Biology subjects

Bell, S.

Publications and source records attributed to Bell, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Differentiation protocol and maturation shape the axial identity and synaptic state in human iPSC-derived spinal motor neurons

Human induced pluripotent stem cell (iPSC)-derived motor neurons are widely used for disease modeling. Stem cells can be differentiated into motor neurons by exposure to specific patterning morphogens, which can ultimately determine terminal cellular composition and developmental state. We compared two small molecule workflows for human iPSC maturation into motor neurons: a rapid direct protocol (diMN protocol) and an extended protocol (purMN protocol), with both protocols matched for 20 days in maturation medium. While the diMN protocol generated mixed neural cultures, the purMN protocol provided cultures with greater motor neuron enrichment, stronger caudal spinal identity, broader synaptic and cholinergic programs, and reduced progenitor-associated signatures. By extending the purMN protocol to 32 days in maturation media, cultures developed reinforced spinal, postsynaptic, presynaptic, calcium-signaling, and cholinergic features. Across four independent reference frameworks, deconvolution aligned diMN cultures with anterior and progenitor-associated states and purMN cultures with spinal and post-mitotic states. In a microfluidic co-culture system, purMNs formed denser, more highly branched distal neurite networks and produced more innervated acetylcholine receptor clusters compared to diMNs. Revealing how purity and maturation jointly define the transcriptomic and structural state of human iPSC-derived spinal motor neuron cultures will help the field choose optimal models for studies of neurodevelopment and neurodegenerative diseases.

neuroscience↗

bioRxiv2026

Single-cell proteomic maps of human induced pluripotent stem cells and their differentiation into motor neurons

The majority of single cell-studies use RNA to identify the cell state. However, many RNAs are transient and decrease in response to elevated protein to control homeostasis. Thus, final cell states are largely defined by their unique and dynamic protein composition not RNA. Here a single-cell proteomics approach was used to identify the proteomic profile of human induced pluripotent stem cells (iPSCs) before and during their in vitro differentiation to motor neurons. By measuring up to 1000 proteins in each cell, novel clusters of growing iPSCs could be characterized along with a new proteomic pathway that defines motor neuron development. Interestingly, there was a dynamic and cell type-specific discordance between the protein levels and their corresponding messenger RNAs. This lays the foundation for drawing new single-cell proteomic maps of developing human tissues. IN BRIEFIn this article, we report the first single-cell proteomic maps of induced pluripotent stem cells (iPSCs) and their differentiation into motor neurons (MNs). By identifying proteomes of individual cells, we resolve iPSC and MN states, their proteomic, metabolomic and organellar heterogeneity. We show considerable, stage-specific discordance between the transcriptome and the proteome in differentiated neurons.

neuroscience↗

bioRxiv2026

A region-delineated snRNA-seq atlas of mouse spinal cord across lifespan resolves the interaction of normative aging programs with SOD1-G93A ALS

Aging is the strongest risk factor for amyotrophic lateral sclerosis (ALS), yet how normative aging programs intersect with disease mechanisms remain unclear. Here we generated a lifespan-resolved, cell type-and region-specific single-nucleus RNA-sequencing atlas of the mouse spinal cord spanning embryonic development through advanced age in WT mice and end-stage disease in the SOD1-G93A ALS model. This resource enabled systematic comparison of physiological aging trajectories with disease-associated transcriptional changes across spinal cord cell types and rostrocaudal regions. We found that SOD1-G93A transcript and protein states differed markedly across spinal regions during disease onset and progression, and these molecular patterns paralleled the relative resilience of cervical regions and the heightened vulnerability of lumbar regions to degeneration in this transgenic mouse model. Prior to disease onset, we identified reduced ubiquitin expression that primed region-specific disruption of proteostasis in the SOD1-G93A spinal cord. Despite these disease-associated changes, aging-related transcriptional programs were largely preserved across most cell types, arguing against a global acceleration of aging in ALS. Instead, microglia emerged as a key exception, exhibiting accelerated and rewired aging- and disease-associated gene expression modules regulated by MITF and NRF2. Together, these findings provide an anatomically, cellularly, and temporally resolved framework for understanding how aging programs interact with disease-specific pathways to shape regional dysfunction and neurodegeneration in ALS.

neuroscience↗

bioRxiv2025

Human heart organoids reveal a regenerative strategy for mitochondrial disease

The human heart is among the most complex tissues to replicate in vitro, with vascular, neuronal, and immune elements shaping its development and function. Here we describe cardiomorphs, self-organising human cardiac organoids that recapitulate the cellular diversity, structural organisation, vascularisation, and innervation of the myocardium and mature along a developmental trajectory from early cardiogenesis to adult tissue. Using patient-derived cardiomorphs, we establish the first three-dimensional human tissue model of Kearns-Sayre syndrome (KSS), a rare mitochondrial disorder characterised by large-scale mtDNA deletions. KSS-cardiomorphs faithfully reproduce disease-associated metabolic, contractile, and ultrastructural hallmarks. Leveraging this platform, we identify Betaxolol, an FDA-approved selective {beta}1-adrenergic antagonist, as a modulator of mitochondrial quality control. Betaxolol increases intracellular oxygenation, selectively eliminates dysfunctional mitochondria via mitophagy, and promotes biogenesis of functional organelles, restoring contractility in KSS tissues. This dual-action, mutation-agnostic mechanism suggests a therapeutic principle with broad relevance to mitochondrial disease, cardiac pathology, and age-associated decline.

cell biology↗

bioRxiv2025

Seagrass Extent Expansion in the Gulf of Mexico and Northwestern Caribbean (1987-2021)

Historically, the areal extent of seagrass beds in the Gulf of Mexico, Florida peninsula, and Northwestern Caribbean (Mexico and Cuba) have been estimated to cover approximately 35,510 km2. However, the absence of regular monitoring limits our ability to detect interannual variability and up-to-date health conditions, and to respond to stressors, such as degraded water quality. Seagrass areal extent is one of the core Essential Ocean variables (EOV) of the Global Ocean Observing System (GOOS). Resource managers and researchers are interested in how this seagrass extent and the distribution of this habitat changes over time to focus possible action to mitigate impacts of various stressors, such as degraded water quality. In this study, we mapped 19,405 km2 of seagrasses for the region for the period 2019-2021, using satellite imagery from Landsat 5, Landsat 7, Landsat 8, and Sentinel-2. Interannual changes in seagrass areal extent at 17 representative sites indicated that seagrass habitats increased by 12.3% between 1987 and 2021. Sites off the West Florida coast showed the highest increasing rates in seagrass extent (up to 3.1% yr-1) and lowest rate (-0.43% yr-1) was observed in Biscayne Bay, South Florida. Seagrasses in the Mexican Caribbean showed positive extent expansion rates (1.3-1.8% yr-1), while in Texas were stable over the period of study. Continuous observations of seagrasses like these help managers to understand spatial and temporal patterns of change and encourage further studies on seagrass ecology and carbon stocks.

ecology↗

bioRxiv2025

Dynamics of Macrophage Polarization Reveal Unique Phenotypes During Mouse Postpartum Uterine Remodeling

BackgroundMacrophages play essential roles in uterine physiology during pregnancy and the postpartum (PP) period. In various organ systems, macrophages exhibit distinct M1 (pro-inflammatory) and M2 (anti-inflammatory) polarization states, the balance of which is key not only in scarless wound healing but also in pathological fibrosis. While macrophages are central players in PP uterine remodeling, their polarization dynamics during this period and associated spatial distribution remain largely unknown. MethodsUterine tissues were collected from C57BL/6J wild-type mice at various PP days (PPD 1, 3, 7, 14, 21, 28) and non-pregnant controls. Multicolor flow cytometry was used to analyze immune populations and macrophage polarization states. Macrophage polarization was determined using CD86 (M1 marker) and CD206 (M2 marker). Immunofluorescence (IF) and immunohistochemistry (IHC) were used to examine the colocalization of M1 and/or M2 markers alongside F4/80 to assess macrophage polarization status and tissue distribution. ResultsOn PPD1, uterine macrophage numbers were higher compared to all other time points, with significantly increased M2 macrophages (CD86-CD206+) (43% p<0.0001) compared to PPD3 (5.1%), PPD7 (2.4%), PPD14 (2.3%), and non-pregnant (1.9%). A rapid polarization shift to M1 macrophages (CD86+CD206-) occurred on PPD3 (50.6%), PPD7 (66.5%), and PPD14 (58.8%) compared to PPD1 (11.9% p<0.0001). Additionally, there was a trend of increased M2 macrophages on PPD21 (10%) and PPD28 (5%). We observed a unique macrophage subset of mixed phenotype (co-expressing CD86+CD206+) significantly higher on PPD 1 (37.2% p<0.05) compared to NP (7.8%), PPD7 (11.6%), and PPD14 (26.4%). IF co-staining confirmed these dynamics, showing the highest percentage of macrophages co-expressing CD206+F4/80+ on PPD1 (77.2%), significantly higher than all other time points. IHC revealed the specific temporal and spatial distribution of F4/80+ and CD206+ cells within the uterine endometrial stroma adjacent to the myometrial junction in the early PP period. ConclusionsThe predominance of M2-polarized macrophages on PPD1 followed by a rapid shift to M1 phenotype from PPD3 to PPD14 indicates an evolving inflammatory response during the early postpartum period. Repolarization to M2 profile on PPD21, along with increased abundance of a mixed population (M1/M2), uncovers the dynamic complexity of macrophage polarization during PP uterine remodeling, providing new insights into scarless uterine tissue repair.

immunology↗

bioRxiv2025

Human iPSC-derived prostate organoids with germline BRCA2 mutation undergo tumorigenic transformations

The lack of physiologically relevant in vitro prostate models has impeded studies of organ development and prostate tumorigenesis. We reprogrammed peripheral blood mononuclear cells (PBMCs) from individuals with and without pathogenic-germline BRCA2 mutation (MUT_BRCA2, CON_BRCA2) into induced pluripotent stem cells (iPSCs), which showed no differences in morphology, proliferation, or pluripotency markers. Differentiation of MUT_BRCA2 iPSCs into prostate organoids (iPROS) using defined growth factors and signaling molecules resulted in disrupted morphology, impaired polarity, increased proliferation, and elevated prostate-specific antigen (PSA) secretion compared to CON_BRCA2 iPROS. Transcriptomic profiling revealed early prostate cancer (PCa) signatures. Upon exposure to dietary carcinogens, MUT_BRCA2 iPROS showed further PSA elevation, enhanced proliferation, AMACR upregulation, p63 reducetion are markers of aggressive PCa. In vivo, MUT_BRCA2 iPROS formed tumors in immunodeficient mice. This patient-derived iPROS-platform recapitulates human-prostate mopphology and function, models early tumorigenesis events, and provides a valuable tool for studying PCa biology and enabling personalized drug discovery. IN BRIEFIn this study, we developed patients iPSC-derived prostate organoids (iPROS) with or without a pathogenic BRCA2 germline mutation that display human-prostate like morphology and function. MUT_BRCA2 iPROS displayed disrupted morphology, early tumorigenic changes, and formed tumors in mice. Upon carcinogen exposure, they showed markers of aggressive prostate cancer. This platform models early prostate tumorigenesis and enables personalized studies of cancer initiation and therapeutic response.

cancer biology↗

bioRxiv2025

Dynamic Transcriptomic Remodeling in Human Neural Progenitor Cells Reveals Mechanisms for Vision Preservation in Retinitis Pigmentosa Model

Human neural progenitor cells (hNPCs) have shown promise in slowing down retinal degeneration in animal models and are currently being tested in clinical trials for treating retinitis pigmentosa (RP). However, the status of grafted hNPCs and their interaction with host retinal cells over time is largely unknown. Here, we investigated single-cell transcriptomic changes in grafted hNPCs and host retinal cells following injection into a rodent model for RP. Grafted hNPCs and host retinal cells undergo dynamic transcriptomic changes in the degenerative retinal environment. Grafted hNPCs protect vision through multiple mechanisms, including trophic factor support, modulation of metabolic activity, reduction of apoptosis, oxidative stress, and inflammation, alongside extracellular matrix remodeling. CellChat analysis revealed a progressive decline in intercellular signaling and communication strength between hNPCs and host retinal cells over time. This study indicates that enhancing trophic factor supports and improving host retinal environment are key targets to enable long-term vision preservation.

neuroscience↗

bioRxiv2024

NRBP1 pseudokinase binds to and activates the WNK pathway in response to osmotic stress

WNK family kinases are regulated by osmotic stress and control ion homeostasis by activating SPAK and OXSR1 kinases. Using a proximity ligation approach, we found that osmotic stress promotes the association of WNK1 with the NRBP1 pseudokinase and TSC22D2/4 adaptor proteins, results that are confirmed by immunoprecipitation and mass spectrometry and immunoblotting studies. NRBP1 pseudokinase is closely related to WNK isoforms and contains a R{Phi}-motif binding conserved C-terminal (CCT) domain, similar to the CCT domains in WNKs, SPAK and OXSR1. Knockdown or knock-out of NRBP1 markedly inhibited sorbitol-induced activation of WNK1 and downstream components. We demonstrate recombinant NRBP1 can directly induce the activation of WNK4 in vitro. AlphaFold-3 modelling predicts that WNK1, SPAK, NRBP1, and TSC22D4 form a complex, in which two TSC22D4 R{Phi}-motifs interact with the CCTL1 domain of WNK1 and the CCT domain of NRBP1. Our data indicates NRBP1 functions as an upstream activator of the WNK pathway. TeaserNRBP1 functions as a scaffolding component regulating the assembly of a multi-subunit complex, required for the activation of the WNK Lysine Deficient Protein Kinase family in response to osmotic stress. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/628181v2_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@5b37eborg.highwire.dtl.DTLVardef@b4661corg.highwire.dtl.DTLVardef@19bc3e9org.highwire.dtl.DTLVardef@15b052e_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2024

New imaging tools reveal live cellular collagen secretion, fibril dynamics and network organisation.

Although light microscopy has been used to examine the early trafficking of collagen within the cell, much of our understanding of the detailed organisation of cell deposited collagen is from static electron microscopy studies. To understand the dynamics of live cell collagen deposition and fibril organisation, we generated a bright photostable mNGCol12 fusion protein and employed a range of microscopy techniques to follow its intracellular transport and elucidate extracellular fibril formation. Our findings reveal the dynamics of fibril growth and the dynamic nature of collagen network interactions at the cellular level. Notably we observed molecular events that build network organisation, including fibril bundling, bifurcation, directionality along existing fibrils, and looping/intertwining behaviours. Strikingly, mNGCol12 fluorescence intensity maxima can mark a fibril before another growing collagen fibril intersects at this location. Our study shows that N-terminal protease site is not an absolute requirement for collagen fibril incorporation and is, to our knowledge, the first time that cell-directed collagen fibrillogenesis has been visualised at high resolution in real time. The approach paves the way for assessing the dynamic organisation and assembly of collagen into the extracellular matrix in skin models and other tissues during health, ageing and disease.

cell biology↗

bioRxiv2024

Unveiling lipid chemodiversity in root exudates: A comprehensive characterizaton of the exudate metabo-lipidome in Tall Wheatgrass

The rhizosphere, where plant roots meet soil, is a hub of biogeochemical activity with ecosystem impacts on carbon stocks. Root derived carbon has been found to contribute more to soil carbon stocks than aboveground litter. Nonetheless, the molecular chemodiversity of root exudates remains poorly understood due to limited characterization and annotation. Here our goal was to discover the molecular chemodiversity of metabolites and lipids in root exudates to advance our understanding of plant root inputs belowground. We worked with mature, field-grown tall wheatgrass (Thinopyrum ponticum) and optimized exudate collection protocols to enable the capture of non-polar lipids in addition to polar and semi-polar metabolites. Rates of carbon input via hydrophobic exudates were approximately double that of aqueous exudates and carbon/nitrogen ratios were markedly higher in hydrophobic compared to aqueous exudates, emphasizing the importance of lipids, due to their high carbon content. To maximize molecular coverage of exudate chemodiversity, we used liquid chromatography coupled tandem mass-spectrometry for paired untargeted metabolomics and lipidomics or metabo-lipidomics. We substantially increased the characterization of exudate chemodiversity by employing both tandem mass spectral library searching and deep learning-based chemical class assignment. Notably, in this unprecedented characterization of intact lipids in root exudates, we discovered a diverse variety of lipids, including substantial levels of triacylglycerols ([~]19 g/g fresh root per min), fatty acyls, sphingolipids, sterol lipids, and glycerophospholipids. Comparison of the root exudate and tissue lipidomes revealed minimum glycerophospholipids in exudates, suggesting the exudate protocol did not extract lipids from root cell membranes.

plant biology↗

bioRxiv2023

Aging and freezing of active nematic dynamics of cancer-associated fibroblasts by fibronectin matrix remodeling

Cancer-associated fibroblasts (CAFs) are one of the most abundant cell types in tumor stroma. Exhibiting an elongated morphology, CAFs align with each other, closely resembling nematic ordering in liquid crystal physics. CAFs play a pivotal role in the genesis and remodeling of the extracellular matrix (ECM), with ECM proteins, especially fibronectin, reciprocally modulating CAF alignment and coherence. Yet, the intricate feedback loops between fibronectin deposition and CAF structuring remain largely unexplored. Here, we combined CAF live imaging, traction force microscopy, ECM microfabrication, and theoretical modeling to assess how the ECM influences the dynamics of nematically ordered CAFs. We found that CAFs dynamically orchestrate a fibronectin network that mirrors their nematic ordering. Over time, this passive nematic ordering of fibronectin, in turn, steers CAF rearrangement. Contrary to most cellular systems, where defects remain dynamic at a steady state, the ECM/CAF interplay profoundly alters the behavior of both CAF and ECM nematics, leading to aging-massive slowdown, and even freezing of defect dynamics. This results in a CAFs capsule where aligned areas and defects are spatially and temporally fixed, yet active, exerting forces at the substate and transmitting forces between cells. Functionally, while defects may be permissive, it is the fibronectin loss-induced fluidization of the CAF capsule that critically undermines its barrier function.

cell biology↗

bioRxiv2023

Targeting cancer with small molecule pan-KRAS degraders

Despite the high prevalence of cancers driven by KRAS mutations, to date only the G12C mutation has been clinically proven to be druggable via covalent targeting of the mutated cysteine amino acid residue (1). However, in many cancer indications other KRAS mutations, such as G12D and -V, are far more prevalent and small molecule concepts that can address a wider variety of oncogenic KRAS alleles are in high clinical demand (2). Here we show that a single small molecule can be used to simultaneously and potently degrade 13 out of 17 of the most prevalent oncogenic KRAS alleles, including those not yet tractable by inhibitors. Compared with inhibition, degradation of oncogenic KRAS results in more profound and sustained pathway modulation across a broad range of KRAS mutant cell lines. As a result, KRAS degraders inhibit growth of the majority of cancer cell lines driven by KRAS mutations while sparing models without genetic KRAS aberrations. Finally, we demonstrate that pharmacological degradation of oncogenic KRAS leads to tumour regression in vivo. Together, these findings unveil a new path towards addressing KRAS driven cancers with small molecule degraders. One-Sentence SummaryThe most prevalent KRAS variants which drive tumour growth in a major share of cancer patients can be targeted with a single small molecule degrader.

pharmacology and toxicology↗

bioRxiv2023

A novel human iPSC model of COL4A1/A2 small vessel disease unveils a key pathogenic role of matrix metalloproteinases in extracellular matrix abnormalities

Abstract/SummaryCerebral small vessel disease (SVD) affects the small vessels in the brain and is a leading cause of stroke and dementia. Emerging evidence supports a role of the extracellular matrix (ECM), at the interface between blood and brain, in the progression of SVD pathology but this remains poorly characterized. To address ECM role in SVD, we developed a co-culture model of mural and endothelial cells using human induced pluripotent stem cells from patients with COL4A1/A2 SVD-related mutations. This model revealed that these mutations induce apoptosis, migration defects, ECM remodelling and transcriptome changes in mural cells. Importantly, these mural cell defects exert a detrimental effect on endothelial cells tight junctions through paracrine actions. COL4A1/A2 models also express high levels of matrix metalloproteinases (MMP) and inhibiting MMP activity partially rescues the ECM abnormalities and mural cell phenotypic changes. These data provide a basis for targeting MMP as a therapeutic opportunity in SVD. HighlightsO_LIA novel human iPSC-derived model of genetic SVD due to collagen IV (COL4A1/A2) mutations is described C_LIO_LIMural cells expressing COL4A1/A2 mutations have prominent ECM abnormalities as seen in patients and mouse models and contribute to endothelial cells defects C_LIO_LIECM and endothelial cells abnormalities can be rescued by MMP inhibition in the COL4A1/A2 model C_LI

cell biology↗

bioRxiv2021

An extremes of phenotype approach confirms significant genetic heterogeneity in patients with ulcerative colitis.

Ulcerative colitis (UC) is a major form of inflammatory bowel disease with increasing global incidence. There is significant phenotypic heterogeneity defined by a range of clinical variables including age of onset and disease extent. Clinical outcomes range from long-term remission on minimal therapy to surgical resection. Close to 70% of UC risk can be attributed to genetics and understanding the genetic mechanisms contributing to this risk and disease heterogeneity is vital for understanding disease pathogenesis and improving patient outcomes through targeted screening and therapies. This study aims to characterise the genetic heterogeneity of UC by identifying genomic risk variants specific to mild and/or severe forms of UC, exploring variations in the effect size of known risk variants and assessing the clinical value of a genetic risk score (GRS). We conducted genome-wide association (GWA) analyses in 287 patients with mild UC, 311 patients with severe UC and 583 age- and gender-matched controls. Odds ratios (OR) for mild vs control, severe vs control and combined mild and severe UC vs control were calculated. Using the combined UC data, two independent loci in the HLA region reached genome-wide significance. An additional genome-wide significant signal on chromosome 1 was identified in severe cases only. OR for known risk loci varied between mild and severe patients and were similar to previously published results. Effect estimates from the most recent UC GWA meta-analysis were used to calculate a GRS for each individual. A higher mean GRS was observed in both mild and severe UC cases compared to controls however, there was no difference between the mean GRS for mild and severe UC. Heterogeneity in effect sizes of UC associated variants between mild and severe disease burden suggests the presence of genetically distinct signatures. While large consortium data are needed to identify genome-wide significant variants, additional risk loci may be identified by targeted recruitment of individuals with a history of severe disease. Author SummaryUlcerative colitis (UC) is a chronic and often debilitating form of inflammatory bowel disease affecting approximately 0.3% of the population in industrialized economies. The disease displays significant clinical heterogeneity including age at presentation, disease severity, and the propensity to develop disease-related complications. Several previous studies have demonstrated the heritability of UC, identifying over 30 loci specific to the disease. The majority of these loci have small to modest effect sizes other than those within the Human Leucocyte Antigen (HLA) region on chromosome 6. Using stringent clinical criteria for defining mild and severe forms of UC in an extremes of phenotype approach, we undertook a genome wide association study in a dataset of 1222 participants to investigate genetic heterogeneity in this disease. We demonstrated substantial differences in genetic associations in severe UC as compared to mild UC. While over 2,000 SNPs achieved genome-wide significance in the severe UC analysis, none reached significance for mild UC. These results were reflected in significant differences in odds ratios. We identified Complement Factor B (CFB) as a potential susceptibility gene for severe UC in the Caucasian population with additional tissue gene expression demonstrating a positive correlation with disease severity.

genetics↗

bioRxiv2021

Rosin Soap Exhibits Virucidal Activity

Chemical methods of virus inactivation are used routinely to prevent viral transmission in both a personal hygiene capacity but also in at-risk environments like hospitals. Several virucidal products exist, including hand soaps, gels and surface disinfectants. Resin acids, which can be derived from Tall oil produced from trees, have been shown to exhibit anti-bacterial activity. However, whether these products or their derivatives have virucidal activity is unknown. Here, we assessed the capacity of Rosin soap to inactivate a panel of pathogenic mammalian viruses in vitro. We show that Rosin soap can inactivate the human enveloped viruses: influenza A virus (IAV), respiratory syncytial virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). For IAV, rosin soap could provide a 100,000-fold reduction in infectivity. However, Rosin soap failed to affect the non-enveloped encephalomyocarditis virus (EMCV). The inhibitory effect of Rosin soap against IAV infectivity was dependent on its concentration but not dependent on incubation time nor temperature. Together, we demonstrate a novel chemical inactivation method against enveloped viruses, which could be of use in preventing virus infections in certain settings. ImportanceViruses remain a significant cause of human disease and death, most notably illustrated through the current Covid-19 pandemic. Control of virus infection continues to pose a significant global health challenge to the human population. Viruses can spread through multiple routes, including via environmental and surface contamination where viruses can remain infectious for days. Methods to inactivate viruses on such surfaces may help mitigate infection. Here we present evidence identifying a novel virucidal product in Rosin soap, which is produced from Tall oil from coniferous trees. Rosin soap was able to rapidly and potently inactivate influenza virus and other enveloped viruses.

microbiology↗

bioRxiv2021

Animal lifestyle changes acceptable mass limits for attached tags

O_LIAnimal-attached devices have transformed our understanding of vertebrate ecology. To minimize tag-related harm for these studies, researchers have long advocated that tag masses should not exceed 3% of the animals body mass. However, this proposition ignores tag forces generated as a result of animal movement. C_LIO_LIUsing data from collar-attached accelerometers on diverse free-ranging terrestrial animals, we detail a tag-based acceleration method (TbAM) in which we quantify animal athleticism in terms of fractions of animal movement time devoted to different collar-recorded accelerations. The varying accelerations are converted to forces imposed on the animals based on the acceleration and tag mass and allow derivation of defined force limits, including those amounting to 3% of the animals mass, for specified fractions of any animals active time. C_LIO_LIWe demonstrate how species athleticism is the principal determinant of tag forces, whereas body mass is of little importance. Forces exerted by 3% tags were mostly equivalent to 4-19% of the animals masses during moving, with a maximum of 54% in a hunting cheetah. Cumulative frequency curves of tag acceleration for periods when animals were active, all showed a characteristic sigmoid pattern, which was displaced further to the right as higher acceleration activities accounted for an increasing proportion of any animals time. Specifying that tags should exert forces that are less than 3% of the animals body mass for 95% of the time led to corrected tag masses constituting between 1.6% and 2.98% of our study animals masses, with values depending on animal athleticism. C_LIO_LIRecognition that animal athleticism affects tag forces of their carriers fundamentally changes how acceptable tag mass limits should be determined by ethics bodies. In order to have a scientifically robust acceptable threshold to limit the forces experienced by an animal carrier, we suggest practitioners derive a similar cumulative acceleration profile for their study species and use a minimum of the 95% limits on the plot (although higher limits may be more appropriate). C_LI

zoology↗

bioRxiv2021

cellxgene: a performant, scalable exploration platform for high dimensional sparse matrices

Quickly and flexibly exploring high-dimensional datasets, such as scRNAseq data, is underserved but critical for hypothesis generation, dataset annotation, publication, sharing, and community reuse. cellxgene is a highly generalizable, web-based interface for exploring high dimensional datasets along categorical, continuous and spatial dimensions, as well as feature annotation. cellxgene is differentiated by its ability to performantly handle millions of observations, and bridges a critical gap by enabling computational and experimental biologists to iteratively ask questions of private and public datasets. In doing so, cellxgene increases the utility and reusability of datasets across the single-cell ecosystem. The codebase can be accessed at https://github.com/chanzuckerberg/cellxgene. For questions and inquiries, please contact cellxgene@chanzuckerberg.com.

systems biology↗