Biology subjects

Freeman, B.

Publications and source records attributed to Freeman, B..

18 recordsLinked to original sources

bioRxiv2026

SpectroBird: Event-Level Vocalization Detection and Curation for Avian Ecology

Passive acoustic monitoring often summarizes long recordings as fixed-window presence predictions, but many ecological questions require records of individual vocal events: how many occurred, when they occurred, whether they overlapped, how long they lasted, what frequency band they occupied, and whether each event was complete enough for structural measurement. We address this event-level measurement problem with SpectroBird, a spectrogram-based method for localizing and curating avian vocalizations in noisy field recordings. SpectroBird first applies a detection-localization model to identify candidate vocalizations as time-frequency boxes. An event-consolidation step merges repeated detections from overlapping windows while preserving overlapping vocalizations as separate events. A completeness-curation model then classifies each consolidated event as complete or incomplete before downstream event-level analysis. We demonstrate SpectroBird on breeding-season Hume's Leaf Warbler buzz vocalizations recorded in the Himalaya across a 3,200-3,800 m elevational gradient. Under shared window-level scoring, the detection-localization model remained competitive with AST and YOLOv11-cls baselines while retaining event timing and frequency bounds; event-level evaluation achieved AP > 0.999 for complete buzzes. Applied to two field seasons, the resulting event records showed that duration of complete buzzes declined with elevation, complete-buzz occurrence showed no simple elevation trend, and relative day-of-year occurrence patterns were strongly correlated between years. These results show how event-level detection and curation can support ecological analyses that depend on individual vocalizations rather than fixed-window presence alone.

bioinformatics↗

bioRxiv2026

Compact adenine base editors to enable therapeutic rescue of Duchenne muscular dystrophy

Adenine base editors (ABEs) have emerged as a powerful gene-editing technology enabling precise and programmable adenine-to-guanine substitutions across the genome. However, their translation into in vivo therapeutics is limited by delivery challenges, as their size exceeds the packaging capacity of adeno-associated virus (AAV). Here, we report the discovery, structural characterization, and engineering of two compact, highly active ABEs built on novel deaminases and Cas9d nucleases, enabling all-in-one, single-vector AAV delivery. Applying these compact ABEs to Duchenne muscular dystrophy (DMD), we demonstrate efficient disruption of conserved splice-acceptor sites at dystrophin exons 45 and 51 in human skeletal muscle cells, enabling therapeutically relevant exon skipping. Together, these ABEs help expand the therapeutic reach of base editing towards diverse tissue types and disease targets.

bioengineering↗

bioRxiv2026

Coevolution of Species' Borders: Interactions Between Interspecific Competition, Gene Flow, and Matching Habitat Choice

Existing theory examining the coevolutionary dynamics of species range borders assumes random dispersal, which causes maladaptive gene flow from the range core to the range margins and contributes to the formation of range limits. However, dispersal is unlikely to be random for many organisms in nature, calling into question existing theoretical predictions. For example, if individuals exhibit phenotype-dependent adaptive dispersal strategies such as matching habitat choice, then the resulting adaptive gene flow toward species range margins could facilitate range expansions and potentially prevent the formation of range limits by interspecific competition. To test this idea, we use a comprehensive mathematical model to develop a quantitative theory of range border coevolution that incorporates phenotype-optimal dispersal--a particular form of matching habitat choice in which individuals follow the gradient in an environmental optimum phenotype to settle in the habit best suited for their phenotype. We find that instead of preventing competitively formed range limits, adaptive dispersal leads to sharper range limits and reduced character displacement in sympatry. These differences are particularly remarkable when natural selection is weak, when individuals are specialized in their resource use, or when individuals are highly sensitive to environmental conditions. We show that matching habitat choice causes backward edge-to-core movements which dynamically interact with the effects of interspecific competition to establish the range limits. Thus, the formation of range limits by interspecific competition is robust to assumptions about individual dispersal. Further, our results identify the competitive advantage of evolving matching habitat choice in steep environmental gradients, especially for slowly-growing species in rapidly fluctuating climates.

ecology↗

bioRxiv2024

AB-free kava enhances resilience against the adverse health effects of tobacco smoke in mice

Tobacco smoke remains a serious global issue, resulting in serious health complications, contributing to the onsets of numerous preventive diseases, and imposing significant financial burdens. Despite regulatory policies and cessation measures aimed at curbing its usage, novel interventions are urgently needed for effective damage reduction. Our preclinical and pilot clinical studies showed that AB-free kava has the potential to reduce tobacco smoke-induced lung cancer risk, mitigate tobacco dependence, and reduce tobacco use. To understand the scope of its benefits in damage reduction and potential limitations, this study evaluated the effects of AB-free kava on a panel of health indicators in mice exposed to 2 - 4 weeks of daily tobacco smoke exposure. Our comprehensive assessments included global transcriptional profiling of the lung and liver tissues, analysis of lung inflammation, evaluation of lung function, exploration of tobacco nicotine withdrawal, and characterization of the causal PKA signaling pathway. As expected, Tobacco smoke exposure perturbed a wide range of biological processes and compromised multiple functions in mice. Remarkably, AB-free kava demonstrated the ability to globally mitigate tobacco smoke-induced deficits at the molecular and functional levels with promising safety profiles, offering a unique promise to mitigate tobacco smoke-related health damages. Further pre-clinical evaluation and clinical translation are warranted to fully harness the potential of AB-free kava in combating tobacco smoke-related harms. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=105 SRC="FIGDIR/small/599576v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@1f6ee4corg.highwire.dtl.DTLVardef@96e062org.highwire.dtl.DTLVardef@16579a0org.highwire.dtl.DTLVardef@1140a8e_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

bioRxiv2024

Bone morphogenetic protein (BMP) signaling determines neuroblastoma cell fate and sensitivity to retinoic acid.

Retinoic acid (RA) is a standard-of-care neuroblastoma drug thought to be effective by inducing differentiation. Curiously, RA has little effect on primary human tumors during upfront treatment but can eliminate neuroblastoma cells from the bone marrow during post-chemo consolidation therapy--a discrepancy that has never been explained. To investigate this, we treated a large cohort of neuroblastoma cell lines with RA and observed that the most RA-sensitive cells predominantly undergo apoptosis or senescence, rather than differentiation. We conducted genome-wide CRISPR knockout screens under RA treatment, which identified BMP signaling as controlling the apoptosis/senescence vs differentiation cell fate decision and determining RAs overall potency. We then discovered that BMP signaling activity is markedly higher in neuroblastoma patient samples at bone marrow metastatic sites, providing a plausible explanation for RAs ability to clear neuroblastoma cells specifically from the bone marrow, seemingly mimicking interactions between BMP and RA during normal development.

cancer biology↗

bioRxiv2024

RBM39 degrader invigorates natural killer cells to eradicate neuroblastoma despite cancer cell plasticity

The cellular plasticity of neuroblastoma is defined by a mixture of two major cell states, adrenergic (ADRN) and mesenchymal (MES), which may contribute to therapy resistance. However, how neuroblastoma cells switch cellular states during therapy remains largely unknown and how to eradicate neuroblastoma regardless of their cell states is a clinical challenge. To better understand the lineage switch of neuroblastoma in chemoresistance, we comprehensively defined the transcriptomic and epigenetic map of ADRN and MES types of neuroblastomas using human and murine models treated with indisulam, a selective RBM39 degrader. We showed that cancer cells not only undergo a bidirectional switch between ADRN and MES states, but also acquire additional cellular states, reminiscent of the developmental pliancy of neural crest cells. The lineage alterations are coupled with epigenetic reprogramming and dependency switch of lineage-specific transcription factors, epigenetic modifiers and targetable kinases. Through targeting RNA splicing, indisulam induces an inflammatory tumor microenvironment and enhances anticancer activity of natural killer cells. The combination of indisulam with anti-GD2 immunotherapy results in a durable, complete response in high-risk transgenic neuroblastoma models, providing an innovative, rational therapeutic approach to eradicate tumor cells regardless of their potential to switch cell states.

cancer biology↗

bioRxiv2023

Latitudinal gradients in predation persist in urban environments

Urbanization can profoundly disrupt local ecology. But while urban areas now stretch across latitudes, little is known about urbanizations effects on macroecological patterns. We used standardized experiments to test whether urbanization disrupts latitudinal gradients in seed predation, a macroecological pattern that shapes community assembly and diversity. Using >56,000 seeds, we compared predation in urbanized and natural areas across 14,000 km of latitude, spanning the Americas. Predation increased 5-fold from high latitudes to the tropics, and latitudinal gradients in predation persisted in urban areas despite significant habitat modification. Urbanization reduced predation by vertebrates, but not invertebrates, and seemed to increase ant predation specifically. Our results show that macroecological patterns in predation intensity can persist in urbanized environments, even as urbanization alters the relative importance of predators. One-Sentence SummaryAcross 56,000 seeds and 112{degrees} of latitude, latitudinal gradients in seed predation are equally strong in natural vs. urban areas

ecology↗

bioRxiv2021

Genomic and Metabolic Hallmarks of SDH- and FH-Deficient Renal Cell Carcinomas

PurposeSuccinate dehydrogenase-deficient and fumarate hydratase-deficient renal cell carcinomas (SDHRCC and FHRCC) are rare kidney cancers driven by loss of metabolically proximal enzymes. We sought to define and compare the genomic and metabolomic hallmarks of these entities. Experimental DesignWe analyzed SDHRCC and FHRCC tumors with either immunohistochemical evidence of loss of protein expression or genomically-confirmed biallelic inactivation of SDHA/B/C/D/AF2 or FH. Somatic alterations were identified using clinical pipelines, and allele-specific copy number changes were identified using FACETS. Mass-spectrometry-based metabolomic profiling was performed on available SDHRCC and FHRCC tumors. ResultsForty two patients were analyzed (25 FHRCC, 17 SDHRCC). In the germline analysis, 16/17 SDHRCC harbored a germline alteration in SDHB, whereas only 17/22 FHRCC had pathogenic germline FH variants. SDHRCC had a lower mutation burden (p = 0.02) and copy number alteration burden (p = 0.0002) than FHRCC. All SDHRCC presented with deletion of chromosome 1p (overlapping SDHB), whereas FHRCC demonstrated high but not ubiquitous loss of 1q (FH locus). Both SDHRCC and FHRCC demonstrated significant, idiopathic accumulation of the metabolite guanine. FHRCC tumors had elevated levels of urea cycle metabolites (argininosuccinate, citrulline, and fumarate), whereas SDHRCC had elevation of numerous acylcarnitines. These characteristic metabolic changes enabled the identification of a previously unrecognized SDH-deficient RCC. ConclusionDespite sharing similar genetic etiology, SDHRCC and FHRCC represent distinct molecular entities with unique genetic and metabolic abnormalities. Translational RelevanceMutations to the TCA cycle enzymes Succinate Dehydrogenase (SDH) and Fumarate Hydratase (FH) predispose individuals to unique subtypes of renal cell carcinoma (SDHRCC and FHRCC, respectively). Defining the genetic and metabolic hallmarks of these diseases is critical for advancing new diagnostic and therapeutic approaches for these rare but biologically intriguing entities. Despite a superficially similar genetic etiology, SDHRCC and FHRCC demonstrated significantly fewer secondary mutations to other cancer-associated genes and copy number aberrations than FHRCC, and was distinguished by universal loss-of-heterozygosity of chromosome 1p. Metabolomic analysis identified pathways disrupted in both SDHRCC and FHRCC, including the massive accumulation of free guanine, as well as pathways uniquely disrupted in each of the two entities. These metabolomic findings enabled the identification of a previously unidentified case of unclassified RCC with SDH deficiency, suggesting that metabolomic profiling may aid in phenotypic classification of tumors and uncover novel therapeutic targets.

cancer biology↗

bioRxiv2021

Predicting Bird Distributions Under Global Change

An introduction to predictive distribution modelling for conservation to encourage novel perspectives. The rapid pace and potentially irreversible consequences of global change create an urgent need to predict the spatial responses of biota for conservation to better inform the prioritization and management of terrestrial habitats and prevent future extinctions. Here, we provide an accessible entry point to the field to guide near-future work building predictive species distribution models (SDMs) by synthesizing a technical framework for the proactive conservation of avian biodiversity. Our framework offers a useful approach to navigate the challenges surrounding the large spatio-temporal resolution of datasets and datasets that favor hypothesis testing at broad spatio-temporal scales and coarse resolutions, which can affect our ability to assess the validity of current predicted distributions. We explain how to improve the accuracy of predictive models by determining the extent to which: 1) dispersal limitation impacts the rate of range shifts, 2) taxa are rare at their range limits, and 3) land use and climate change interact. Finally, we offer approaches to filling knowledge gaps by creatively leveraging existing methods and data sources. RESUMENUna introduccion a la modelizacion predictiva de la distribucion para la conservacion con el fin de fomentar nuevas perspectivas. El rapido ritmo y las consecuencias potencialmente irreversibles del cambio global crean una necesidad urgente de predecir las respuestas espaciales de la biota para la conservacion, con el fin de informar mejor la priorizacion y gestion de los habitats terrestres y prevenir futuras extinciones. Aqui proporcionamos un punto de entrada accesible al campo para guiar el trabajo del futuro proximo en la construccion de modelos predictivos de distribucion de especies (SDM), sintetizando un marco tecnico para la conservacion proactiva de la biodiversidad aviar. Nuestro marco ofrece un enfoque util para navegar por los retos que rodean a la gran resolucion espacio-temporal de los conjuntos de datos y a los conjuntos de datos que favorecen la comprobacion de hipotesis a escalas espacio-temporales amplias y resoluciones gruesas, lo que puede afectar a nuestra capacidad para evaluar la validez de las distribuciones predichas actuales. Explicamos como mejorar la precision de los modelos predictivos determinando hasta que punto 1) la limitacion de la dispersion influye en el ritmo de los cambios de area de distribucion, 2) los taxones son raros en los limites de su area de distribucion, y 3) el uso del suelo y el cambio climatico interactuan. Por ultimo, proponemos enfoques para colmar las lagunas de conocimiento aprovechando de forma creativa los metodos y fuentes de datos existentes.

ecology↗

bioRxiv2021

Efficacy of oseltamivir treatment in influenza virus infected obese mice

Obesity has been epidemiologically and empirically linked with more severe disease upon influenza infection. To ameliorate severe disease, treatment with antivirals, such as the neuraminidase inhibitor oseltamivir, are suggested to begin within days of infection, especially in hosts at higher risk for poor outcomes. However, this treatment is often poorly effective and can generate resistance variants within the treated host. Here, we hypothesized that oseltamivir treatment would not be effective in genetically obese mice and would generate a more diverse and drug resistant viral population. We demonstrated that oseltamivir treatment does not improve viral clearance in obese mice. While no traditional variants associated with oseltamivir resistance emerged, we did note that drug treatment failed to quench the viral population and did lead to phenotypic drug resistance in vitro. Mechanistically, we demonstrate the blunted interferon response in obese hosts may be contributing to treatment failure, as type I interferon receptor deficient mice also fail to clear influenza virus infection upon oseltamivir administration. Together, these studies suggest that the unique pathogenesis and immune responses in obese mice could have implications for pharmaceutical interventions and the within-host dynamics of the influenza virus population. IMPORTANCEInfluenza virus infections, while typically resolving within days to weeks, can turn critical especially in high-risk populations. Prompt antiviral administration is crucial to mitigating these severe sequalae, yet concerns remain if antiviral treatment is effective in hosts with obesity. Here, we show that oseltamivir does not improve viral clearance in genetically obese or type I IFN receptor-deficient mice and increases the genetic entropy of the within-host viral population. This suggests a blunted immune response may impair oseltamivir efficacy and render a host more susceptible to severe disease. This study furthers our understanding of oseltamivir treatment dynamics both systemically and in the lungs of obese mice, as well as the consequences of oseltamivir treatment for the within-host emergence of drug-resistant variants.

microbiology↗

bioRxiv2021

The chemotherapeutic CX-5461 primarily targets TOP2B and exhibits selective activity in high-risk neuroblastoma.

Survival in high-risk pediatric neuroblastoma has remained around 50% for the last 20 years, with immunotherapies and targeted therapies having had minimal impact. Here, we identify the small molecule CX-5461 as selectively cytotoxic to high-risk neuroblastoma and synergistic with low picomolar concentrations of topoisomerase I inhibitors improving survival in vivo in orthotopic patient-derived xenograft neuroblastoma mouse models. CX-5461 recently progressed through phase I clinical trial as a first-in-human inhibitor of RNA-POL I. However, we also use a comprehensive panel of in vitro and in vivo assays to demonstrate that CX-5461 has been mischaracterized and that its primary target at pharmacologically relevant concentrations, is in fact topoisomerase II beta (TOP2B), not RNA-POL I. These findings are important because existing clinically approved chemotherapeutics have well-documented off-target interactions with TOP2B, which have previously been shown to cause both therapy-induced leukemia and cardiotoxicity--often-fatal adverse events, which can emerge several years after treatment. Thus, while we show that combination therapies involving CX-5461 have promising anti-tumor activity in vivo in neuroblastoma, our identification of TOP2B as the primary target of CX-5461 indicates unexpected safety concerns that should be examined in ongoing phase II clinical trials in adult patients before pursuing clinical studies in children.

cancer biology↗

bioRxiv2020

Sclerostin depletion induces inflammation in the bone marrow of mice

Romosozumab, a humanized monoclonal antibody specific for sclerostin, has been approved for treatment of post-menopausal women with osteoporosis at high risk for fracture. In several Phase III clinical trials, romosozumab decreased the risk of vertebral fractures up to 73% and increased total hip area bone mineral density by 3.2%. Previous work in 12 to 15-week-old sclerostin-knockout (Sost-/-) mice indicated that changes in immune cell development occur in the bone marrow (BM), which could be a possible side effect to follow in human patients. Our overall goal was to define the mechanisms that guide behavior of long-term hematopoietic stem cells (LT-HSCs) after exposure to an irregular BM microenvironment. SOST plays an important role in maintaining bone homeostasis, as demonstrated by the increased ratio of bone volume to total volume observed in Sost-/- mice. Here, we examined the effects of short-term sclerostin depletion in the BM on hematopoiesis in young (8 week-old) mice receiving sclerostin-antibody (Scl-Ab) treatment for 6 weeks, and the effects of long-term Sost-deficiency on wild-type (WT) LT-HSCs transplanted into older (16-22 week-old) cohorts of Sost-/- mice. Our analyses revealed an increased frequency of granulocytes and decreased frequency of lymphocytes in the BM of Scl-Ab treated mice and WT[->]Sost-/- hematopoietic chimeras, indicating myeloid-biased differentiation in Sost-deficient BM microenvironments. This myeloid bias extended to extramedullary hematopoiesis in the spleen and was correlated with an increase in inflammatory cytokines TNF, IL-1 and MCP-1 in the serum of the Sost-/- BM. Additionally, we observed alterations in erythrocyte differentiation in the BM and spleen of Sost-/- mice. Taken together, our current study indicates novel roles for Sost in the regulation of myelopoiesis and control of inflammation in the BM. Our animal studies strongly recommend tracking of hematopoietic function in patients treated with romosozumab.

immunology↗

bioRxiv2020

The latitudinal gradient in the rate of evolution of a biotic interaction trait

Where is evolution fastest? The biotic interactions hypothesis proposes that greater species richness creates more ecological opportunity, driving faster evolution at low latitudes, whereas the "empty niches" hypothesis proposes that ecological opportunity is greater where diversity is low, spurring faster evolution at high latitudes. Here we tested these contrasting predictions by analyzing rates of bird beak evolution for a global dataset of 1141 sister pairs of birds. Beak size evolves at similar rates across latitudes, while beak shape evolves faster in the temperate zone, consistent with the empty niches hypothesis. We show in a meta-analysis that trait evolution and recent speciation rates are faster in the temperate zone, while rates of molecular evolution are slightly faster in the tropics. Our results suggest that drivers of evolutionary diversification are more potent at higher latitudes, thus calling into question multiple hypotheses invoking faster tropical evolution to explain the latitudinal diversity gradient.

evolutionary biology↗

bioRxiv2020

Montane species and communities track recent warming more closely in the tropics

Many species are responding to global warming by shifting their distributions upslope to higher elevations, but the observed rates of shifts vary considerably among studies. Here we test the hypothesis that this variation is in part explained by latitude, with tropical species being generally more responsive to warming temperatures than are temperate species. We find support for this hypothesis in each of two independent empirical datasets--shifts in species elevational ranges, and changes in composition of forest inventory tree plots. Tropical species are tracking rising temperatures 2.1-2.4 times (range shift dataset) and 10 times (tree plot dataset) better than their temperate counterparts. Models predict that for a 100 m upslope shift in temperature isotherm, species at the equator have shifted their elevational ranges 93-96 m upslope, while species at 45{degrees} latitude have shifted only 37-42 m upslope. For tree plots, models predict that a 1{degrees}C increase in temperature leads to an increase in community temperature index (CTI), a metric of the average temperature optima of tree species within a plot, of 0.56 {degrees}C at the equator but no change in CTI at 45{degrees} latitude (-0.033). This latitudinal gradient in temperature tracking suggests that tropical montane biotas may be on an "escalator to extinction" as global temperatures continue to rise.

ecology↗

bioRxiv2020

Validation of a SARS-CoV-2 spike ELISA for use in contact investigations and serosurveillance

Since emergence of SARS-CoV-2 in late 2019, there has been a critical need to understand prevalence, transmission patterns, to calculate the burden of disease and case fatality rates. Molecular diagnostics, the gold standard for identifying viremic cases, are not ideal for determining true case counts and rates of asymptomatic infection. Serological detection of SARS-CoV-2 specific antibodies can contribute to filling these knowledge gaps. In this study, we describe optimization and validation of a SARS-CoV-2-specific-enzyme linked immunosorbent assay (ELISA) using the prefusion-stabilized form of the spike protein [1]. We performed receiver operator characteristic (ROC) analyses to define the specificities and sensitivities of the optimized assay and examined cross reactivity with immune sera from persons confirmed to have had infections with other coronaviruses. These assays will be used to perform contact investigations and to conduct large-scale, cross sectional surveillance to define disease burden in the population.

immunology↗

bioRxiv2020

Identification of an antiretroviral small molecule that appears to be a host-targeting inhibitor of HIV-1 assembly

Given the projected increase in multidrug resistant HIV-1, there is an urgent need for development of antiretrovirals that act on virus life-cycle stages that are not targeted by antiretrovirals currently in use. Host-targeting drugs are of particular interest because they can offer a high barrier to resistance. Here we report identification of two related small molecules that inhibit HIV-1 late events, a stage of the HIV-1 life cycle for which potent and specific inhibitors are lacking. This chemotype was discovered using cell-free protein synthesis and assembly systems that recapitulate intracellular host-catalyzed viral capsid assembly pathways. These compounds inhibit replication of HIV-1 in human T cell lines and PBMCs and are effective against a primary isolate. They reduce virus production, likely by inhibiting a post-translational step in HIV-1 Gag assembly. Notably, the compound colocalizes with HIV-1 Gag in situ; however, unexpectedly, selection experiments failed to identify compound-specific resistance mutations in gag or pol, even though known resistance mutations developed in a parallel nelfinavir selection. Thus, we hypothesized that instead of binding to Gag directly, these compounds might localize to assembly intermediates, the intracellular multiprotein complexes containing Gag and host factors that are formed during immature HIV-1 capsid assembly. Indeed, imaging of infected cells showed colocalization of the compound with two host enzymes found in assembly intermediates, ABCE1 and DDX6. While the exact target and mechanism of action of this chemotype remain to be determined, these findings suggest that these compounds represent first-in-class, host-targeting inhibitors of intracellular events in HIV-1 assembly. IMPORTANCEThe success of antiretroviral treatment for HIV-1 is at risk of being undermined by the growing problem of drug resistance. Thus, there is a need to identify antiretrovirals that act on viral life cycle stages not targeted by drugs in use, such as the events of HIV-1 Gag assembly. To address this gap, we developed a compound screen that recapitulates the intracellular events of HIV-1 assembly, including viral-host interactions that promote assembly. This effort led to identification of a new chemotype that inhibits HIV-1 replication at nanomolar concentrations by inhibiting virus production. This compound colocalized with Gag and two host enzymes that facilitate capsid assembly but resistance selection did not result in compound-specific mutations in gag, suggesting that the chemotype does not directly target Gag. We hypothesize that this chemotype may represent a first-in-class inhibitor of virus production that acts by targeting a viral-host complex important for HIV-1 Gag assembly.

microbiology↗

bioRxiv2019

Mixed support for the idea that lower elevation animals are better competitors than their upper elevation relatives

What factors set species range edges? One general hypothesis, often attributed to Darwin and MacArthur, is that interspecific competition prevents species from inhabiting the warmest portions along geographic gradients (i.e., low latitudes or low elevations). A prediction arising from the Darwin-MacArthur hypothesis is that lower elevation species are better competitors than are related upper elevation species. I tested this prediction by conducting a meta-analysis of studies that have measured behavioral competition between related species along elevational gradients. I found that (1) interspecific aggression appears to be a reliable indicator of interspecific competition; (2) as predicted, lower elevation species showed stronger interspecific aggression, but only for tropical species-pairs tested with playback experiments (nearly all songbirds); (3) for a broader range of taxa where authors directly observed behavioral interactions, upper elevation species showed stronger interspecific aggression; and (4) in general, larger species showed greater interspecific aggression. One potential explanation for why upper elevation species often show more interspecific aggression is that they tend to be larger (Bergmanns rule; larger body sizes in colder environments). Supporting this possibility, tropical species tested with playback experiments, which do not follow Bergmanns rule, were the only group that matched predictions arising from the Darwin-MacArthur hypothesis. Hence, available evidence does not consistently support the longstanding hypothesis that relative range position predicts the outcome of interspecific competition. Instead, body size is a better predictor of behavioral competition. Last, I consider these results in the context of the hypothesis that behavioral interactions may impact rates of upslope range shifts associated with recent warming.

ecology↗

bioRxiv2019

Adaptation and latitudinal gradients in species interactions: nest predation in birds

The "biotic interactions" hypothesis--that stronger interspecific interactions in the tropics drive faster evolution and speciation, giving rise to the latitudinal diversity gradient--has inspired many tests of whether certain biotic interactions are indeed stronger in the tropics. However, the possibility that populations have adapted to latitudinal differences in species interactions, blunting effects on evolutionary rates, has been largely ignored. Here we show that mean rates of nest predation experienced by land birds vary minimally with latitude in the Western Hemisphere. This result is surprising because nest predation in birds is a canonical example of a strong tropical biotic interaction. We explain our finding by demonstrating that (1) rates of nest predation are in fact higher in the tropics, but only when controlling for the length of the nesting period, (2) long nesting periods are associated with reduced predation rates, and (3) tropical birds have evolved particularly long nesting periods. We suggest this is a case example of how adaptation to a biotic interaction can alter observed latitudinal gradients in interaction strength, potentially equalizing evolutionary rates among latitudes. More broadly, we advocate for tests of the biotic interactions hypothesis to consider both latitudinal patterns in interaction strength and evolutionary responses to these interactions.

evolutionary biology↗