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Clark, J.

Publications and source records attributed to Clark, J..

At least 19 recordsLinked to original sources

Evidence from the field that multiple processes maintain hidden adaptive capacity to a novel environment in a wild daisy

Populations often persist in novel environments despite predictions that adaptive capacity to such conditions should be limited by a lack of genetic variation. A leading hypothesis is that genetic variation for adapting to novel environments is maintained but remains hidden under native conditions. However, direct evidence for the mechanisms that maintain this adaptive potential in natural populations is scarce. Here, we integrate data from four large-scale field experiments to test whether variation in selection across life history and environments, together with genetic architecture, maintains genetic variation important for adapting to novel environments. Using a quantitative genetic breeding design, we generated families of the Sicilian daisy, Senecio chrysanthemifolius (Asteraceae), and planted seeds and cuttings across native and novel elevations on Mount Etna. We tracked fitness across elevations, life stages, seasons and generations. Genotypes with higher survival and flowering success at the novel elevation increased adaptive potential, but were only weakly selected against in the native environment where they had slightly lower fitness at a later life-history stage. A negative genetic correlation in seedling survival across seasons indicated that different genotypes were favoured across temporal variation in native environments. Crosses between genotypes with low and high fitness in the novel environment revealed that genotypes that increased adaptive potential had heritable effects on plasticity and fitness across generations, but were recessive and therefore largely hidden in heterozygotes. Together, these results provide rare field-based evidence that weak selection in native environments, temporal variation in selection and dominance effects act together to maintain cryptic adaptive potential in natural populations.

evolutionary biology↗

Optimal virulence in ageing populations

Global populations are ageing at an unprecedented rate. For many diseases, age is a strong indicator of susceptibility, morbidity, or mortality. Principles of evolutionary biology can be leveraged to understand how pathogens may optimally exploit new populations, and the impact of this on the global burden of infectious-disease-induced mortality. We parameterised an age-specific R0 model with 2017 epidemiological data on Measles, Tuberculosis, Meningitis, and Ebola, and age-specific demographic estimates for 2017 and 2050, for the seven Global Burden of Disease super-regions. We explored the theoretical trade-offs between pathogen virulence & transmission, and virulence & host recovery, parameterising trade-off parameters using Latin Hypercube Sampling. Population ageing between 2017-2050 saw an increase in virulence induced mortality in four settings: 1) Ebola in sub-Saharan Africa, 2) Measles in central/eastern Europe & central Asia region, 3) Measles in North Africa & the Middle East and 4) Tuberculosis in the central/eastern Europe & central Asia region. The decrease in infection duration due to an increase of elderly people drives pathogen virulence down for diseases in the remaining settings. Understanding the mechanisms that shape pathogen dynamics and leveraging this to predict future challenges is key to endemic disease management in a rapidly changing world. Author SummaryKey aspects of disease transmission including susceptibility to infection, the severity of infection, and the probability of dying from that infection, are affected by host age. Global populations are rapidly ageing, so that the mean age of most populations is generally higher than it used to be and is set to continue on this trajectory. This suggests that the dynamics of infectious diseases are also likely to change, although infectious disease dynamics tend to be non-linear as these key parameters interact. We have developed a dynamic modelling framework to explore how changes in population age structure might impact the optimal level of pathogen virulence in a population. We have chosen four infectious diseases as case studies, that differentially impact certain age classes to illustrate these dynamics. We have parameterised this framework with open access data for each of the seven Global Burden of Disease super-regions and show that population ageing can increase virulence for several diseases in differing global regions, whilst increased background rates of mortality can drive virulence down in others.

evolutionary biology↗

Activating Ras-MAPK pathway variants drive hippocampal clonal competition in human epilepsy

Mesial (a.k.a., medial) temporal lobe epilepsy (MTLE) is the most common focal epilepsy1,2 and, in drug-resistant cases, is treated by surgical removal of the anterior temporal lobe, which often shows neuronal loss and gliosis consistent with hippocampal sclerosis (HS)2. MTLE with HS has minimal contribution from germline genetic variation3, and is associated with prior precipitating insults such as prolonged childhood seizures and head trauma4-6. Somatic variants in Ras-MAPK pathway genes were recently reported in a few MTLE surgical specimens7,8, but their prevalence, clinical relevance, and underlying biological mechanisms remain unknown. Targeted duplex sequencing of hippocampal DNA from 462 surgical resections revealed significant enrichment of deleterious somatic variants in MTLE versus controls, with >40% of MTLE specimens harboring activating Ras-MAPK variants in PTPN11, NF1, BRAF, KRAS, and twelve genes not previously associated with focal epilepsy. Eight Ras-MAPK genes showed positive clonal selection in MTLE. Increased somatic variant burden predicted worse surgical outcome. Somatic Ras-MAPK variants at ultra-low (<0.5%) variant allele fractions were associated with older seizure onset and HS pathology, supporting a late prenatal or postnatal origin. Ras-MAPK variants in MTLE were enriched in cells derived from hippocampal progenitors--neurons, astrocytes, oligodendrocytes--in line with the known neuronal hyperexcitability and seizures induced by Ras-MAPK overactivation9,10; in contrast, Alzheimer disease hippocampi exhibited microglial enrichment of Ras-MAPK variants, consistent with prior reports11. Single-nucleus RNA sequencing showed increased expression of Ras-MAPK genes in neurons and upregulation of pathways mediating neurogenesis and neural development in MTLE. Functional validation of novel, recurrent PTPN11 variants confirmed gain-of-function, while cellular modeling in induced pluripotent stem cells demonstrated proliferative/survival advantages for mutant cells in mosaic culture. Overall, our data suggest that somatic Ras-MAPK variants and acquired risk factors may converge on clonal competition in the hippocampus to modulate epilepsy risk.

genetics↗

B Lymphocyte Protein Factories produced by Hematopoietic Stem Cell Gene Editing

Long-term in vivo production of therapeutic proteins and development of vaccines that elicit protective levels of broadly neutralizing antibodies (bNAbs) against major pathogens face challenges. Here we report on an alternative gene-editing approach using small numbers of hematopoietic stem and progenitor cells (HSPCs) to direct long-term, high-level expression of antibodies or cargo proteins. Edited B lymphocyte offspring can be activated by cognate antigen to undergo clonal expansion and develop into specific antibody or cargo protein-synthesizing plasma cells. These cells produce long-lasting, therapeutic levels of serum antibody against HIV-1 or malaria and an anti-influenza virus bNAb that mediated universal protection from heterologous lethal challenge. Our data provide a paradigm for cell therapy approaches to prevent or treat disease using self-amplifying B cell protein factories.

immunology↗

The pharmacokinetics, bio-distribution and therapeutic efficacy of a trimeric nanobody against SARS-CoV-2 in the Syrian golden hamster COVID-19 model

The rapid emergence of SARS-CoV-2 prompted the development of anti-viral therapies and vaccines to combat the COVID-19 pandemic. The continuous emergence of variants of concern has necessitated the development of platforms that can be rapidly adapted. Nanobodies, offer advantages over conventional monoclonal antibodies, including low molecular weight, high antigen-binding affinity, enhanced tissue penetration, blood-brain barrier permeability, and simplified production. Previous studies have demonstrated the efficacy of nanobodies against respiratory viruses such as SARS-CoV-2, respiratory syncytial virus, and influenza A virus in animal models. We previously reported the protective effects of nanobody trimers against SARS-CoV-2. However, pharmacokinetic and biodistribution data for nanobodies remain limited. To address this, we evaluated the efficacy, biodistribution and longevity of action of a nanobody trimer (A8) administered intranasally (IN) or intraperitoneally (IP) in Syrian golden hamsters. Our findings revealed that the A8 trimer reached peak concentrations shortly after administration and was subsequently cleared from the system via both routes. Importantly, early administration of A8 trimer reduced virus mediated weight loss and viral load compared with untreated controls supporting its potential as a therapeutic candidate for SARS-CoV-2 infection.

microbiology↗

The evolution lifecycle of ribosome hibernation factors

Bacteria defend against hostile environments through a variety of molecular mechanisms, including ribosome hibernation. Previously, bacteria were shown to initiate ribosome hibernation by activating protective proteins known as hibernation factors. It was demonstrated that hibernation factors prevent ribosome degradation by nucleases, which allows bacteria to safely store their inactive ribosomes and survive under starvation or persistent stress. Because homologs of hibernation factors were found in diverse lineages of bacteria, it is currently assumed that the mechanism of ribosome hibernation is highly conserved across species. Here, we assess 46,015 complete bacterial genomes to reveal the principles underlying the origin and evolution of these essential proteins in bacterial cells. We find that hibernation factors emerged in ancient bacteria as relatively large proteins that then gradually reduced in size and have undergone complete extinction in over 10% of studied bacteria. We then demonstrate that the degeneration of ancient hibernation factors is often accompanied by "borrowing" hibernation factors from other species via gene transfers, de novo gene birth or fusion of truncated hibernation factors with fragments from other stress-response proteins. These findings reveal a unique evolutionary pathway in which bacteria respond to the reductive evolution of hibernation machinery by inventing novel hibernation mechanisms, thus restoring their capacity to survive starvation and stress. This model implies that most ribosome hibernation factors are yet to be discovered and predicts the organisms that rely on currently unknown hibernation mechanisms.

microbiology↗

Risk factors, patterns and seropositivity of inter-epizootic Rift Valley fever virus of cattle in northern Tanzania.

1.1BackgroundRift Valley Fever (RVF) is a zoonotic viral disease affecting both animals and humans, with significant public health and economic implications. In Tanzania, a series of RVF outbreaks in livestock have been reported. The epidemiological information about hosts exposures status, time, location and risk factors that contribute to virus maintenance between one epizootic and the other, is important for preparedness and intervention plans. This study investigated the seroprevalence and potential determinants of RVFV exposure in cattle in Babati, Hai, and Moshi Districts between the last RVF outbreak in 2007 and the anticipated El Nino rains of 2024, which could precipitate the next outbreak. MethodsA total of 1,627 cattle serum samples (790 from Babati, 518 from Moshi, and 319 from Hai), were collected between August and October 2023 from both urban and rural areas, were analyzed using a competitive ELISA to detect RVFV-specific antibodies. Data on cattle biodata, management practices, environmental factors, were obtained through structured questionnaires and field records. Sero-prevalence was determined by descriptive statistics, while risk factors were quantified by multivariable logistic regression and RVF seropositivity was plotted on administrative boundaries of Babati, Moshi, and Hai districts by using QGIS. ResultsThe overall RVFV seroprevalence was 15.0% (95% CI: 13.26 - 16.73). Seropositivity was 22.2% (95% CI: 18.62-25.78) in Moshi, 12.2% (95% CI: 8.63-15.82) in Hai and 11.4% (95% CI 9.18-13.61) in Babati. Age (OR = 1.22, 95% CI: 1.15-1.3, p<0.001), sex (OR = 0.53, 95% CI: 0.36-0.79, p = 0.0017), herd size (OR=0.2201; 95% CI: 0.095-0.5101; p=0.0004), water access along irrigated crop fields (OR=3.7181; 95% CI: 1.5868-8.7121; p=0.0025), and geographical location (OR = 2.23, 95% CI: 1.63-3.06, p < 0.001) were significant predictors of seropositivity. Spatial visualization revealed clustering of seropositive herds in villages near lake Manyara and Tarangire National parks in Manyara region, also seropositive clusters in villages near irrigated areas, Nyumba ya Mungu dam and floodplains in lower Moshi. ConclusionThis study highlights ongoing inter-epizootic exposure of cattle to RVFV in northern Tanzania. The RVFV is not randomly distributed during inter-epizootic periods, but rather forms seropositive clusters. Most significant determinants of seropositivity includes age, sex, herd size, water access along irrigated crop fields and geographical location Moshi showing higher seropositivity.

ecology↗

Lysyl oxidase-mediated intermolecular crosslinks fine-tune collagen I molecular dynamics and regulate cell-matrix interactions through focal adhesions

Lysyl oxidase (LOX)-mediated intermolecular crosslinking is essential for collagen I fibril stability, yet its influence on collagen molecular conformation and dynamics, and the downstream consequences for cell-matrix interactions remain poorly understood. Here, we genetically modulated LOX in collagen I-producing MC3T3-E1 cells to generate matrices with elevated (overexpression, OX) or absent (knockout, KO) crosslinking. Enhanced crosslinking yielded thick, continuous, aligned fibrils, whereas reduced crosslinking produced friable, dissociated fibrils. Solid-state nuclear magnetic resonance spectroscopy (SSNMR) revealed local triple-helix unfolding and altered nanosecond- and microsecond-scale molecular motions in both OX and KO matrices, changes largely reversible upon decellularization, implicating a synergistic role of crosslinking chemistry and cell-applied forces in regulating the dynamically-accessible conformations of collagen I. Changes in the molecular structure and dynamics of collagen had a functional impact on cell adhesion and mechanotransduction. These findings identify collagen crosslinking as a tunable element of the extracellular matrix "mechanical code," integrating biochemical modification with molecular-scale mechanics to regulate cell-matrix adhesion and mechanosignalling.

biophysics↗

Functional Integration of Different-Sex Gonad Transplants into the Adult Mouse Hypothalamic Pituitary Gonadal Axis

Gender-affirming hormone therapy (GAHT) relies on exogenous hormones to produce hormonal milieus that achieve and/or maintain embodiment goals. Another potential route to these endpoints is transplantation of novel steroidogenic tissue. To develop a pre-clinical model, we asked whether different-sex gonad transplants can be functionally integrated into the adult mouse hypothalamic-pituitary-gonadal (HPG) axis. Adult male and female mice were gonadectomized and implanted with gonads from genetically matched but different-sex pups. Controls received gonads from same-sex pups. Temporal changes to gonadotropin and steroid hormone levels reveal the decoupling of the HPG following gonadectomy and gonad-dependent levels after transplanting donor gonads. After six weeks, histological structures in transplanted gonads were consistent with expected steroidogenesis and gametogenesis. Interestingly, pituitary, ARC and AVPV mRNA showed gonad- and sex-dependent expression patterns. Future work with this technique could lead to translation to gender affirming care and explorations of gonad-dependent sex differences in biomedical and basic research.

cell biology↗

Genetic and plastic effects on trait variability in two major tree species: insights from common garden experiments across Europe

Phenotypic plasticity and genetic adaptation are key mechanisms that enable species to respond to changing environments. Tree traits do not vary independently but rather in coordination. However, our understanding of whether functional traits are governed by the same mechanism is far from complete. Thus, we aim at assessing the drivers of trait variability of sessile oak and European beech provenances across their distribution ranges. We estimated growth-related and leaf morphological traits from 9 and 11 provenances of oak and beech, respectively, grown in four different common gardens distributed across their respective distribution areas. Overall, phenotypic plasticity played a dominant role in explaining individual trait variability. For most oak traits, variation among provenances and genetically based plasticity were correlated with the climate of origin, whereas fewer significant associations were found for beech. In oak, climate-transfer distance analyses revealed that traits such as DBH, height, specific leaf area, and long-term growth responses to summer temperature decreased when provenances were moved away from their local precipitation regime. In beech, significant climate-transfer distances were fewer and primarily related to temperature-related parameters. These results suggest that natural selection and local adaptation may play a secondary but notable role. The pattern of multi-trait phenotypes indicates that resource-use strategies among provenances covary with the temperatures of origin in both species. The limited genetic responses in beech could hinder its survival if it reaches the boundaries of trait plasticity, while oak may better adjust through adaptation. Our study contributes to a better understanding of the interplay between genetic adaptation and phenotypic plasticity in long-lived forest trees.

ecology↗

Genetic basis of traits and local adaptation in UK silver birch

Knowledge of the genomic basis of phenotypes in forest trees lags that of other economically important organisms. We sequenced the genomes of 2054 silver birch trees from 20-year-old field trials at three locations in Britain. Each trial site contains trees from the same 29 source populations, and one trial site (Drummond) is outside the climate envelope of the source sites. We discovered many single nucleotide polymorphisms (SNP), and a structural polymorphism, associated with several growth traits. Using models trained with genome-wide SNPs we estimate the genomic breeding values of 148 plus trees. We discover 117 SNPs significantly associated with source-site environmental variables, but genetic offset estimates using these SNPs provide poor predictions of tree growth rates (Drummond excluded). They are outperformed in this task by offset estimates using thousands of non-significant SNPs. Such estimates for Drummond in current climates are higher than for source sites under a future worst case climate scenario.

genomics↗

Wheat - black-grass competition is a non-zero-sum game influenced by root growth

Interactions with neighbouring plants have profound effects on plant growth, especially in crop-weed interactions, which can cause major crop-losses in agricultural systems. Black-grass (Alopecurus myosuroides) is the most problematic weed for UK agriculture, causing dramatic yield losses in winter wheat, but the basis of its competitive advantage is not clear. We aimed to fundamentally reappraise the nature of wheat - black-grass competition. Here, we show that black-grass is slow to establish, and requires long periods to demonstrate any competitive advantage over wheat. We show that black-grass grows significantly faster under winter conditions than wheat, and has much more vigorous root growth, collectively suggesting that prolonged root growth over winter is key to black-grasss competitive advantage over wheat. We tested the competitiveness of a range of wheat and barley germplasm against black-grass in three distinct environmental set-ups, and show that competitiveness under controlled conditions reflects competitiveness under field conditions. In controlled conditions, we identified significant variation in crop varietal competitiveness against black-grass, in both ability to suppress black-grass growth, and to continue to grow in the presence of black-grass (tolerance). We further identified that this competition is not a zero-sum game, with loss in crop biomass not necessarily equal to gain in black-grass biomass. Finally, we found that the black-grass suppression, but not tolerance, is correlated with crop root growth, supporting our root growth hypothesis for black-grass competition. Overall, our results suggest that breeding for increased root growth and/or winter growth rate can create more competitive wheat cultivars for grassweed suppression.

plant biology↗

Genetic differences in plasticity across environmental scales determine fitness along an ecological gradient

When populations suffer reduced fitness in novel environments, genotypes that better adjust their phenotype to cope with environmental change can aid persistence by reducing the severity of fitness declines. However, we know little about how plastic changes in phenotype allow different genotypes to track environmental variation across ecological gradients, particularly as environments become novel. We transplanted numerous clones of 19 genotypes of a Sicilian daisy, Senecio chrysanthemifolius, at four elevations on Mt Etna. We assessed fitness at native and novel elevations and quantified leaf plasticity among and within elevations. Genotypes with higher fitness at novel elevations showed lower variance in fitness, lower plasticity across elevations, but higher plasticity within elevations compared to those with higher fitness in the native range. Our results suggest that there are genotypes hidden in a population whose plasticity better tracks novel environmental variation at multiple scales, which will be crucial for population persistence under rapid environmental change.

evolutionary biology↗

Convergent and clonotype-enriched mutations in the light chain drive affinity maturation of a public antibody

Public antibodies that recognize conserved epitopes are critical for vaccine development, and identifying somatic hypermutations (SHMs) that enhance antigen affinity in these public responses is key to guiding vaccine design for better protection. We propose that affinity-enhancing SHMs are selectively enriched in public antibody clonotypes, surpassing the background frequency seen in antibodies carrying the same V genes, but with different epitope specificities. Employing a human IGHV4-59/IGKV3-20 public antibody as a model, we compare SHM signatures in antibodies also using these V genes, but recognizing other epitopes. Critically, this comparison identified clonotype-enriched mutations in the light chain. Our analyses also show that these SHMs, in combination, enhance binding to a previously uncharacterized viral epitope, with antibody responses to it increasing after multiple vaccinations. Our findings offer a framework for identifying affinity-enhancing SHMs in public antibodies based on convergence and clonotype-enrichment and can help guide vaccine design aimed to elicit public antibodies. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=138 SRC="FIGDIR/small/642041v1_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@1c4559eorg.highwire.dtl.DTLVardef@d12202org.highwire.dtl.DTLVardef@fca57org.highwire.dtl.DTLVardef@ad5041_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIClonotype-enriched SHMs are identified in the light chain of a public antibody, M15 C_LIO_LIThese light chain SHMs enhance affinity of M15 C_LIO_LIM15 targets a previously undescribed, conserved viral epitope C_LIO_LISerum antibody levels targeting this epitope increase after repeated vaccinations C_LI

immunology↗

An experimental test of the influence of microbial manipulation on sugar kelp (Saccharina latissima) supports the the core influences host function hypothesis

Kelp are valued for a wide range of commercial products and for their role in kelp forest ecosystems, making kelp cultivation a rapidly expanding economic sector. Microbes associated with kelp and other macroalgae play a critical role in processes such as nutrient exchange, chemical signaling, and defense against pathogens. Thus, manipulating the microbiome to enhance macroalgal growth and resilience is a promising yet underexplored approach for sustainable kelp cultivation. The core microbiome hypothesis suggests that the bacteria that are consistently found on a host (the core microbes) are likely to have a disproportionate impact on host biology, making them an attractive target for microbiome manipulation. In this study, we surveyed wild Saccharina latissima and their surrounding environment to identify core bacterial taxa, compared them to cultivated kelp, and experimentally tested how cultured bacterial isolates affect kelp development. We found that core bacteria are nearly absent in cultivated juvenile sporophytes in nurseries but eventually colonized them after outplanting to ocean farm sites. Bacterial inoculants had both positive and negative effects on kelp development. Notably, the strength of association of a bacterial genus with kelp in the wild positively correlated with its impact on gametophyte settlement and sporophyte development in kelp co-culture experiments, aligning with predictions from the core microbiome influences host function hypothesis. These findings affirm the feasibility of using microbial manipulations to improve current kelp aquaculture practices and provide a framework for developing these techniques. IMPORTANCEMicroorganisms consistently associated with hosts are widely thought to be more likely to impact host biology and health. However, this intuitive concept has not been experimentally evaluated. This study formalizes this concept as the Core microbiome Influences Host Function hypothesis and experimentally tests this hypothesis in sugar kelp (Saccharina). The distribution of bacteria on wild kelp and core microbes were first identified by compiling a broad dataset of the kelp microbiome sampled across space and time. Bacterial cultures were isolated from the surface of sugar kelp and individually grown in laboratory co-culture with sugar kelp spores to assess the ability of bacterial isolates to influence kelp growth and development. In support of the core influences host function hypothesis, isolates belonging to bacterial genera that are more strongly associated with wild sugar kelp are more likely to influence development in laboratory experiments.

ecology↗

HIF1α gates tendon response to overload and drives tendinopathy independently of vascular recruitment

Tendons are mostly avascular dense connective tissues that link muscles to bones, withstanding some of the highest mechanical stresses in the body. Mechanical overload and tissue hypervascularity are implicated in tendinopathy, a common musculoskeletal disorder, but mechanistic understanding of their roles is largely lacking. Here, we identify HIF1 not only as a marker but as a driver of tendinopathy. Initial histological and multi-omics evaluation of human tendinopathic samples revealed extensive extracellular matrix remodeling, including pathological collagen crosslinking coinciding with active hypoxic signaling. Hypothesizing a causal contribution of hypoxia signaling, we generated mice with tenocyte-targeted deletions of the Von Hippel-Lindau (VHL) gene, which controls hypoxia signaling by regulating HIF degradation. We demonstrated that VHL inactivation suffices to induce pathological hallmarks of tendinopathy, such as collagen matrix disorganization, crosslinking, altered mechanics and neuro-vascular ingrowth. This phenotype was HIF1-dependent, since co-deleting HIF1 rescued tendon morphology and mechanics. Moreover, deleting vascular endothelial growth factor A (VEGFA) alongside VHL effectively decoupled the effects of vascular ingrowth from persistently aberrant extracellular matrix remodeling and mechanical dysfunction, emphasizing a direct role of HIF1 in driving tendon disease that is independent of angiogenesis. Mechanistically, we linked tendon mechanical overload to the onset of HIF1 signaling in primary cultured human tendon cells. Furthermore, genetically removing HIF1 from tenocytes prevented aberrant tendon remodeling in response to chronic overload. These findings position HIF1 signaling as a central driver of tendinopathy that acts through a maladaptive tissue response to chronic overload, providing mechanistic insights that could be leveraged for improved therapeutic approaches. One Sentence SummaryHIF1 activation promotes tendinopathy and its inhibition prevents overload-induced maladaptation, suggesting therapeutic potential.

cell biology↗

Novel pink-spot disease in North American kelpnurseries

Macroalgal cultivation is a growing industry in North America, but is well established in Asia and Africa, where macroalgal disease cause crop losses, placing a significant economic burden on farmers. As kelp cultivation intensifies in North America, kelp disease prevalence is expected to increase in tandem. With input from the kelp-growing community through an online survey, we describe the prevalence of a novel kelp disease, pink-spot disease, which has been observed in Canada and the United States on Saccharina latissima, Alaria marginata, Nereocystis luetkeana, and Macrocystis tenuifolia. Eight of the fourteen (57%) surveyed kelp growers report bright pink spots (pink-spot disease) on their kelp spools in the land-based nursery stage. Along with the grower survey, we conducted 16S rRNA amplicon sequencing in 2021 and 2022 to investigate the causative agent of pink-spot disease and associated bacterial community changes on infected Saccharina latissima (sugar kelp) spools. Our data in both years show that a member of the genus Algicola is enriched on visibly diseased spool regions compared to asymptomatic spool regions and may be the causative agent of pink-spot disease. As macroalgal cultivation continues to intensify, monitoring diseases is important to mitigate potential negative impacts.

ecology↗

Fraxinus excelsior updated long-read genome reveals the importance of MADS-box genes in tolerance mechanisms against ash dieback

Ash dieback caused by the fungus Hymenoscyphus fraxineus has devastated the European ash tree population since it arrived in Europe in 1992. Great effort has been put into breeding programmes to increase the genetic diversity of ash trees and find heritable genetic markers associated with resistance, or tolerance mechanisms, to ash dieback. To facilitate identification of molecular markers, we used Oxford Nanopore Technologies combined with Illumina sequencing to obtain an accurate and contiguous ash genome. We used this genome to reanalyse transcriptome data from a Danish ash panel of 182 tree accessions. Using associative transcriptomics, we identified 175 gene expression markers (GEMs), including 11 genes annotated as dormancy MADS-box transcription factors which are associated with ash bud dormancy, flowering and senescence. We hypothesize that tolerant trees both break dormancy earlier in the year by increasing the expression of flowering-related SOC1 MADS-box and reducing the expression of SVP-like MADS-box, whilst also accelerating senescence by increasing the expression of JOINTLESS MADS-box genes. DNA methylation differences in the promoters of MADS-box genes between one tolerant and one susceptible tree indicate potential epigenetic regulation of these traits. Article SummaryAsh dieback has devastated European ash tree populations. To aid in breeding programmes focused on finding solutions against this pathogen, we have assembled a new ash genome. This new genome helped us to identify genes related to tree biological life cycles, expressed differently in tolerant and susceptible trees. For the first time, we have also discovered that susceptible and tolerant trees showed different DNA methylation frequencies in those genes, suggesting epigenetic regulation. DNA methylation can turn on/off gene expression without changing the DNA sequence. These genes, and their regulatory elements, are ideal targets during breeding programmes combating this pathogen.

plant biology↗