Biology subjects

Collins, S.

Publications and source records attributed to Collins, S..

At least 19 recordsLinked to original sources

bioRxiv2026

An ice-bucket challenge: investigating ice algae physiology in laboratory microcosms.

John Raven pioneered the field of algae ecophysiology, advancing our understanding of cellular resource economics, carbon acquisition, and energy allocation. His work laid the foundation for investigating integrative physiology, linking growth-survival trade-offs across diverse environments. The sea ice habitat provides an excellent framework to continue the research John championed. With steep temperature-salinity gradients, algae survival requires a shift in physiology that we are only beginning to understand. We developed two small scale, reproducible icecosms to investigate physiological changes associated with incorporation into sea ice and survival potential post-melt. Fragilariopsis cylindrus and Nitzschia frigida, known for their association with the ice environment, and Porosira glacialis, known for its association with the ice edge, were used to mechanistically link physical properties with algal physiology and post-melt survival. We observe incorporation into the ice of F. cylindrus and N. frigida alongside vertical photophysiological profiles of F. cylindrus revealing inhospitable conditions in the top compared to the bottom layers of ice. N. frigida and P. glacialis remain viable within the ice and retain the capacity to seed populations following melt. Our results establish icecosms as experimental framework to investigate ecophysiological responses of sea ice algae and provide a foundation toward ecological and evolutionary questions.

ecology↗

bioRxiv2026

Single-cell resolution of resection-dependent chromatin accessibility in response to DNA double-strand breaks reveals specific gene expression programs

Chromatin structure is extensively modified and remodeled to allow for efficient signaling and repair of DNA double-strand breaks (DSBs), a process which is influenced by the nature and properties of the damaged locus or the repair pathway involved. However, the extent of cell-to-cell variability in these DSB-induced chromatin modifications remains poorly characterized. Here, we report how chromatin accessibility is reshuffled at the damaged locus at high resolution. Notably, we identify a long-range increase in chromatin accessibility which is dependent on functional resection. We report that resection-dependent chromatin remodeling events at individual damaged loci display significant heterogeneity in single cells which are only partly explained by the cell cycle, and can frequently be detected as asymmetric and unidirectional. Moreover, we identify strong transcriptional phenotypes upon sustained DNA damage as well as subpopulations of S and G2/M cells for which similar resection-dependent chromatin accessibility patterns occur simultaneously at multiple DSBs. These coordinated chromatin accessibility patterns at multiple DSBs are associated with specific gene expression programs, including DNA damage checkpoint signaling, inflammation and apoptosis. Altogether, our results highlight the heterogeneity in chromatin remodeling during DSB repair and suggest unexpected links between DNA end resection and specific gene expression programs mounted in response to genotoxic stress.

cell biology↗

bioRxiv2026

Simulation-guided design of exotendons to reduce the energetic cost of running

A passive device that attaches to the feet, called an exotendon, can reduce the energetic cost of running at moderate speeds, but its efficacy and optimal design parameters at higher speeds are unknown. Identifying optimal parameters at new speeds experimentally would require many experimental trials with different exotendon designs, which is challenging for participants at higher running speeds. We developed a muscle-driven simulation framework to predict the effect of various exotendon designs on the energetic cost of running at an experimentally untested speed (4 m/s). We used these predictions to select four designs, which we evaluated experimentally as users ran at this speed. The framework correctly predicted that an exotendon that reduced energetic cost at 2.7 m/s would also reduce energetic cost at 4 m/s (10% predicted vs. 5.7% measured) and that a short, stiff exotendon and a long, compliant exotendon would not significantly reduce energetic cost. However, exotendon parameters predicted by the simulation to maximize energetic savings did not significantly reduce energetic cost when evaluated experimentally. There was variability between participants in both the magnitude of maximum energy savings and the exotendon condition associated with those savings. In a 5-km time trial performed with and without the exotendon condition that elicited the largest energy savings for each participant during the experiment, we observed a lower average heart rate (-3.9 {+/-} 3.8 beats/min; P=0.03; mean {+/-} standard deviation) and increased cadence (15.9 {+/-} 9.6 steps/min; P=0.002) when participants ran with the exotendon but did not observe a statistically significant difference in finishing time (-13.5 {+/-} 24.6 sec; P=0.3). These results demonstrate exotendons can reduce energetic cost across multiple running speeds and that predictive simulations provide a framework for guiding experiments to evaluate assistive device designs. Author summaryDesigning assistive devices that help people move more efficiently usually requires many experimental trials. These studies can be time-consuming and physically demanding, especially when testing multiple device designs. In this study, we explored whether computer simulations could help guide the design of an assistive device for running called an exotendon. The exotendon is a simple elastic band that connects the feet and can help runners use less energy. Previous experiments showed that the device reduces the energy needed to run at moderate speeds, but it was unclear whether it would also work at faster speeds or which design would lead to energetic savings. We first used simulations of human running to test many possible exotendon designs at a faster speed. These simulations allowed us to identify promising designs before conducting experiments. We then tested a small number of these designs with runners. The experiments confirmed that the exotendon can reduce the energy required to run at faster speeds, although the efficacy of different designs varied between individuals. Our results show that computer simulations can help researchers rapidly evaluate a variety of assistive device ideas and focus experimental testing on the most promising designs.

bioengineering↗

bioRxiv2026

Intra-annual precipitation variability mutes or magnifies the impact of wet and dry years on plant biomass.

As the atmosphere warms, both the amount and timing of precipitation are changing, but how those two trends interact to influence plant growth remains unresolved. Using 5-15 years of data from 48 globally distributed grassland sites, we quantified how the temporal distribution of precipitation within the year (evenness) interacts with annual precipitation amount and nutrient limitation to influence plant biomass. Annual precipitation anomalies had a large influence on plant biomass when intra-annual precipitation was more evenly distributed (frequent small events) and little impact when less even (infrequent large events). This relationship was consistent across aridity gradients and nutrient limitations and strongest in systems with warm wet seasons. Our work shows that the response of plant systems to changes in annual precipitation amount are largely dependent on how evenly it is temporally distributed.

ecology↗

bioRxiv2026

Variation in survival and growth following prolonged darkness in a polar diatom species

O_LIPhytoplankton are the major primary producers in the Southern Ocean, participate in the global carbon cycle, nutrient cycles, and are at the base of the food-web. These polar ecosystems are unique in their extended periods of darkness in the winter. C_LIO_LIProlonged darkness has the potential to exert selection that affects the composition of diatom communities if there is differential survival of diatoms in the dark, variation in population growth rates in subsequent light periods, or both. C_LIO_LIWe tested whether prolonged darkness has the potential to exert within-species selection on a model polar diatom species by exposing 5 strains of the polar diatom Porosira glacialis to prolonged darkness at two different temperatures in the laboratory. We measured population survival in the dark, growth rate upon re-illumination, and between strain variability in these traits. C_LIO_LIWe found a pronounced decline in survival and growth rate with time spent in the dark, as well as important intraspecific variation in these. C_LIO_LIHigher temperature exacerbated declines in growth and survival. C_LIO_LIOur results show that the darkness of polar night can exert selection within diatom species, with implications for phytoplankton community composition and subsequent impacts on Southern Ocean biogeochemical cycles. C_LI

ecology↗

bioRxiv2025

Phylogenomics supports monophyly of marsupial crustaceans: a journey to direct development

Peracarida (marsupial crustaceans) represent one of the most diverse and ecologically important crustacean groups, yet their evolutionary relationships have long been debated. Here, we present the most comprehensive phylogenomic analysis of Peracarida to date, incorporating the relict taxa Thermosbaenacea, Mictacea, Ingolfiellida, and Spelaeogriphacea for the first time in a phylogenomic framework. Our results robustly confirm peracarid monophyly and recover a well-supported clade uniting Mancoida (Isopoda, Tanaidaca, Cumacea), Mictacea, and Spelaeogriphacea. We propose the new taxon Panmancoida to encompass this expanded lineage defined by shared developmental and morphological traits. The inferred phylogeny further suggests that peracarid evolution involved a transition from an intermediate "pseudodirect" developmental mode to the direct development seen in most lineages. We further show that the shift to extensive brood care within the marsupium, accompanied by the loss of a free-swimming larval stage, may have accelerated rates of molecular evolution across lineages. Together, these findings provide a robust evolutionary framework for this major malacostracan lineage and highlight how key reproductive innovations reshaped the genomic and life-history trajectories of the marsupial crustaceans.

evolutionary biology↗

bioRxiv2025

Wnt5a-mediated Adipo-Cardiac Interorgan Communication in HFpEF

BackgroundObesity is an important risk factor in heart failure with preserved ejection fraction (HFpEF), but the precise mechanisms that drive obesity-associated cardiac remodeling are not well understood. Our previous work has shown that increased expression of the natriuretic peptide clearance receptor (Nprc) may drive cardiac remodeling in response to high fat diet. In this study, we hypothesized that Nprc plays a central role in preventing and reversing experimental HFpEF. MethodsNprc knockout mice were generated to induce global, cardiomyocyte-specific, or adipocyte-specific disruption of the Nprc (Npr3) gene. HFpEF was induced by the 2-hit stress of L-NAME and high fat diet. Outcomes measured included echocardiography, exercise endurance, invasive catheterization, and histologic assessment. Differential gene expression in adipocyte Nprc knockout visceral adipose tissue was investigated via bulk RNA sequencing and validated by RT-qPCR and culture of H9C2 cells with or without Wnt5a treatment. Adipocyte-mediated Wnt ligand release was interrupted in vivo via LGK974 injection in mice subjected to HFpEF conditions. ResultsGlobal inducible Nprc knockout prevented and reversed structural, hemodynamic, echocardiographic, and exercise tolerance features of HFpEF. This effect was found to be driven by adipocyte-specific, not cardiomyocyte-specific Nprc expression. Bulk RNA sequencing of adipocyte-specific Nprc knockout in peri-gonadal visceral adipose tissue identified downregulation of several secretory pathways, including Wnt pathways. Wnt5a was identified as one of the most downregulated genes by RNA sequencing and specifically validated by qPCR. Wnt5a exposure increased cardiomyocyte hypertrophy in vitro, and LGK974 (PORCN inhibitor) treatment in vivo decreased circulating Wnt5a levels and improved cardiac remodeling in HFpEF. ConclusionsOur study identifies a novel crosstalk mechanism between cardiomyocytes and adipocytes in obesity-associated HFpEF driven by natriuretic peptide-mediated inhibition of release of Wnt5a from adipocytes.

molecular biology↗

bioRxiv2025

Salt-inducible kinase inhibition promotes weight loss and improves the diastolic function of obesity-related heart failure with preserved ejection fraction in mice

BackgroundObesity negatively impacts cardiac function and is closely associated with heart failure with preserved ejection fraction (HFpEF). Salt-inducible kinases (SIKs) are critical regulators of energy metabolism and cardiovascular function. Small molecule SIK inhibitors have been developed but their effect in treating obesity-related HFpEF remains unexplored. We recently discovered that pharmacological SIK inhibition promotes the adipose tissue thermogenesis and mitochondrial biogenesis gene program. We reason that targeting SIKs to treat obesity-related complications would be beneficial for HFpEF. MethodsWe employed a preclinical HFpEF mouse model induced by two-hit stress of high-fat diet (HFD) and nitric oxide synthase (NOS) inhibition using L-NAME in drinking water. Eight-week-old C57BL/6J mice received a regular low-fat chow diet or HFD/L-NAME for 5 weeks and were treated with vehicle or a pan-SIK inhibitor YKL-05-099 (YKL) via daily intraperitoneal injection in the last 4 weeks. Body weight and parameters of adiposity, energy balance and glucose tolerance were assessed. Cardiovascular function was characterized by echocardiography and in vivo pressure-volume loop hemodynamic analysis. Myocardial transcriptomic data were analyzed to determine if changes in SIK gene expression are associated with human HFpEF. ResultsYKL treatment limits body weight gain mainly by reducing the fat mass in obese HFpEF mice. YKL-treated mice show better glucose tolerance, enhanced adipose tissue browning and decreased lipid deposition. YKL-treatment mice demonstrate preserved left ventricular (LV) ejection fraction, reduced LV filling pressure and improved diastolic function. Myocardial expression of SIK1, SIK2, and SIK3 mRNA is down-regulated in patients with HFpEF. However, higher SIK mRNA expression is associated with a subgroup of HFpEF patients that has a greater risk for HF hospitalization and/or death. ConclusionsTaken together, our study reveals a pathological role for SIKs in obesity-related HFpEF and suggests that pharmacological SIK inhibition would be a disease-modifying strategy for obese HFpEF, for which evidence-based therapy has been limited.

physiology↗

bioRxiv2024

Endogenous neuronal DNA double-strand breaks are not sufficient to drive brain aging and neurodegeneration

Loss of genomic information due to the accumulation of somatic DNA damage has been implicated in aging and neurodegeneration1-3. Somatic mutations in human neurons increase with age4, but it is unclear whether this is a cause or a consequence of brain aging. Here, we clarify the role of endogenous, neuronal DNA double-strand breaks (DSBs) in brain aging and neurodegeneration by generating mice with post-developmental inactivation of the classical non-homologous end-joining (C-NHEJ) core factor Xrcc4 in forebrain neurons. Xrcc4 is critical for the ligation step of C-NHEJ and has no known function outside of DSB repair5,6. We find that, unlike their wild-type counterparts, C-NHEJ-deficient neurons accumulate high levels of DSB foci with age, indicating that neurons undergo frequent DSBs that are typically efficiently repaired by C-NHEJ across their lifespan. Genome-wide mapping reveals that endogenous neuronal DSBs preferentially occur in promoter regions and other genic features. Analysis of 3-D genome organization shows intra-chromosomal clustering and loop extrusion of neuronal DSB regions. Strikingly, however, DSB accumulation caused by loss of C-NHEJ induces only minor epigenetic alterations and does not significantly affect gene expression, 3-D genome organization, or mutational outcomes at neuronal DSBs. Despite extensive aging-associated accumulation of neuronal DSBs, mice with neuronal Xrcc4 inactivation do not show neurodegeneration, neuroinflammation, reduced lifespan, or impaired memory and learning behavior. We conclude that the formation of spontaneous neuronal DSBs caused by normal cellular processes is insufficient to cause brain aging and neurodegeneration, even in the absence of C-NHEJ, the principal neuronal DSB repair pathway.

neuroscience↗

bioRxiv2024

Replicating retroviral delivery of an IL-15 superagonist improves antitumor immunity and long-term survival in poorly immunogenic glioblastoma models

Glioblastoma (GBM) is the most lethal primary brain neoplasm due to its highly immunosuppressive microenvironment and resistance to conventional therapies. To overcome this challenge, we engineered a replicating retrovirus (RRV) to deliver a superagonist interleukin-15 receptor-linked fusion protein (RLI) directly to tumor cells, engineering them into local immunotherapy biofactories. This strategy leverages the tumor-selective replication of RRV to achieve localized and sustained RLI expression within the tumor microenvironment. In two orthotopic poorly immunogenic GBM mouse models, intratumoral administration of RRV RLI significantly reduced tumor growth and prolonged survival compared to controls, with some mice achieving long-term remission and demonstrating immunologic memory upon rechallenge. Transcriptomic and flow cytometric analyses revealed that RRV RLI treatment enhanced infiltration and activation of CD8 T cells, NK cells, and upregulated antigen presentation pathways within the tumor microenvironment. Depletion studies indicated that the therapeutic efficacy of RRV RLI is dependent on both CD4 and CD8 T cells. Notably, combining RRV RLI with the GBM standard of care chemotherapeutic agent temozolomide (TMZ) synergistically improved survival outcomes. Subsequent single-cell RNA and T cell receptor sequencing identified enhanced effector cell activation, antigen presentation, and clonal T cell expansion in the combination therapy group. Further T cell receptor analysis and clustering implied a tumor-specific immune response rather than one targeting the viral delivery vehicle, suggesting that this therapeutic approach could be reapplied without eliciting anti-vector immunity. Our findings suggest that RRV-mediated delivery of RLI effectively transforms GBM tumors into immunostimulatory hubs, eliciting a potent anti-tumor immune response. This novel viral immunotherapy holds significant promise for clinical translation in the treatment of GBM and other difficult-to-treat solid tumors.

cancer biology↗

bioRxiv2024

Extensive haplotype diversity in a butterfly colour pattern supergene is fuelled by incomplete recombination suppression

Supergenes can evolve when recombination-suppressing mechanisms like inversions promote co-inheritance of alleles at two or more polymorphic loci that affect a complex trait. Theory shows that such genetic architectures can be favoured under balancing selection or local adaptation in the face of gene flow, but they can also bring costs associated with reduced opportunities for recombination. These costs may in turn be offset by rare gene flux between inverted and ancestral haplotypes, with a range of possible outcomes. We aimed to shed light on these processes by investigating the BC supergene, a large genomic region comprising multiple rearrangements associated with three distinct wing color morphs in Danaus chrysippus, a butterfly known as the African monarch, African queen and plain tiger. Using whole-genome resequencing data from 174 individuals, we first confirm the effects of BC on wing color pattern: background melanism is associated with SNPs in the promoter region of yellow, within an inverted subregion of the supergene, while forewing tip pattern is most likely associated with copy number variation in a separate subregion of the supergene. We then show that haplotype diversity within the supergene is surprisingly extensive: there are at least six divergent haplotype groups that experience suppressed recombination with respect to each other. Despite high divergence between these haplotype groups, we identify an unexpectedly large number of natural recombinant haplotypes. Several of the inferred crossovers occurred between adjacent inversion modules, while others occurred within inversions. Furthermore, we show that new haplotype groups have arisen through recombination between two pre-existing ones. Specifically, an allele for dark coloration in the promoter of yellow has recombined into distinct haplotype backgrounds on at least two separate occasions. Overall, our findings paint a picture of dynamic evolution of supergene haplotypes, fuelled by incomplete recombination suppression.

evolutionary biology↗

bioRxiv2024

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology

BackgroundApolipoprotein E {varepsilon}4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimers disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimers Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects. MethodsWe introduced the R136S variant into mouse Apoe (ApoeCh) and investigated its effect on the development of AD-related pathology using the 5xFAD model of amyloidosis and the PS19 model of tauopathy. We used immunohistochemical and biochemical analysis along with single-cell spatial transcriptomics and proteomics to explore the impact of the ApoeCh variant on AD pathological development and the brains response to plaques and tau. ResultsIn 5xFAD mice, ApoeCh enhances a Disease-Associated Microglia (DAM) phenotype in microglia surrounding plaques, and reduces plaque load, dystrophic neurites, and plasma neurofilament light chain. By contrast, in PS19 mice, ApoeCh suppresses the microglial and astrocytic responses to tau-laden neurons and does not reduce tau accumulation or phosphorylation, but partially rescues tau-induced synaptic and myelin loss. We compared how microglia responses differ between the two mouse models to elucidate the distinct DAM signatures induced by ApoeCh. We identified upregulation of antigen presentation-related genes in the DAM response in a PS19 compared to a 5xFAD background, suggesting a differential response to amyloid versus tau pathology that is modulated by the presence of ApoeCh. ConclusionsThese findings highlight the ability of the ApoeCh variant to modulate microglial responses based on the type of pathology, enhancing DAM reactivity in amyloid models and dampening neuroinflammation to promote protection in tau models. This suggests that the Christchurch variants protective effects likely involve multiple mechanisms, including changes in receptor binding and microglial programming.

neuroscience↗

bioRxiv2024

TET2 regulates early and late transitions in exhausted CD8+ T-cell differentiation and limits CAR T-cell function

CD8+ T-cell exhaustion hampers disease control in cancer and chronic infections and limits efficacy of T-cell-based therapies, such as CAR T-cells. Epigenetic reprogramming of CAR T-cells by targeting TET2, a methylcytosine dioxygenase that mediates active DNA demethylation, has shown therapeutic potential; however, the role of TET2 in exhausted T-cell (TEX) development is unclear. In CAR T-cell exhaustion models and chronic LCMV infection, TET2 drove the conversion from stem cell-like, self-renewing TEX progenitors towards terminally differentiated and effector (TEFF)-like TEX. In mouse T-cells, TET2-deficient terminally differentiated TEX retained aspects of TEX progenitor biology, alongside decreased expression of the transcription factor TOX, suggesting that TET2 potentiates terminal exhaustion. TET2 also enforced a TEFF-like terminally differentiated CD8+ T-cell state in the early bifurcation between TEFF and TEX, indicating a broad role for TET2 in mediating the acquisition of an effector biology program that could be exploited therapeutically. Finally, we developed a clinically actionable strategy for TET2- targeted CAR T-cells, using CRISPR/Cas9 editing and site-specific adeno-associated virus transduction to simultaneously knock-in a CAR at the TRAC locus and a functional safety switch within TET2. Disruption of TET2 with this safety switch in CAR T-cells restrained terminal TEX differentiation in vitro and enhanced anti-tumor responses in vivo. Thus, TET2 regulates pivotal fate transitions in TEX differentiation and can be targeted with a safety mechanism in CAR T-cells for improved tumor control and risk mitigation. One Sentence SummaryModulation of exhausted CD8+ T-cell differentiation by targeting TET2 improves therapeutic potential of CAR T-cells in cancer.

immunology↗

bioRxiv2024

Wild bird mass mortalities in eastern Canada associated with the Highly Pathogenic Avian Influenza A(H5N1) virus, 2022

In 2022, a severe outbreak of clade 2.3.4.4b Highly Pathogenic Avian Influenza (HPAI) H5N1 virus resulted in unprecedented mortality among wild birds in eastern Canada. Tens of thousands of birds were reported sick or dead, prompting a comprehensive assessment of mortality spanning the breeding season between April 1 and September 30, 2022. Mortality reports were collated from federal, Indigenous, provincial, and municipal agencies, the Canadian Wildlife Health Cooperative, non-governmental organizations, universities, and citizen science platforms. A scenario analysis was conducted to refine mortality estimates, accounting for potential double counts from multiple sources under a range of spatial and temporal overlap. Correcting for double counting, an estimated 40,966 wild birds were reported sick or dead in eastern Canada during the spring and summer of 2022. Seabirds and sea ducks, long-lived species that are slow to recover from perturbations, accounted for 98.7% of reported mortalities. Mortalities were greatest among Northern Gannets (Morus bassanus; 26,193), Common Murres (Uria aalge; 8,133), and American Common Eiders (Somateria mollissima dresseri; 1,945), however, these figures underestimate total mortality as they exclude unreported deaths on land and at sea. In addition to presenting mortality estimates, we compare mortalities with known population sizes and trends and make an initial assessment of whether population-level impacts are possible for the Northern Gannet, a species that has suffered significant global mortality, and two harvested species, Common Murre and American Common Eider, to support management decisions. We hypothesize that population-level impacts in eastern Canada are possible for Northern Gannets and American Common Eiders but are unlikely for Common Murres. This study underscores the urgent need for further research to understand the broader ecological ramifications of the HPAI outbreak on wild bird populations.

zoology↗

bioRxiv2023

Bi-allelic variants in WDR47 lead to neuronal loss causing a rare neurodevelopmental syndrome with corpus callosum dysgenesis in humans.

The corpus callosum (CC) is the largest interhemispheric connection that is largely formed by the axons of layer 2/3 callosal projection neurons (CPNs) through a series of tightly regulated cellular events, including neuronal specification, migration, axon extension and branching. Defects in any of those steps may prevent the proper development of the corpus callosum resulting in a spectrum of disorders collectively referred to as corpus callosum dysgenesis (CCD). Here, we report four unrelated families carrying bi-allelic variants in WDR47 presenting with CCD together with other neuroanatomical phenotypes such as microcephaly, cerebellar abnormalities and hydrocephalus. Using a combination of in vitro and in vivo mouse models and complementation assays, we show that independently from its previously identified functions in neuronal migration and axonal extension, WDR47 is required for survival of callosal neurons by contributing to the maintenance of mitochondrial and microtubule homeostasis. We further provide evidence that severity of the CCD phenotype is determined by the degree of the loss of function caused by the human variants. Taken together, we identify WDR47 as a causative gene of a new neurodevelopmental syndrome characterized by corpus callosum abnormalities and other neuroanatomical malformations.

neuroscience↗

bioRxiv2023

Bayesian phylogenetics on globally emerging SARS-CoV-2 variant BA.2.86 suggest global distribution and rapid evolution

Using bioinformatic pipelines and Bayseian phylogenetic analyses, we characterized a SARS-CoV-2 variant designated by the World Health Organization as a variant under monitoring in August 2023. Here we analyze the genomes of this SARS-CoV-2 variant, BA.2.86, deposited into GISAID within the two weeks of its emergence (2023-08-14 first submission to 2023-08-31), including the first BA.2.86 genome reported from a traveler originating from Japan. We present bioinformatics methods using publicly available tools to help analysts identify the lineage-defining 12 nucleotide insertion (S:Ins16MPLF), which is often masked by most bioinformatics pipelines. We also applied maximum-likelihood and Bayesian phylogenetics to demonstrate the high mutational rate of the tree branch leading to the emergence of BA.2.86, hinting at possible origins, and predict that BA.2.86 emerged around May 2023 and spread globally rapidly. Taken together, these results provide a framework for more rigorous bioinformatics approaches for teams performing genomic surveillance on viral respiratory pathogens.

bioinformatics↗

bioRxiv2023

Transposable element insertions are associated with Batesian mimicry in the pantropical butterfly Hypolimnas misippus

Hypolimnas misippus is a Batesian mimic of the toxic African Queen butterfly (Danaus chrysippus). Female H. misippus butterflies use two major wing patterning loci (M and A) to imitate the four colour morphs of D. chrysippus found in different regions of Africa. In this study, we examine the evolution of the M locus and identify it as an example of adaptive atavism. This phenomenon involves a morphological reversion to an ancestral character that results in an adaptive phenotype. We show that H. misippus has re-evolved a wing pattern present in other Hypolimnas species for Batesian mimicry of a D. chrysippus morph. Using haplotagging, a linked-read sequencing technology, we discover two large transposable element (TE) insertions located at the M locus and establish that these insertions are present in the dominant allele responsible for producing the ancestral and mimetic phenotype. By conducting a comparative analysis involving additional Hypolimnas species, we demonstrate that the dominant allele is derived. This suggests that the TEs disrupt a cis-regulatory element, leading to the reversion to an ancestral phenotype that is then utilized for Batesian mimicry of a distinct model, a different morph of D. chrysippus. Our findings present a compelling instance of convergent evolution and adaptive atavism, in which the same pattern element has independently evolved multiple times in Hypolimnas butterflies, repeatedly playing a role in Batesian mimicry of diverse model species.

evolutionary biology↗

bioRxiv2023

Enabling Success Through Transformative Practices in STEM: The Effects of Applying an Anti-Deficit Framework to Diversity and Equity Programming

Diversity, equity, and inclusion (DEI) programming and literature for historically underrepresented and marginalized students in science, technology, engineering, and mathematics degree programs often focuses on illuminating the challenges they face. The repeated emphasis on negative experiences creates a deficit-focused thread of inquiry that may unintentionally reinscribe persistent disparities and inequities. In this practice brief, we describe the positive effect of adapting anti-deficit framework with social career cognitive theory in developing and evaluating an Initiative for Maximizing Student Development program at a biomedical sciences graduate school, as well as how other institutions can explore, implement, and evaluate transformative DEI practices. In identifying and emphasizing the enablers of success while facilitating structured opportunities for personal and professional identity development, students and program leadership align values and goals to increase academic and scientific development, as well as community and social support.

scientific communication and education↗