increasingly relies on genomic information to guide crop improvement. Although some genes are characterized, additional tools are needed to effectively identify and characterize genes associated with crop traits. To address this need, the mPing element from rice was modified to serve as an activation tag to induce expression of nearby genes. Embedding promoter sequences in mPing resulted in a decrease in overall transposition rate; however, this effect was negated by using a hyperactive version of mPing called mmPing20. Transgenic soybean events carrying mPing-based activation tags and the appropriate transposase expression cassettes showed evidence of transposition. Expression analysis of a line that contained a heritable insertion of the mmPing20F activation tag indicated that the activation tag induced overexpression of the nearby soybean genes. This represents a significant advance in gene discovery technology as activation tags have the potential to induce more phenotypes than the original mPing element, improving the overall effectiveness of the mutagenesis system.

plant biology↗