Biology subjects

Haider, S.

Publications and source records attributed to Haider, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Mapping the Fragment-Binding Landscape of SARS-CoV-2 nsp14 for Antiviral Drug Discovery

Non-structural protein 14 (nsp14) is a bifunctional coronavirus drug target, combining a 3'-to-5' exoribonuclease domain with an N7-methyltransferase domain. Proof-of-concept data have demonstrated beneficial effects in animal models upon inhibition. Using microscale thermophoresis and X-ray crystallography, we screened full-length nsp14 for fragment hits and developed SAR-by-catalogue analogues with five- to eight-fold improved affinity. Several scaffolds showed pronounced overlap between distinct pockets, complicating structure-based optimisation. Analysis of mutational frequencies across over 14 million SARS-CoV-2 genome sequences identified nsp14 residues with markedly high and very low mutation rates, highlighting sites best suited to pan-coronavirus inhibitor design. Combining these data with all 19 publicly known fragment- and ligand-binding regions on nsp14, most of which have never been directly compared, we introduce a systematic site-naming system and rank every site by its potential for future structure-based development. Weighing criteria include proof-of-principle inhibitor data, cross-coronavirus conservation, mutation frequency, the number of fragments bound per site, and susceptibility to crystallographic artefacts from symmetry mates. This ranked, unified binding-site atlas resolves which of the many previously reported nsp14 sites merit prioritisation, providing a practical resource for future coronavirus antiviral drug development.

biochemistry↗

bioRxiv2026

Functional niche attributes shape species interaction roles in ecological networks

Identifying how species interact in ecological networks is key to understanding species' contributions to ecosystem functioning, but can be difficult to establish in species-rich communities. Functional niches, which capture broader ecological strategies, are often easier to assess and could help approximate species' interaction roles. We tested this by integrating species interaction and leaf functional trait data of tree species and leaf-associated interaction types from a large-scale forest biodiversity experiment. We found that identity, variability, and similarities of functional niches shaped corresponding aspects of interaction roles. Interestingly, however, this association inversed in the case of functional niche variability, which decreased instead of increased the variability of species interactions. This suggests a potential trade-off between processes that determine variability in functional and interaction space. Furthermore, effects were not constrained within aspects, with similarities of interactions being particularly responsive to most tested niche aspects, indicating that interaction-based competition among plants is particularly sensitive to functional niche differences. Moreover, many effects of functional niches depended on tree species biomass and tree species richness, highlighting the importance of the larger ecological context for determining species interaction roles. Together, our findings show that species' interaction roles, while clearly altered by, are not simply a consequence of functional niches. Instead, interaction roles integrate multiple aspects of functional niches depending on species performances and community composition and can therefore be crucial for anticipating ecosystem change.

ecology↗

bioRxiv2026

Linezolid Acts as a Selective Inhibitor of the JAK2V617F Mutation

The JAK2V617F (JAK2VF) driver mutation is found in 95% of patients with polycythemia vera (PV), a progressive myeloproliferative neoplasm. Current treatments suppress excessive hematopoiesis but lack specificity for targeting JAK2VF cells, are unable to deplete mutant stem/progenitor cells and ultimately result in drug resistance. We discovered that the FDA-approved antibiotic, linezolid (LZD), ameliorates the PV phenotype across multiple model systems. LZD suppressed cell proliferation and STAT5 signaling, altered the cell cycle, and increased apoptosis of JAK2VF-harboring human erythroleukemia cells, but not in wild-type acute leukemia cells. Computational modelling indicated that LZD interacts specifically with mutant JAK2VF but not with wild-type JAK2 protein. We further showed that, in JAK2VF mice that faithfully recapitulate human PV, LZD mitigates disease burden by selectively targeting JAK2VF stem cells thereby normalizing spleen size and blood counts. LZD also inhibited hematopoietic colony formation by patient-derived peripheral blood mononuclear cells, with the more primitive progenitors being preferred targets. Importantly, LZD selectively decreased JAK2VF+ colony numbers, without impacting wild-type JAK2 colonies. In all, the data provide a firm foundation for evaluating LZD-like molecules as an effective therapy for PV and other myeloproliferative neoplasms. Key pointsO_LILinezolid acts as a JAK2V617FIZselective inhibitor in PV mouse models and PV patient samples while sparing wildIZtype hematopoiesis. C_LIO_LILinezolid acts directly on JAK2V617F hematopoietic stem cells. C_LI

cancer biology↗

bioRxiv2026

Trait dissimilarity-based tree species loss affects tree diversity effects on herbivory

O_LIBiodiversity loss can alter interactions not only through changes in tree species richness, but also through the loss of particular functional strategies from ecological communities. Working in a subtropical forest diversity experiment we asked whether tree species richness effects on arthropod herbivory and leaf pathogen infestation depend on community functional diversity, and whether trait dissimilarity-based, non-random species loss alters these relationships compared to random loss. To address this, we combined already established planted scenarios with newly constructed extinction pathways. C_LIO_LIWe tested the responses of herbivory and leaf pathogen infestation (i) to tree species richness, functional diversity (Raos Q), community structure and resource strategies (i.e. ever-greenness) and community-weighted trait means as well as predation, and (ii) trait dissimilarity-based extinction pathway analyses that contrasted directed loss of functionally similar versus functionally distinct tree species. C_LIO_LIHerbivory increased with tree species richness and this increase was significantly stronger in communities with higher tree functional diversity. Under directed species loss scenarios, herbivory differed most strongly from random-loss expectations when similar tree species were lost first. By contrast, losing functionally distinct species first produced richness effects that were much closer to the random-loss scenarios. Trait-based species loss will therefore modify trophic interactions more strongly than random loss. For pathogen infestation tree richness effects depended on evergreenness and among planted extinction scenarios (three-way interaction), with only minor deviations of trait-based extinction path-ways from random-loss expectations. Pathogen infestation also tended to increase with community-weighted mean leaf nitrogen. Predation showed no clear relationship with tree species richness or functional diversity but was positively associated with herbivory. The strength of this association differed among extinction scenarios, providing no evidence for consistent top-down regulation. C_LI SynthesisThe ecological consequences of biodiversity loss for leaf damage depend on which functional strategies are lost, not only on how many tree species remain. By integrating ob-served tree diversity gradients with trait-based extinction pathways, this study shows that functional diversity and host redundancy help explain why herbivores and pathogens are shaped by the same changes in tree diversity through different functional constraints and im-prove predictions of interaction strength under non-random species loss.

ecology↗

bioRxiv2026

Reversion mutations define minimal BRCA1/2 requirements for therapy resistance

Although platinum salts or PARP inhibitors are effective in delivering anti-tumor responses in people with BRCA1 or BRCA2 mutated cancers, drug resistance is common and is often caused by secondary BRCA1/2 reversion mutations that restore function. By collating and analyzing 848 BRCA1/2 reversion mutations in 384 cancer patients with drug resistance, we confirm that pathogenic BRCA1/2 mutation type influences the acquisition of reversions, and that large BRCA1/2 deletions are an underappreciated form of reversion. Integrating reversion data with systematic CRISPR-Cas9 screens that delete BRCA1/2 exons, we also show that both proteins contain privileged domains whose structure is essential for drug resistance, including the PALB2 interacting domains of both BRCA1 and BRCA2. Reversions in PALB2 also conserve both BRCA1 and BRCA2 binding domains. Surprisingly, exon 11 of BRCA2, which encodes BRC repeats 1-8, is not essential for resistance. Using this patient and functional information, we estimate the likelihood of pathogenic BRCA2 mutations to revert. We show that risk of reversion correlates with both the presence of clinical reversions and the response to treatment, suggesting that the propensity to revert could be a useful clinical parameter.

cancer biology↗

bioRxiv2026

Molecular and phenotypic footprints of climate in native Arabidopsis thaliana

Climate change poses a major threat to humanity by driving biodiversity loss and reducing crop yields1,2. To understand the molecular and developmental impacts of rising temperatures, plant science has relied heavily on the model organism Arabidopsis thaliana. Despite decades of research, its development under fully natural conditions remains poorly understood, and only [~]30% of genes have experimental functional annotations, largely because many functions are subtle or manifest only in specific laboratory or ecological contexts3. Here, we address this gap with a landscape transcriptomic approach that integrates intensive phenotyping and transcriptomic profiling of naturally occurring plants in their native habitats4. Across two contrasting field sites and five growing seasons (2021-2025), we phenotyped more than 3,000 A. thaliana plants and generated >1,600 matching transcriptomes. The resulting >30,000 quantitative trait measurements provide a unique opportunity to link climate fluctuations with plant traits and gene expression. Seasons characterized by extreme temperature anomalies directly influenced plant traits, and climatic variables together explained up to 17% of phenotypic variation. In situ transcriptomes carried clear temperature and local environmental signatures, closely matching temperature-response programs known from the laboratory. Leveraging paired per-plant transcriptomes and phenotypes, we applied machine learning to predict regulators of climate-relevant and other plant traits under natural conditions. The models recovered canonical thermomorphogenesis regulators, including PHYTOCHROME INTERACTING FACTOR 4 (PIF4)5,6, providing ecological evidence that temperature signaling pathways defined in controlled environments operate in the wild, and expanded this regulatory landscape by identifying hormonal receptors, signaling components, and previously uncharacterized genes, some of which we functionally validated. Together, this work demonstrates that landscape transcriptomics, by integrating natural field transcriptomes with phenotypes, and thus, capturing environmental and regulatory states, enables the predictive identification of genetic regulators of temperature responses and broader plant traits. This makes landscape transcriptomics a scalable framework for climate-aware functional genomics in plants.

plant biology↗

bioRxiv2026

FAK Inhibition Remodels the Metastatic ECM and Restores CD8+ T Cell Trafficking and Immunosurveillance

Metastatic breast cancer remains largely incurable, driven in part by immunosuppressive microenvironments that limit CD8+ T cell-mediated clearance. Using a murine pulmonary metastatic breast cancer model, we show that the focal adhesion kinase (FAK) inhibitor VS-4718 promotes a CD8+ T cell-dependent regression of metastatic lesions by reprograming the metastatic microenvironment. VS-4718 reduced immunosuppressive myeloid and regulatory T cells while increasing CD8+ T cell infiltration. Cellular and secreted proteome profiling revealed that VS-4718 downregulates ECM components such as laminin 5 and collagen VIII1, which we show impair CD8+ T cell migration and activity. In human breast cancer cohorts, elevated LAMA5/COL8A1 expression and a FAK-dependent ECM signature associate with poor outcome and prognostic for residual disease. Intravital imaging demonstrated that VS-4718 enhances CD8 T cell extravasation and induces T cell-tumor cell contacts necessary for cytotoxicity. Ex vivo lung slice cultures recapitulated these findings, showing enhanced T cell swarming, metastatic cluster shrinkage, and apoptosis. These findings reveal how FAK inhibition remodels the metastatic ECM to potentiate coordinated CD8+ T cell responses. VS-4718 might aid in clearing metastases in breast cancer patients through modulating both stromal and immune components. STATEMENT OF SIGNIFICANCEFocal adhesion kinase (FAK) inhibition remodels collagen- and laminin-rich extracellular matrix barriers and alleviates physical constraints that limit CD8 T cell access and activity in metastases. This enhances infiltration, migration, and tumor cell engagement, and synergizes with PD-1 blockade, supporting combined therapeutic strategies in metastatic breast cancer.

cancer biology↗

bioRxiv2025

Moving Beyond Binary Biomarkers: Machine Learning Model Resolves Concurrent and Molecularly Heterogeneous Mismatch Repair and Homologous Recombination Deficiencies in Prostate Cancer

Current DNA damage repair (DDR) biomarkers employ binary classifications that fail to capture the molecular complexity of tumors with concurrent repair deficiencies. We used genomics analysis to stratify 672 metastatic prostate cancer patients into 11 DDR subgroups, identifying 51 molecular signatures with weighted roles in class identity. We identified a tumor-mutational-burden very-high subset, characterized by 19 mutations/Mb or more, as a molecularly distinct group characterized by preserved genomic integrity and enhanced immunogenicity. Critically, 2.3 percent of tumors exhibited concurrent TMB-High and HRR mutant phenotypes, while 1.5 percent harbored MMR bi-allelic loss without MMRd (mismatch-repair-deficiency) signatures. Clinical validation in 130 patients demonstrated superior immunotherapy responses in tumors with very high TMB levels. We developed CHIMERA DDR, a probabilistic machine learning tool that integrates these 51 genomic features using a nested Random Forest architecture to infer seven clinically relevant DDR subgroups. After negating model overfit concerns, CHIMERA-DDR showed exceptional classification performance (AUCs 0.919-0.999) to accurately detect MMRd and HRR mutant molecular subtypes with or without concurrent DDR deficiencies, resolving admixed phenotypes to enable precision therapeutic stratification beyond binary methods.

genomics↗

bioRxiv2025

A Physically-Realistic Simulator and Cosine-Based Decoder for MERFISH Spatial Transcriptomics

Imaging-based spatial transcriptomics technologies have opened new avenues for studying cellular organization and gene expression within intact tissues. However, the accuracy of downstream analyses depends critically on the decoding step that reconstructs barcodes from fluorescence patterns and maps them to gene identities. Despite a growing number of decoding methods, systematic benchmarking has been limited. Here, we introduce Serval, a modular framework for developing and benchmarking decoding methods across diverse spatial transcriptomics platforms. Serval separates key decoding stages into independently configurable modules, enabling flexible integration of alternative algorithms. Using this framework, we develop the Cosine decoder, a novel method that improves transcript recovery by optimizing cosine similarity to known barcodes. We evaluate Cosine and baseline methods on synthetic and real MERFISH datasets, showing that Cosine achieves higher transcript recovery and superior correlation with expression references compared to existing methods. Furthermore, we demonstrate that the Serval framework generalizes beyond MERFISH. By extending to the DART-FISH platform, we show that Cosine improves transcript recovery, clustering stability and supports more direct annotation of complex biological structures such as the human primary motor cortex. These results establish that modular decoding frameworks facilitate robust, platformagnostic benchmarking, ultimately supporting more accurate spatial transcriptomics analysis across diverse biological samples.

bioinformatics↗

bioRxiv2025

LOX inhibition disrupts a collagen-integrin-MYC axis as a translatable targeting strategy in invasive lobular carcinoma

Invasive lobular carcinoma (ILC) accounts for 15% of breast cancers yet lacks specific therapy because ILCs are underrepresented in clinical trials and preclinical models are lacking. We established intraductal xenograft models to test whether the clinical pan-lysyl-oxidase PXS-5505, now in phase trials for myelofibrosis can exploit the collagen-rich matrix dependency created by CDH1 loss. PXS-5505 remodels fibrillar collagen, and halts tumor expansion and metastatic seeding across ER+ and triple negative models without systemic toxicity. Genome-wide CRISPR screens reveal ITGAV and ITGB5 as synthetic lethal partners of CDH1 and LOX inhibition downregulates their expression together with MYC, NF-{kappa}B, and AP-1 transcriptional programmes. Collagen fibre density/alignment, and MYC/AP-1 gene signatures serve as pharmacodynamic readouts of drug activity. These data uncover a tractable ECM-integrin-MYC axis in ILC and nominate PXS-5505, alone or with endocrine therapy, for window of opportunity trials in this understudied breast cancer subtype. One Sentence SummaryTargeting matrix remodelling in ILC inhibits ILC progression and alters multiple molecular endpoints, providing a translatable therapeutic strategy for this understudied subtype that requires better treatments.

cancer biology↗

bioRxiv2025

Maternal smoking in early pregnancy disrupts placental function through syncytiotrophoblast and macrophage dysregulation.

Smoking in pregnancy is the leading avoidable cause of gestational morbidity and mortality, causally linked to fetal growth restriction (FGR). The placenta, functional interface between mother and fetus is essential for healthy fetal development. For the first time, we studied cell type-resolved smoking effects on placental development at high molecular resolution using single-nucleus RNA sequencing and deep visual proteomics of matched tissues. We validated our findings through an independent cohort and in-vitro cigarette smoke exposure to primary human trophoblast cells. Our results show placental macrophages (Hofbauer cells; HBC) and the syncytiotrophoblast (STB) barrier are most affected by smoking, with dysregulation of cell-cell adhesion, extracellular matrix organization, and stress phenotype. STBs show moderate compositional increases in smokers and in-silico trophoblast differentiation modelling indicates a preferential shift towards the STB lineage in this group. The trophoblast displays a large upregulation of pro-angiogenic effectors, increases in xenobiotic detoxification, reduced mitochondrial function, and vastly altered transmembrane transport. These molecular changes affect placental development with important consequences for fetal growth. We provide insight into placental dysfunction contributing to FGR early in pregnancy, before clinical symptoms appear. We anticipate this data to advance diagnostics and therapies to improve FGR outcomes.

systems biology↗

bioRxiv2025

Could instructor talk drive CURE effectiveness? A comparative study of instructor talk in introductory lab courses

Course-based undergraduate research experiences (CUREs) are thought to enhance students motivation to continue in college, in science, and in research. Yet, how CUREs enhance student motivation is largely undefined. Theories of instructor immediacy, self-efficacy, and task values suggest that CURE instructors may talk in ways that influence students motivational beliefs. We characterized the non-content related talk of instructors teaching 48 introductory biology lab courses, half CUREs and half non-CUREs. We identified 14 types of instructor talk that fit these theoretical perspectives: fostering students closeness with their instructor (i.e., immediacy talk), building students confidence in their scientific abilities (i.e., self-efficacy talk), and promoting students sense of worth in their work (i.e., task value talk). Course type had a medium effect on talk type, with CURE instructors utilizing more immediacy, self-efficacy, and task values talk than non-CURE instructors but also showing more variation in these types of talk. Our results suggest that motivation-related instructor talk is more prevalent in CUREs than non-CUREs, but wide variation in CURE instructor talk indicates additional investigation is needed before non-content talk can be considered a mechanism for the motivational influences of CUREs. HIGHLIGHTThis study compares non-content instructor talk in CURE and non-CURE lab courses using immediacy, self-efficacy, and task value theories. CURE instructors use more talk than non-CURE instructors, but variation in CURE instructor talk leaves open the question of whether talk is a causal factor in the motivational influence of CURE instruction.

scientific communication and education↗

bioRxiv2025

A large global soil carbon sink informed by repeated soil samplings

Partitioning the terrestrial carbon sink between vegetation and soil is crucial for predicting future climate change, but the role of soils remains poorly quantified. Here, we compiled 3,099 soil organic carbon time series spanning five decades. We found a global soil organic carbon sink of 1.83 {+/-} 0.9 (mean {+/-} SE) petagrams per year from 1992 to 2020, driven by extratropical young forests, boreal old forests, and grasslands, while trends in tropical ecosystems remain uncertain. Our findings suggest the net land sink resides almost exclusively belowground as soil carbon, emphasizing the global opportunity of soil conservation and restoration for climate mitigation.

ecology↗

bioRxiv2025

Identification of Injury-Response State Determinants in Glioblastoma Stem Cells

Glioblastoma (GBM) is a common and highly lethal type of primary brain tumor in adults. Therapeutic failure is partly attributed to a fraction of Glioblastoma Stem Cells (GSCs) that show high levels of heterogeneity and plasticity. GSCs exist in a transcriptional gradient between two states: Developmental (Dev) and Injury Response (IR) in which IR-GSCs exhibit more invasive behaviors. While previous studies have identified fitness genes in GSCs, the genes required to establish and maintain the Dev and IR states remain poorly defined. To identify the regulators of the IR GSC state, we performed a phenotypic genome-wide CRISPR-Cas9 knockout (KO) screen in patient-derived GSCs based on cell surface expression of the IR marker CD44. Notably, we found that perturbations of the histone acetyltransferase EP300 in IR GSCs led to decreased CD44 cell surface expression, significant downregulation of gene expression signatures associated with the IR state, and to decreased self-renewal and invasion. Furthermore, genetic targeting of Ep300 in a mouse GBM model delayed tumor initiation and/or progression. Collectively, our results establish EP300 as a regulator of the IR state in GSCs and provide a mechanistic basis for its therapeutic targeting in GBM. SignificanceA genome-wide phenotypic CRISPR-Cas9 screen in a patient-derived Glioblastoma Stem Cell line identified the genes required to maintain the Injury-Response cellular state, with a focus on the histone acetyl transferase gene EP300. This study suggests how therapeutic targeting of cellular state could reduce the aggressiveness of GBM tumors.

cancer biology↗

bioRxiv2025

PWO proteins are associated with PRC2 since their emergence in vascular plants

PWWP-Domain Interactor of Polycombs 1 (PWO1), also known as PWWP1, interacts with the catalytic subunits of the Polycomb Repressive Complex 2 (PRC2) and, together with PWO2/3 proteins, plays a critical role in the development of Arabidopsis thaliana (At). PWOs are unique to plants and impact chromatin structure by enabling crosstalk between active and repressive epigenetic marks through mechanisms that are not yet fully understood. We aimed to understand the evolution of PWO proteins and whether their interaction with PRC2 has been conserved through evolution. Our study reveals that PWO proteins are present in vascular plants, but absent in bryophytes and green algae. The ancestral clade of PWO proteins includes the Selaginella moellendorffii (Sm) PWO orthologs SmPWOa and SmPWOb. Transient expression assays showed that both AtPWO1 and SmPWOa form nuclear speckles where they tether At, Sm, but also Physcomitrium patens (Pp) PRC2 catalytic subunits, despite the absence of PWO proteins in Pp. The PWO-PRC2 interactions were confirmed by protein-protein analyses. A newly identified evolutionarily conserved short C-terminal alpha-helix (c-motif) in PWO proteins contributes to an interaction interface for PWO-PRC2 binding. SmPWOs partially rescue the pwo1;pwo2 mutant phenotype in Arabidopsis, highlighting the functional conservation of PWOs in vascular plants.

plant biology↗

bioRxiv2025

Mechanistic Insights into the Substrate Egress Pathways of Human Glucose Transporters GLUT1 and GLUT9

Glucose transporters (GLUTs) play critical roles in cellular energy homeostasis and substrate-specific transport. Dysfunctional mutations can cause GLUT1 deficiency syndrome and excessive expression of GLUT1 is linked to cancer progression; while abnormal regulation of urate transport by GLUT9 is associated with hyperuricemia and gout. In this study, machine-learning driven molecular dynamics simulations have been employed to investigate the mechanistic insights into the substrate egress pathways of GLUT1 and GLUT9, including the inhibition mechanism of GLUT9 by apigenin. Our findings reveal that intracellular helices play a crucial role in facilitating the transition from inward-closed to inward-open conformations in both transporters. Additionally, aromatic residues, F291 and W388 in GLUT1, and W336 and F435 in GLUT9, are identified as key mediators of conformational changes. Analysis of substrate exit pathways provides mechanistic insights into transport profiles and aligns with clinically observed mutations. Furthermore, the inhibitory effect of apigenin on GLUT9 is shown to arise from steric hindrance due to increased substrate size, rather than stable interactions. These findings enhance our understanding of GLUT transporter dynamics and highlight the potential of targeting substrate pathways for therapeutic intervention.

biophysics↗

bioRxiv2024

Mountain roads across the globe significantly alter local soil microclimates

Mountain roads have repeatedly shown to host significantly different plant species communities compared to the adjacent natural vegetation. Besides the effect of propagule pressure, altered disturbance regime and soil processes, one of the reasons given for the strong influence of mountain roads on species distributions is a significantly altered microclimate in the roadside compared to the adjacent vegetation, a direct consequence of the altered disturbance regime. However, the microclimatic differences between roadside and natural vegetation have rarely been quantified, particularly lacking global analyses, hampering a better understanding of their importance for mountain biodiversity. In this study, we analysed in-situ measured soil temperatures along mountain roads in seven mountain regions across the globe, in order to assess the impact of mountain roads on a range of bioclimatic variables across the elevational gradient. Our results undeniably show the importance of roadsides as unique microhabitats, even in heterogeneous mountain environments. In most regions, roadside soils had warmer maxima (3.95 {+/-} 2.35{degrees}C warmer) and colder minima (0.85 {+/-} 1.11 {degrees}C colder) than the soil in the adjacent vegetation, with higher frost risks in winter. Therefore, we recommend future research to incorporate the notion that the local microclimates created by mountain roads could play a critical role in species redistributions in space and time.

ecology↗

bioRxiv2024

Intraspecific and intraindividual trait variability decrease with tree species richness in a subtropical tree biodiversity experiment

Phenotypic variability within tree species responds to local tree species richness. However, we lack evidence on how different sources of trait variation shape tree-tree interactions. Along a diversity gradient from one to eight tree species, we sampled 4,568 leaves from 381 trees to study changes in intraspecific and intraindividual leaf trait variability and assessed their contribution to community functional diversity. Intraspecific variability decreased with tree species richness, while intraindividual variability barely responded. Functional overlap between conspecific trees increased with tree species richness and through intraindividual variation, but was reduced through intraspecific variability, meaning that intraspecific variability may reduce intraspecific competitive interactions while intraindividual variability could arise due to varying microenvironmental conditions within the canopy. Last, intraspecific and intraindividual variability explained high community functional richness and divergence, respectively, especially in mixtures. Our findings emphasize that fine-scale variability influences tree-tree interactions and can be a driver of local functional diversity. TeaserTrait variability within tree species decreases with diversity and explains high forest functional diversity.

ecology↗