Biology subjects

Johnson, D.

Publications and source records attributed to Johnson, D..

At least 19 recordsLinked to original sources

bioRxiv2026

Bidirectional changes in seabird populations drive terrestrial ecosystem function and biodiversity

Seabird populations fluctuate dramatically in response to perturbations and human activity, such as the current highly pathogenic avian influenza (HPAI) panzootic and fishery practices. Seabirds vector marine nutrients into terrestrial and coastal environments causing cascading effects through ecosystems, but quantifying the inter-related mechanisms underpinning marine-terrestrial cascades in response to changes in seabird populations is challenging. Here we simulate decreases and increases in seabird density, as have occurred due to HPAI and fishing practices respectively, through turf transplant experiments and stratified surveys to quantify marine nutrient cascades and show how they regulate terrestrial ecosystem processes and biodiversity. We use structural equation modelling to quantify the relative strengths of each hypothesised mechanistic pathway in the ecological network. This analysis identified that seabirds shape terrestrial plant and invertebrate biodiversity primarily indirectly, through modifying soil nutrient availability. Our findings highlight the ecosystem changes that are likely occurring, and the pathways through which they operate, due to acute declines and chronic increases in seabirds caused by HPAI, fishing practices or other drivers.

ecology↗

bioRxiv2026

Interferon lambda drives immunological maturation in the infant lung and protects against lethal Bordetella pertussis infection

Serious pertussis infections disproportionately affect infants but the biological basis for this age-dependent susceptibility remains unclear. Infant mouse models recapitulate features of severe human infant pertussis. We investigated the role of interferon lambda (IFN-{lambda}), a key regulator of mucosal immunity, in Bordetella pertussis infection of infant mice. While infected adult mice upregulate lung IFN-{lambda}, infant mice inoculated at P7 fail to upregulate IFN-{lambda} and succumb to infection. We hypothesized that failure to produce IFN-{lambda} during infection represents a critical immunological deficit in infant mice, and that restoring IFN-{lambda} signaling would improve survival outcomes. Whereas wild-type mice gained complete protection from lethal B. pertussis infection by P10, mice lacking the IFN-{lambda} receptor component IFNLR1 did not achieve full protection until P21. Loss of IFNLR1 was associated with enhanced bacterial dissemination to systemic organs. Infant mice possessed a functional IFN-{lambda} receptor in the lungs but failed to upregulate IFN-{lambda} during infection, and supplementing IFN-{lambda} exogenously extended survival. RNA sequencing of lung tissue from infected and uninfected wild-type and IFNLR1-deficient mice inoculated at different ages identified an immune transcriptional framework distinguishing susceptible from resistant animals at a systems level and revealed IFN-{lambda} signaling as a critical driver of immunological maturation in the infant lung. Infected infant IFNLR1-deficient mice had dysregulated immune cell recruitment to the lungs, indicating a quantitatively expanded but qualitatively impaired response. These findings demonstrate that IFN-{lambda} affects immune maturation accounting for a critical window of age-dependent resistance to lethal pertussis with novel therapeutic possibilities for human infants with this disease.

immunology↗

bioRxiv2026

Persistent but variable effect of experimental laboratory burns on microbial community resistance, resilience, and function across contrasting boreal forest soils

Boreal forests stretch across vast swaths of the northern hemisphere, are shaped by wildfire, and play an important role in the global carbon cycle. Microorganisms play a critical role in soil nutrient cycling in these ecosystems, yet there are many open questions about the impacts of wildfire on microbially mediated soil biogeochemical cycles. In this study, we used laboratory burns and soil incubations of intact soil cores collected from two distinct soil types -- Histosols and Gleysols -- from boreal forest within Wood Buffalo National Park, Alberta, Canada, to assess burn effects on soil bacterial and fungal community composition and function. We compared resistance and resilience to burning for microbial communities vs. resistance and resilience to burning for soil pH and soil respiration to assess the relationships between burn-induced shifts in microbial community composition, the soil environment, and microbial activity. To link shifts in microbial community composition to potential community function, we measured glucose-specific carbon use efficiency (CUE) and assessed its relationship with weighted mean predicted 16S rRNA gene copy numbers for bacterial communities and FUNGuild-estimated relative abundance of putative symbiotrophic and saprotrophic fungi in burned and unburned soils. Microbial community resistance and resilience to burning varied across soil type with higher resistance of both bacterial and fungal communities from Histosols compared to the O horizons of Gleysols. This may be explained by a larger impact of burning on microbes in the thinner Gleysol O horizons. The relatively low resilience of bacterial and fungal communities to burning as well as the failure of resilience to increase with time since burning supports previous reports of post-burn microbial community recovery occurring over years rather than months. Burning caused a decrease in CUE with larger decreases following longer, hotter burns, which correlated with an increase in weighted mean predicted 16S rRNA gene copy number, raising the possibility that copy number could serve as a proxy for post-fire CUE in boreal forest soils, though more research is needed to constrain the effects of environmental conditions, substrates, and time since fire on this relationship. These findings suggest several ways in which burn-induced shifts in microbial community composition reflect altered microbial community function in meaningful ways for soil carbon cycling.

ecology↗

bioRxiv2026

Cocaine-Enriched Oral Streptococcus parasanguinis Promotes Neuroimmune Dysfunction and Memory Impairment

Chronic cocaine use is associated with neuroinflammation and cognitive dysfunction, but the underlying mechanisms remain unclear. We previously identified oral enrichment of Streptococcus parasanguinis (SP) and other species in individuals with cocaine use disorder (CUD), and here demonstrate that cocaine selectively enhanced SP growth in vitro. To investigate causality, antibiotic-pretreated wild-type C57BL/6 mice received chronic oral inoculation of SP, S. salivarius, Neisseria flavescens, or vehicle. SP-treated mice exhibited spatial memory impairment, increased brain IL-1{beta}, and non-region-specific microglial activation, without detectable bacterial translocation into the brain. While amyloid-associated signaling changes were observed across all bacterial treatment groups, only SP induced cognitive deficits and neuroinflammation. Untargeted metabolomics identified distinct SP-associated oral-to-brain metabolite signatures, including cysteine S-sulfate (CSS) and altered histamine-associated metabolites. CSS and histamine induced neuroinflammatory and amyloid-associated responses in vitro. Together, these findings identify a cocaine-associated oral pathobiont that promotes neuroinflammation and neurodegeneration, suggesting a novel oral microbiome-brain axis in CUD.

neuroscience↗

bioRxiv2026

The Vagus Nerve conducts viable translocation of gut flora to the lungs that impacts interstitial lung disease severity in mice

Communication between gut microbiota and extraintestinal organs is increasingly recognized, yet elucidation of relevant translocation mechanism(s) remains enigmatic. Vagus neuroanatomy and reports of vagal protein transfer to extraintestinal organs suggest that this "superhighway" could translocate bacteria. Here we explore whether the vagus superhighway can translocate bacteria to extraintestinal organs. Gavage of green fluorescent protein-expressing Escherichia coli (GFP-E. coli) into germ-free (GF) or specific-pathogen free (SPF) C57BL/6 mice yielded high bacillary loads in the stomach and lungs, followed by the heart, stool and peripheral muscles, despite negative blood cultures. Notably, confocal microscopy and culture revealed GFP-E. coli within the vagus nerve within five minutes of gavage suggesting rapid translocation. Metagenomic analysis of stool, lung, heart, vagus nerve, and muscle from non-gavaged SPF mice demonstrated significant microbial overlap, supporting that bacterial translocation occurs despite the presence of endogenous microflora. Remarkably, subdiaphragmatic vagotomy performed prior to GFP-E. coli gavage resulted in marked reductions of bacterial transduction in the lungs and other extraintestinal organs, except muscle. Furthermore, vagotomy significantly reduced lung fibrosis in SPF mice following intranasal bleomycin administration. In lung cancer patients undergoing lobectomy, vagotomy inhibited postsurgical reductions in forced vital capacity. These findings identify the vagus nerve as a literal gut-lung axis, facilitating viable bacterial translocation and influencing lung severity.

microbiology↗

bioRxiv2026

The First 1,000 Days (1kD) Project - Collecting and Analyzing an Ultra-Dense Naturalistic Dataset of Human Baby Development

Human development unfolds in continuous, multimodal environments across seconds, days, and years, yet most developmental datasets capture sparse, context-limited samples of everyday life. We introduce the First 1,000 Days (1kD) Project, an initiative designed to collect ultra-dense, longitudinal, child-centered data that capture developmental trajectories within their full ecological context. Fifteen U.S. homes with 17 infants were recorded 12-14 hours per day over a median of 944 days, yielding [~]1.18 million hours of raw audiovisual data. We present an end-to-end framework for large-scale longitudinal naturalistic measurement and a scalable analysis pipeline of the collected data. In a case study, we describe how we utilized our pipeline to isolate child-centered speech, resulting in the collection of 2,000 to 6,000 hours of transcribed speech for each infant. We demonstrate that dense sampling within the home environment reveals a stable, household-specific lexical structure, which sparse sampling methods consistently fail to capture. The 1kD project offers a blueprint for teams aiming to collect and analyze natural behavior at scale in real-world settings.

neuroscience↗

bioRxiv2026

Localised negative feedback shapes genome-wide patterning of meiotic DNA breaks

Genetic diversity within sexually reproducing species arises via the formation and repair of programmed DNA double-strand breaks (DSBs) created by the evolutionarily conserved topoisomerase-like enzyme, Spo11. Because DSBs threaten genome stability, their formation is tightly regulated in both space and time. In S. cerevisiae, Tel1, the orthologue of mammalian Ataxia Telangiectasia Mutated (ATM) kinase, suppresses nearby DSB formation through local inhibition known as DSB interference. However, whether such local inhibition reshapes the genome-wide DSB landscape remains unclear. Here, we develop a quantitative simulation framework to model how Tel1-mediated feedback shapes Spo11-DSB formation across the yeast genome. We demonstrate that innate chromosome-specific DSB patterns, when combined with interference, generate complex, population-level redistribution of DSBs. We define the spatial range over which interference propagates and provide evidence that this regulatory mechanism requires Tel1 recruitment to DSBs via Xrs2 and Tel1 kinase activity. Although the pro-DSB factor Rec114 contributes to DSB regulation, mutation of potential Rec114 phosphorylation sites indicates that it is not an essential target of Tel1. Together, these findings demonstrate how localised negative feedback can drive broad-scale, emergent patterning of a fundamental genome-modifying process, with the potential in meiosis to influence recombination initiation and, consequently, genetic variation across generations.

cell biology↗

bioRxiv2026

Maximum entropy networks predict fluctuations and stability of food web energetics

A central goal of ecology is understanding how the architecture of food webs, which represent the structural backbone of ecosystems, affects their stability. The analysis of stability in the classical sense of population dynamics (i.e. return to equilibrium) can be successful for a single instance of an empirical food web but ignores the multiplicity of alternative states in which the system could be found as a result of intrinsic variability and fluctuations. Here we propose and test a new methodology to reconstruct, from single empirical observations of a food web, the viable ensemble of alternative realizations respecting the observed resource-consumer linkages and empirical ener-getics. The reconstruction can be handled analytically within a maximum-entropy framework which predicts how empirical food webs access a multitude of alternative states with comparable stability and reactivity. The (measurable) entropy of the reconstructed ensemble directly quantifies this multiplicity and serves as a novel proxy of system resilience, that is the rate of return to equilibrium in response to an external perturbation. We show that the associated ensemble fluctuations provide explicit predictions for the expected response of food webs to external perturbations, such as anthropogenic or climate-induced stresses. We do that by validating the proposed fluctuation-response relation on empirical soil food webs subjected to experimentally controlled perturbations, confirming that intrinsic fluctuations in the unperturbed state predict responses to subsequent stresses. The perturbed states are associated with higher entropy, indicating less likely spontaneous recovery.

ecology↗

bioRxiv2025

DYT1 mutation alters gut microbiome composition and gut-brain axis dynamics in a mouse model

Dystonia is a neurological movement disorder characterized by involuntary, sustained, or intermittent muscle contractions, that result in twisting movements, repetitive motor patterns, or abnormal postures. While genetic mutations such as Tor1a+/{Delta}GAG are known contributors, the environmental and peripheral factors influencing disease onset and progression remain poorly understood. Emerging evidence implicates the gut microbiome in shaping neurodevelopment and host behavioral function, yet its contribution to dystonia pathobiology is largely unexplored. Here, we longitudinally profiled the gut microbiome of Tor1a+/{Delta}GAG mouse model using 16S rRNA gene sequencing and uncovered early emerging, persistent disruptions in microbial diversity and community composition that track with progressive motor impairment. Mutant mice exhibited an alteration of key commensal taxa, and molecular signatures indicative of compromised gut-barrier integrity. Parallel transcriptomic profiling of colonic epithelium reveals coordinated dysregulation of pathways governing epithelial stress responses, endoplasmic reticulum homeostasis, lipid signaling, autophagy, and DNA damage and repair, pointing to a previously unrecognized epithelial stress state in Tor1a+/{Delta}GAG mouse model. Integrative microbial-host interaction correlation analyses uncovered robust associations between specific dysbiotic taxa and host signaling pathways. These peripheral perturbations coincide with longitudinal motor deficits, suggesting a mechanistic gut-brain axis linking intestinal dysfunction to central neuronal vulnerability. Together, our findings provide the first experimental framework connecting microbiome perturbations, gut-barrier disruption, and neuronal vulnerability in a genetic model of dystonia. This work positions the gut microbiome and its regulation of epithelial and neuronal homeostasis as a novel entry point for disease modification in individuals carrying deleterious dystonia-associated variants.

neuroscience↗

bioRxiv2025

Machine perfusion and single-cell spatial transcriptome mapping identifies novel immune escape mechanisms in colorectal cancer liver metastasis

Liver metastasis is the terminal stage of colorectal cancer. Immune checkpoint blockade (ICB) has heralded remarkable clinical success across a range of cancer types, but with limited efficacy in replacement-type colorectal liver metastasis (CRLM), the most common and lethal histological subtype. Using a novel human normothermic perfusion model, we demonstrate for the first time, that T-cells preferentially extravasate within the peri-tumoural liver rather than the CRLM. We use single-cell spatial transcriptomics and multiplexed immunofluorescence to validate CRLM T-cell exclusion and show that CRLM endothelia are anergic, lacking key receptors required for T-cell extravasation. CD4 T-cells that extravasate within the peri-tumoural liver are TCR-reactive, yet exhausted, whilst CD4 T-cells within the CRLM demonstrate a stress response, impaired cytokine expression and lack of TCR reactivity. We identify the spatial cellular and molecular interactions underlying these observations, providing novel targets for future attempts to sensitise to immunotherapeutics and a justification for failed ICB efficacy in CRLM.

cancer biology↗

bioRxiv2025

Arsenic Trioxide Underpins Delayed Neuroinflammation and Impaired Synaptic Integrity involving Integrative Stress Response Signaling

Arsenic trioxide (ATO), an industrial and environmental chemical with potential for accidental or intentional exposure, exerts profound neurotoxic effects. Its single acute exposure has been linked to delayed neurological and neurodegenerative outcomes. However, the molecular and cellular pathways driving these long-term manifestations remain poorly defined. In this study, combining human iPSC-derived neuronal and in vivo mouse model, we uncovered that the acute ATO exposure activates cellular stress pathway, which drives long-term neurotoxic and associated functional outcomes. We found that ATO induces integrated stress response (ISR) signaling in human iPSC-derived neurons. To model the impact of accidental ATO exposure in vivo, we administered a single high dose of ATO to C57BL/6J wild type mice. Four weeks post-treatment, ATO-exposed mice displayed neuropsychological symptoms and cognitive deficits. Brain analyses of ATO-challenged mice revealed elevated ISR activity marked by the increased phosphorylation of PERK and eIF2 and upregulation of the transcription factors, CHOP and ATF4. Transcriptomic profiling using bulk RNAseq revealed activation of pathways associated with stress and neuroinflammatory responses. Consistently, increased DNA damage and dysregulation of the STING-mediated innate immune response were also found in the brain of ATO-challenged mice. Pharmacological inhibition of the ISR with a small-molecule inhibitor, ISRIB mitigated ISR activation and preserved synaptic integrity in mouse hippocampal cells. In conclusion, our data identify ISR activation and DNA damage-driven immune dysregulation as key pathogenic drivers of ATO-induced delayed neurotoxicity and cognitive deficits and highlight ISR inhibitors as promising therapeutics to mitigate these effects.

neuroscience↗

bioRxiv2025

Cannabis-enriched oral Actinomyces induces anxiety-like behavior via impairing mitochondria and GABA signaling

The human oral microbiome is increasingly recognized as a contributor to brain health, yet its mechanisms remain unclear. Our previous work revealed that oral Actinomyces species was enriched in chronic cannabis smokers. Here, we show oral inoculation of cannabis use-associated Actinomyces species, especially A. meyeri, to wild-type C57BL/6 mice leads to anxiety-like behaviors, non-region-specific microglia activation, mitochondrial dysfunction, and reduced GABAergic neurotransmission, without evidence of bacterial translocation to the brain, neuroinflammation, and memory decline. Notably, Actinomyces species-producing metabolites, i.e., arginine and argininosuccinate, were increased in both oral swabs and brain following inoculation in vivo. These Actinomyces species-producing metabolites induced mitochondrial dysfunction and oxidative stress in neurons in vitro, indicating a neuropathogenic role and aligning with reduced GABAergic neurotransmission in vivo. Together, these results suggest that oral cannabis-associated dysbiosis impacts behavior through mitochondrial stress and impaired inhibitory signaling, indicating the oral-brain metabolic axis is potentially consequential in neuropsychiatric disorders. TeaserChronic heavy cannabis use-enriched oral bacteria can drive anxiety and neuropathogenesis in mice. Highlights{whitebullet} Cannabis-associated oral Actinomyces enrichment induces anxiety-like behavior in mice {whitebullet}Microglial activation occurs without neuroinflammation (IL-1{beta}, TNF-, and IL-6) {whitebullet}Mitochondrial hyperactivation and reduced inhibitory GABAergic signaling Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=160 SRC="FIGDIR/small/689724v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@120b0b1org.highwire.dtl.DTLVardef@1304782org.highwire.dtl.DTLVardef@a6aa77org.highwire.dtl.DTLVardef@17d6d_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2025

Elucidating Neurodevelopmental Trajectories in Cancer with Topic Modeling: Revealing Persistent External Granule Layer Lineages in Medulloblastoma

Single-cell transcriptomics transformed our understanding of cellular heterogeneity, yet cross-dataset comparison remains fundamentally limited by batch effects, technology differences, and inconsistent annotation frameworks. These challenges have impeded efforts to connect developmental programs with disease states which creates a critical gap for understanding pediatric cancers with suspected developmental origins. Here, we demonstrate that topic modeling, an unsupervised natural language processing technique, overcomes these barriers by learning transferable transcriptional genetic signatures that generalize across datasets, technologies, and biological contexts without requiring data integration. Applying this framework to over one million fetal cerebellar nuclei, we identify seven distinct topics that capture the developmental spectrum of rhombic lip progenitors through external granule layer (EGL) differentiation, including transitional states missed by conventional clustering. These topics transfer successfully across sequencing technologies (SPLiT-seq to sci-RNA-seq3), developmental timepoints, species (human to mouse), and from single-cell to bulk RNA sequencing of 876 medulloblastoma tumors. We reveal that Sonic hedgehog (SHH) medulloblastoma subtypes retain these topics, corresponding to distinct stages of EGL development. Our findings highlight that developmental timing at tumor initiation fundamentally shapes tumor biology, with immediate implications for subtype-specific therapeutic strategies in pediatric brain cancer. Our workflow establishes topic modeling as a scalable solution for mining expanding genomic atlases with broad applications across different datasets, technologies, and biological contexts.

bioinformatics↗

bioRxiv2025

Harnessing cGAS-STING signaling to counteract the genotoxic-immune nexus in tauopathy

Tauopathies are progressive neurodegenerative disorders characterized by aberrant tau aggregation, cognitive decline, and persistent neuroinflammation, yet the mechanisms driving neuroinflammation and disease progression remain incompletely understood. Here, utilizing human postmortem AD brains and a mouse model of tauopathy, we report that genotoxic stress-induced cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) immune pathway form a self-amplifying loop that fuels neuropathology and cognitive deficits. Targeted disruption of this cycle through either genetic deletion of cGAS or pharmacological inhibition of STING restores immune homeostasis and attenuates tau pathology and cognitive deficits. Our results showed a significant accumulation of DNA double-strand breaks (DDSBs) and impaired DNA repair function, alongside elevated cGAS-STING signaling and type I interferon (IFN-I) responses in human AD brains compared to non-AD. In the PS19 transgenic (PS19Tg) mouse model of tauopathy, we found significantly elevated levels of DDSBs and altered expression of DNA repair proteins during early stages of disease, which preceded the dysregulation of cGAS-STING signaling and emergence of significant neuropathology in the later stage. Interestingly, genetic deletion of cGAS shifted microglial polarization from a pro-inflammatory M1 phenotype toward an anti-inflammatory M2 state, accompanied by a reduction in IFN-I signaling and improved cognitive performance in PS19Tg mice. Pharmacological STING inhibition reshaped the transcriptomic landscape, revealing selective regulation of pathways governing synaptic plasticity, and immune responses. This transcriptional reprogramming was accompanied by suppression of inflammatory responses, reduction in synaptic pathology, and attenuation of tau pathology in PS19Tg mice, underscoring STING as a therapeutic target for tauopathy. In conclusion, our findings reveal that genotoxic-immune crosstalk drives neuroinflammation and tau pathology and identify a conserved, druggable cGAS-STING axis that can be targeted to impede or slow disease progression in tauopathies. O_FIG O_LINKSMALLFIG WIDTH=184 HEIGHT=200 SRC="FIGDIR/small/678980v1_ufig1.gif" ALT="Figure 1"> View larger version (53K): org.highwire.dtl.DTLVardef@1339c89org.highwire.dtl.DTLVardef@16a1d5borg.highwire.dtl.DTLVardef@1ad4631org.highwire.dtl.DTLVardef@db4615_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2025

Systemic translocation of S. aureus Drives Anti-CD4 Autoimmunity in Treated HIV Infection

BackgroundIn 2017, our group first demonstrated that autoimmunity contributes to HIV pathogenesis, even without autoimmune disease. This concept is now broadly recognized, exemplified by the role of autoimmunity in severe COVID-19. In people with HIV (PWH) on suppressive ART, anti-CD4 autoantibodies may impair CD4+ T cell recovery, though the mechanisms driving their production remain unclear. Building on evidence from our group and others that Staphylococcus aureus and its peptidoglycan (PGN) promote autoimmunity, we investigated their contribution to anti-CD4 IgG in HIV. MethodsPlasma from 32 ART-naive PWH, 53 ART-treated PWH, and 32 HIV-negative controls was analyzed for IgG autoantibodies and markers of S. aureus translocation using protein array, ELISA, and microarray. EcoHIV mice were injected intraperitoneally with saline, S. aureus PGN, or Bacillus subtilis PGN. PGN structures were compared by mass spectrometry. ResultsAmong 87 autoantibodies, 40% were elevated in ART-naive PWH and largely normalized by ART; however, anti-CD4 IgGs remained elevated in PWH on ART. Anti-CD4 IgG levels inversely correlated with CD4+ T cell counts in ART-treated PWH and positively with S. aureus translocation. In mice, S. aureus PGN induced anti-CD4 IgGs, reduced gut CD4+ T cells, and promoted surface IgG binding and apoptosis in CD4+ T cells. ConclusionS. aureus and its PGN translocation may drive anti-CD4 autoimmunity and hinder immune recovery in PWH on suppressive ART, highlighting S. aureus colonization as a therapeutic target and supporting the development of competitive probiotic interventions such as Bacillus subtilis.

immunology↗

bioRxiv2025

Burn-induced decreases in soil microbial carbon use efficiency vary across soil types and substrates

Wildfires cause immediate changes in above and belowground carbon (C) stocks in boreal forest ecosystems with long-term repercussions for C cycling. Understanding the role of soil microbes in mediating post-fire C cycling and recovery is an important step to predicting how these ecosystems will respond to novel wildfire regimes caused by climate change. Wildfires can cause large shifts in soil bacterial and fungal community composition that can persist for years post-fire. Less is known about the effects of fire on soil microbial community function, such as C use efficiency (CUE). In this study, we measured the effects of burning on substrate-specific CUE using a laboratory incubation of boreal forest soils. We amended burned and unburned soils with either 13C-labelled ground pine roots or glucose and measured the amount of added substrate C that was incorporated into microbial biomass C versus respired as CO2 in order to calculate CUE. Burning caused a decrease in the amount of soil microbial biomass and respiration derived from soil organic C. Glucose-specific CUE declined with burning, driven by a decrease in glucose-derived microbial biomass. This decrease in glucose-specific CUE following burning correlated with an increase in weighted mean predicted 16S rRNA gene copy number, raising the possibility of using copy number as a proxy for post-fire CUE in boreal forest soils. Overall, pine-specific CUE was lower than glucose-specific CUE, likely reflecting the difference in chemical complexity between the two substrates; burning had a much smaller effect on pine-specific CUE, highlighting the variability of CUE between substrates in burned soils.

ecology↗

bioRxiv2025

Cells stably expressing shRNA against MYO10 display altered cell motility

Myosin-X (MYO10) is an actin-based motor protein involved in cytoskeletal dynamics, membrane interactions, and integrin-mediated adhesion. To investigate MYO10s cellular roles, we generated MYO10 knockdown (MYO10KD) HeLa and COS7 cell lines using lentiviral shRNA. Compared to wild-type cells, both MYO10KD lines showed reduced proliferation and impaired cell migration in wound assays. There were fewer edge filopodia in HeLa cells. Additionally, MYO10KD cells demonstrated increased spreading on laminin-coated substrates, suggesting altered integrin activation and cytoskeletal linkage. Our results reinforce MYO10s importance in cell proliferation, adhesion, and migration; these MYO10KD lines provide an accessible cell culture model for further study of MYO10.

cell biology↗

bioRxiv2025

Litter biota and quality as drivers of litter decomposition in mature oak forests subject to drought or elevated CO2

1.) Increasing atmospheric CO2 concentrations alongside more frequent and severe droughts are key global change factors impacting litter decomposition and global carbon cycles. Yet, we have a poor understanding of how these perturbations impact interactions between initial litter chemical properties and the abiotic and biotic properties of the decomposition environment, especially under field conditions. 2.) We tested how drought and elevated atmospheric CO2 concentrations modify litter decomposition via litter properties and decomposition environment using two separate, long-term manipulative drought or elevated CO2 field experiments in mature oak woodlands. Litterbags were deployed in a reciprocal transplant design within each experiment, where we measured litter mass loss, carbon-biochemistry, C:N ratios, moisture content, and microbial and mesofaunal properties. 3.) We found that litter placed in droughted plots decomposed slower than in control plots and experimental litter derived from elevated CO2 plots decomposed slower over the first three harvests compared to control litter. Under drought, litter mass loss rates and C:N ratio was regulated by initial litter properties and the decomposition environment, while elevated CO2 impacted mass loss via changes in initial litter properties. 4.) Synthesis: We show that drought and elevated atmospheric CO2 can modify the decomposability of litter prior to litterfall and during the subsequent decomposition, highlighting the need to disentangle their individual and interactive effects to better predict how global change factors influence decomposition.

ecology↗