Biology subjects

Qiu, F.

Publications and source records attributed to Qiu, F..

17 recordsLinked to original sources

bioRxiv2026

The cellular and genetic basis of inflorescence divergence between maize and teosinte

The domestication of maize from teosinte involved dramatic remodeling of the ear, yet the cellular and genetic bases of this transformation remain unclear. Here, we generate a single-nucleus and spatial transcriptome atlas of developing maize and teosinte ears. Comparative analysis reveals divergence in cob-associated cell types, with enhanced cytokinin signaling and reduced growth-inhibitory signals collectively driving cob thickening and enlargement in maize. We further demonstrate that domestication expanded the spatial expression domain of key transcription factors in maize meristem cells, enhancing the potential for increasing kernel number. Additionally, we verified a major domestication gene, ZmSPD1, in which two nonsynonymous SNPs differentiate maize from teosinte and alter jasmonic acid (JA) levels in the ear, thereby suppressing spikelet abortion to effectively double kernel production. These findings provide a cell-resolved mechanistic framework for how cob architecture and kernel number were shaped during maize domestication, offering new insights into the formation of key agronomic traits.

plant biology↗

bioRxiv2026

STING agonist-mediated endothelial cell activation drives NK cells and neutrophils-dependent pulmonary inflammation

Stimulator of interferon genes (STING) agonists and derivative molecules have been extensively developed for tumor immunotherapy. However, systemic exposure toxicity risks have constrained clinical trial progression and even threatened patient lives. Currently, systematic toxicity assessments for STING agonists remain lacking, with the mode of action for major organ injury yet to be elucidated. Here, we focused on STING agonist-induced lung injury, revealing that systemic administration of STING agonists caused pulmonary hemorrhage, inflammatory alterations, and respiratory dysfunction. Through single-cell RNA sequencing and immune deletion studies, we found that lung endothelial cells could be stimulated by STING agonists and then secreted chemokines and IL-15 to recruit and activate NK cells. NK cells could induce endothelial cell apoptosis via IFN-{gamma}. Tbx21+ NK subpopulations, which activated by endothelial cells, could produce chemokines to recruit neutrophils. Neutrophils secreted IL-1{beta} through positive feedback pathways and form neutrophil extracellular traps during lung injury. This study elucidates the critical role of the endothelial cell-NK cell-neutrophil axis in mediating STING agonist-associated pneumonia, offering insights for developing intervention strategies for STING agonist toxicity.

pharmacology and toxicology↗

bioRxiv2026

CTLA-4 inhibitors drive colitis through metabolic reprogramming-mediated Treg/Th17 imbalance

Immune checkpoint inhibitors (ICIs), especially CTLA-4 inhibitors (CTLA-4), exhibit a high incidence of colitis as an immune-related adverse event (irAE) during cancer treatment, severely limiting patient benefit. Clinically, both treatment interruption and existing intervention drugs for ICI-mediated colitis may compromise antitumor efficacy. However, there is inadequate research on the pathogenesis of ICI-mediated colitis, with findings often conflicting. Here, we first established multiple clinically relevant animal models, including an immuno-humanized ICI-mediated colitis model. Through time-series transcriptomics, we discovered that CTLA-4-induced colonic toxicity exhibits characteristics ranging from early metabolic reprogramming represented by glycolysis to later immune disorders represented by Th17 responses. By targeting colonic CTLA-4+ T cells, CTLA-4 blocked CD80/CD86-CTLA-4 interaction, thereby activating the PI3K-AKT-mTOR pathway. Subsequently, mTOR mediated metabolic reprogramming in T cells, shifting them from Treg-biased oxidative phosphorylation to Th17-biased glycolysis. The colonic toxicity of CTLA-4 has also been demonstrated to depend on the PI3K-AKT-mTOR pathway, glycolysis, and Th17 responses. Notably, metformin significantly relieved ICI-mediated colitis by inhibiting mTOR without impeding antitumor efficacy. Collectively, these findings highlighted the metabolic-immune axis in the colonic toxicity of ICI and provided a clinically superior intervention strategy.

pharmacology and toxicology↗

bioRxiv2025

Neutrophil extracellular traps-mediated thrombosis drive pyrrolizidine alkaloid-induced hepatic sinusoidal obstruction syndrome

Hepatic sinusoidal obstruction syndrome (HSOS) caused by pyrrolizidine alkaloid (PA) is a life-threatening disease with limited treatments, yet the initiating vascular event remains undefined. Neutrophil extracellular traps (NETs), as key driver of immunothrombosis in various thromboinflammatory diseases, may represent a critical yet uncharacterized component in the pathogenesis of PA-HSOS. Rats and mice were separately administered monocrotaline (MCT) or senecionine (SEN) via gavage to induce HSOS. Human hepatic sinusoidal endothelial cell (HHSEC) and primary human neutrophil treated with MCT, SEN, or corresponding metabolites were used as in vitro models. In separate experiments, animals received a neutrophil elastase (NE) inhibitor or neutrophil-depleting antibody to evaluate the contribution of NETs. We detected NETs within the sinusoids of necrotic liver lobes, as evidenced by robust immunostaining for NETs markers, accompanied with elevated level of circulating cell-free DNA, and hepatic citrullinated histone H3. Sinusoidal microthrombi containing VWF, CD41, and fibrin(ogen) were also stained positive for neutrophils in PA-HSOS models. Treatment with NE inhibitor or neutrophil depletion markedly attenuated PA-induced liver injury by concomitantly suppressing NETs formation and intrahepatic thrombogenesis. In vitro, conditioned medium from HHSEC exposed to MCT or SEN metabolites potently induced NETs formation. HHSEC injured by PA metabolites released CXCL8. Furthermore, hepatic mRNA and protein levels of CXCL1 and CXCL2 (murine homologous to human CXCL8) were up-regulated in PA-HSOS models, accompanied by a parallel elevation of their high-affinity receptors, CXCR1 and CXCR2. Our study identifies NETs-mediated immunothrombosis as a key driver in HSOS, which provides a promising target for PA-HSOS treatment.

pharmacology and toxicology↗

bioRxiv2025

Development of LYTACs via incorporating a nucleolin-targeting and lysosome-directed aptamer

Lysosomal targeting chimeras (LYTACs) represent an emerging class of bifunctional molecules that bridge extracellular target proteins with intrinsic lysosome-targeting receptors (LTRs) on the cell surface, facilitating endocytic internalization and subsequent lysosomal degradation of the targets. However, the therapeutic potential of LYTACs has been limited by the scarcity of suitable intrinsic LTRs. We previously identified an aptamer, SAPT8, that selectively targets nucleolin, a shuttling protein overexpressed on the surface of pathogenic FLSs in rheumatoid arthritis (RA), and induced its lysosomal degradation. In this study, we repurposed SAPT8 as a tumor-targeting and lysosome-directed ligand, leveraging the elevated expression of NCL on tumor cell surfaces. By conjugating SAPT8 with either the c-Met-binding aptamer SL1 or the small molecule inhibitor Tepotinib, we engineered novel LYTACs that demonstrated potent tumor-targeting capability and induced concurrent degradation of both c-Met and NCL, leading to significant antitumor effects. Furthermore, fusion of SAPT8 with VEGFR-2-targeting aptamer Apt02 generated LYTACs that simultaneously degraded VEGFR-2 and NCL, effectively suppressing RA-FLS activity. These results establish SAPT8 as a versatile platform for developing next-generation LYTACs, overcoming current limitations in extracellular protein degradation by circumventing dependence on endogenous LTRs. Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=69 SRC="FIGDIR/small/672993v1_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@975b74org.highwire.dtl.DTLVardef@f55565org.highwire.dtl.DTLVardef@b9639corg.highwire.dtl.DTLVardef@13aaba7_HPS_FORMAT_FIGEXP M_FIG C_FIG

pathology↗

bioRxiv2024

CDC5L surveils cellular stress responses and stress granule formation through transcriptional repression

Cells have evolved a variety of mechanisms to respond to stress, such as activating the PERK- eIF2 pathway and forming stress granules (SGs). It is important that these mechanisms are inducted only when necessary and exerted at appropriate levels, to prevent spontaneous or excessive activation of stress responses. However, the mechanisms by which cells keep the stress response programs in check are elusive. In this study, we discovered that downregulation of Cell Division Cycle 5 Like (CDC5L) causes spontaneous SG formation in the absence of any stress, which is independent of its known functions in the cell cycle or the PRP19 complex. Instead, we found that CDC5L binds to the PERK promoter through its DNA-binding domains and represses PERK mRNA transcription. As a result, it negatively regulates the abundance of PERK protein and the phosphorylation levels of eIF2, thereby suppressing the PERK-eIF2 signaling pathway and preventing undesirable SG assembly. Further RNA-sequencing (seq) and chromatin immunoprecipitation (ChIP)-seq analyses reveal a dual function of CDC5L in gene transcription: it acts as a transcriptional activator in cell cycle control but as a repressor in cellular stress responses. Finally, we show that the loss of CDC5L decreases cell viability and fly survival under mild stress conditions. Together, our findings demonstrate a previously unknown role and mechanism of CDC5L in the surveillance of cellular stress through transcriptional repression, which serves as a gatekeeper for the stress response programs such as the PERK-eIF2 pathway and SG formation. Significance statementCells need to respond to stress promptly for survival. Meanwhile, it is equally important to prevent spontaneous or excessive activation of stress response programs when no stress or only minor stress is present. Here, we reveal that the DNA/RNA-binding protein CDC5L represses the transcription of a cluster of stress response genes including PERK. In doing so, CDC5L suppresses the PERK-eIF2 pathway and prevents spontaneous SG assembly. Downregulation of CDC5L releases the restraint on these genes, resulting in an exaggerated response to stress and decreased viability in both cell and fly models. Taken together, this study demonstrates the existence of a gatekeeper mechanism that surveils the stress response programs and highlights the crucial role of CDC5L-mediated transcriptional repression in this regulation.

cell biology↗

bioRxiv2023

Characterization of m6A modifiers and RNA modifications in uterine fibroids

Uterine leiomyoma or fibroids are the most common prevalent noncancerous tumors of the uterine muscle layer. Common symptoms associated with fibroids include pelvic pain, heavy menstrual bleeding, anemia, and pelvic pressure. These tumors are a leading cause of gynecological care but lack long-term therapy as the origin and development of fibroids are not well understood. Several next-generation sequencing technologies have been performed to identify the underlying genetic and epigenetic basis of fibroids. However, there remains a systemic gap in our understanding of molecular and biological process that define uterine fibroids. Recent epitranscriptomics studies have unraveled RNA modifications that are associated with all forms of RNA and are thought to influence both normal physiological functions and the progression of diseases. We quantified RNA expression profiles by analyzing publicly available RNA-seq data for 15 known epigenetic mediators to identify their expression profile in uterine fibroids compared to myometrium. To validate our findings, we performed RT-qPCR on a separate cohort of uterine fibroids targeting these modifiers confirming our RNA-seq data. We then examined protein profiles of key m6A modifiers in fibroids and their matched myometrium. In concordance with our RNA expression profiles, no significant differences were observed in these proteins in uterine fibroids compared to myometrium. To determine abundance of RNA modifications, mRNA and small RNA from fibroids and matched myometrium were analyzed by UHPLC MS/MS. In addition to the prevalent N6-methyladenosine (m6A), we identified 11 other known modifiers but did not identify any aberrant expression in fibroids. We then mined a previously published dataset and identified differential expression of m6A modifiers that were specific to fibroid genetic sub-type. Our analysis also identified m6A consensus motifs on genes previously identified to be dysregulated in uterine fibroids. Overall, using state-of-the-art mass spectrometry, RNA expression and protein profiles, we characterized and identified differentially expressed m6A modifiers in relation to driver mutations. Despite the use of several different approaches, we identified limited differential expression of RNA modifiers and associated modifications in uterine fibroids. However, considering the highly heterogenous genomic and cellular nature of fibroids, and the possible contribution of single molecule m6A modifications to fibroid pathology, there is a need for greater in-depth characterization of m6A marks and modifiers in a larger and varied patient cohort.

cancer biology↗

bioRxiv2023

Structural insights into Rad18 targeting by the SLF1 BRCT domains

Rad18 interacts with the SMC5/6 localization factor 1 (SLF1) to recruit the SMC5/6 complex to DNA damage sites for repair. The mechanism of the specific Rad18 recognition by SLF1 is unclear. Here, we present crystal structure of the tandem BRCT repeat (tBRCT) in SLF1 (SLF1tBRCT) bound with the interacting Rad18 peptide. Our structure and biochemical studies demonstrate that SLF1tBRCT interacts with two phosphoserines and adjacent residues in Rad18 for high affinity and specificity Rad18 recognition. We found that SLF1tBRCT utilizes mechanisms common among tBRCTs as well as unique ones for Rad18 binding, the latter include interactions with an -helical structure in Rad18 that has not been observed in other tBRCT-bound ligand proteins. Our work provides structural insights into Rad18 targeting by SLF1 and expands the understanding of BRCT-mediated complex assembly.

biochemistry↗

bioRxiv2023

Human Retinal Ganglion Cells Respond to Evolutionarily Conserved Chemotropic Cues for Intra Retinal Guidance and Regeneration

Retinal ganglion cells (RGCs) connect the retina with the higher centers in the brain for visual perception. Their degeneration leads to irreversible vision loss in glaucoma patients. Since human RGCs (hRGCs) are born during fetal development and connections with the central targets are established before birth, the mechanism underlying their axon growth and guidance remains poorly understood. Here, using RGCs directly generated from human embryonic stem cells, we demonstrate that hRGCs express a battery of guidance receptors. These receptors allow hRGCs to read the spatially arrayed chemotropic cues in the developing rat retina for the centripetal orientation of axons toward the optic disc, suggesting that the mechanism of intra-retinal guidance is conserved in hRGCs. The centripetal orientation of hRGCs axons is not only in response to chemo-repulsion but also involves chemo-attraction, mediated by Netrin-1/DCC interactions. The spatially arrayed chemotropic cues differentially influence hRGCs physiological responses, suggesting that neural activity of hRGCs may facilitate axon growth during inter-retinal guidance. Additionally, we demonstrate that Netrin-1/DCC interactions, besides promoting axon growth, facilitate hRGCs axon regeneration by recruiting the mTOR signaling pathway. The diverse influence of Netrin-1/DCC interactions ranging from axon growth to regeneration may involve recruitment of multiple intracellular signaling pathways as revealed by transcriptome analysis of hRGCs. From the perspective of ex-vivo stem cell approach to glaucomatous degeneration, our findings posit that ex-vivo generated human RGCs are capable of reading the intra-retinal cues for guidance toward the optic disc, the first step toward connecting with the central target to restore vision.

developmental biology↗

bioRxiv2022

FGFR1 governs iron metabolism via regulating post-translational modification of IRP2 in prostate cancer cells

The acquisition of ectopic fibroblast growth factor receptor 1 (FGFR1) expression is well documented in prostate cancer (PCa) progression. However, how FGFR1 facilitates PCa progression is not fully revealed, although it is known to confer tumor growth advantage and metastasis. Here we report that FGFR1 deletion in DU145 human PCa cells retards the iron metabolism and reduces transferrin receptor 1 (TFR1), which synergistically enhances the anti-cancer effect of iron chelator. FGFR1 and TFR1 are highly expressed in PCa, and FGFR1 overexpression increased TFR1 in PCa cell lines. Furthermore, we first time demonstrate that FGFR1 deletion boosts and shifts the degradation of iron regulatory proteins 2 (IRP2) to downregulate TFR1. Detailed characterization revealed that based on FGFR1 deletion the stability of IRP2 is broken, whose degradation is accelerated, which can be not observed without FGFR1 deletion. In addition, IRP2 overexpression rescue the malignancy degree of DU145 cells. Our results here unravel a novel mechanism by which FGFR1 promotes PCa progression by upregulating iron metabolism, and that the FGFR1/IRP2/TFR1 axis can be a potential target for managing PCa progression.

cancer biology↗

bioRxiv2022

Neuronal activity-related transcription is blunted in immature compared to mature dentate granule cells

Immature dentate granule cells (DGCs) generated in the hippocampus during adulthood are believed to play a unique role in dentate gyrus function. Although immature DGCs have hyperexcitable membrane properties in vitro, the consequences of this hyperexcitability in vivo remain unclear. In particular, the relationship between experiences that activate the dentate gyrus, such as exploration of a novel environment (NE), and downstream molecular processes that modify dentate gyrus circuitry in response to cellular activation are unknown in this cell population. We first performed quantification of immediate early gene proteins in immature (5-week-old) and mature (13-week-old) DGCs from mice exposed to a NE. Paradoxically, we observed lower immediate early gene protein expression in hyperexcitable immature DGCs. We then isolated nuclei from active and inactive immature DGCs and performed single nuclei RNA-Sequencing. Compared to mature nuclei collected from the same animal, immature DGC nuclei showed less activity-induced transcriptional change, even though they were classified as active based on expression of ARC protein. These results demonstrate that the coupling of spatial exploration, cellular activation, and transcriptional change differs between immature and mature DGCs, with blunted activity-induced changes in immature cells.

neuroscience↗

bioRxiv2022

Expansion and Adaptive Evolution of the mTERF Gene Family in Plants

Mitochondrial transcription termination factor (mTERF) genes are encoded in the nucleus and bind to nucleic acids to regulate the replication, transcription and translation of mitochondrial genomes. Plants possess a large family of mTERF genes that play important roles in regulating organellar gene expression and stress response. However, their origin and expansion in land plants has not been examined. Here, we conducted a comprehensive molecular evolution analysis of 611 mTERF genes identified in 18 plant species, including algae, moss, fern, gymnosperm and flowering plants. Higher plants have more mTERF genes compared to lower plants, forming a huge higher plant-specific clade (M-class mTERF genes). M-class mTERF genes occur in clusters, suggesting that tandem duplication contributed to their expansion. Compared to other mTERF genes, M-class mTERF genes have undergone rapid evolution, and several significant positively selected sites were located in nucleic acid-binding sites. The strong correlation between the number of M-class mTERF genes and corresponding mitochondrial genome variation suggests that the rapid evolution of M-class mTERF genes might account for the changes in the complex machinery for expression regulation of plant mitochondrial genomes, providing molecular evidence for the host-parasite interaction hypothesis between the nucleus and mitochondria.

plant biology↗

bioRxiv2022

Reduced synaptic activity and dysregulated extracellular matrix pathways are common phenotypes in midbrain neurons derived from sporadic and mutation-associated Parkinson's disease patients

Several mutations that cause Parkinsons disease (PD) have been identified over the past decade. These account for 15-25% of PD cases; the rest of the cases are considered sporadic. Currently, it is accepted that PD is not a single monolithic disease but rather a constellation of diseases with some common phenotypes. While rodent models exist for some of the PD-causing mutations, research on the sporadic forms of PD is lagging due to a lack of cellular models. In our study, we differentiated PD patient-derived dopaminergic (DA) neurons from induced pluripotent stem cells (iPSCs) of several PD-causing mutations as well as from sporadic PD patients. Strikingly, we observed a common neurophysiological phenotype: Neurons derived from PD patients had a severe reduction in the rate of synaptic currents compared to those derived from healthy controls. While the relationship between mutations in genes such as the SNCA and LRRK2 and a reduction in synaptic transmission has been investigated before, here we show evidence that the pathogenesis of the synapses in neurons is a general phenotype in PD. Analysis of RNA sequencing results displayed changes in gene expression in different synaptic mechanisms as well as other affected pathways such as extracellular matrix-related pathways. Some of these dysregulated pathways are common to all PD patients (monogenic or idiopathic). Our data, therefore, shows changes that are central and convergent to PD and suggests a strong involvement of the tetra-partite synapse in PD pathophysiology.

neuroscience↗

bioRxiv2021

Deep oncopanel sequencing reveals fixation time- and within block position-dependent quality degradation in FFPE processed samples

Clinical laboratories routinely use formalin-fixed paraffin-embedded (FFPE) tissue or cell block cytology samples in oncology panel sequencing to identify mutations that can predict patient response to targeted therapy. To understand the technical error due to FFPE processing, a robustly characterized normal cell line was used to create FFPE samples with four different pre-tissue processing formalin fixation times. A total of 96 FFPE sections were then distributed to different laboratories for targeted sequencing analysis by four oncopanels, and variants resulting from technical error were identified. Tissue sections that failed more frequently showed low cellularity, lower than recommended library preparation DNA input, or target sequencing depth. Importantly, sections from block surfaces were more likely to show FFPE-specific errors, akin to "edge effects" seen in histology, and the depth of formalin damage was related to fixation time. To assure reliable results, we recommend avoiding the block surface portion and restricting mutation detection to genomic regions of high confidence.

cancer biology↗

bioRxiv2020

Recombinant SARS-CoV-2 RBD molecule with a T helper epitope as a built in adjuvant induces strong neutralization antibody response

Without approved vaccines and specific treatment, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is spreading around the world with above 20 million COVID-19 cases and approximately 700 thousand deaths until now. An efficacious and affordable vaccine is urgently needed. The Val308 - Gly548 of Spike protein of SARS-CoV-2 linked with Gln830 - Glu843 of Tetanus toxoid (TT peptide) (designated as S1-4) and without TT peptide (designated as S1-5), and prokaryotic expression, chromatography purification and the rational renaturation of the protein were performed. The antigenicity and immunogenicity of S1-4 protein was evaluated by Western Blotting (WB) in vitro and immune responses in mice, respectively. The protective efficiency of it was measured by virus neutralization test in Vero E6 cells with SARS-CoV-2. S1-4 protein was prepared to high homogeneity and purity by prokaryotic expression and chromatography purification. Adjuvanted with Alum, S1-4 protein stimulated a strong antibody response in immunized mice and caused a major Th2-type cellular immunity compared with S1-5 protein. Furthermore, the immunized sera could protect the Vero E6 cells from SARS-CoV-2 infection with neutralization antibody GMT 256. The candidate subunit vaccine molecule could stimulate strong humoral and Th1 and Th2-type cellular immune response in mice, giving us solid evidence that S1-4 protein could be a promising subunit vaccine candidate.

bioengineering↗

bioRxiv2020

Microbubble-Mediated Cavitation Promotes Apoptosis and Suppresses Invasion in AsPC-1 Cells

This study aimed to identify the potential and mechanisms of microbubble-mediated cavitation in promoting apoptosis and suppressing invasion in cancer cells. AsPC-1 cells were used and divided into four groups: control group, microbubble-only (MB) group, ultrasound-only (US) group, and ultrasound combined with microbubbles (US+MB) group. Pulse ultrasound was used with a frequency of 360 kHz and an intensity of 0.7 W/cm2 for 1 min (duty rate=50%). Then cells in four groups were cultured for 24 h. Cell counting kit-8 illustrated that US+MB could decrease cell viability. Western blot confirmed that US+MB increased cleaved Caspase-3, Bcl-2-associated X protein (BAX), and decreased the B-cell lymphoma-2 (Bcl-2) levels. Besides, US+MB increased intracellular calcium ions and down-regulated cleaved Caspase-8. For proliferation ability, cells in US+MB group had a lower expression of Ki67 and the weakened colony formation ability. The transwell invasion assay showed that US+MB could decrease invasion ability in AsPC-1 cells. Further evidence showed that cells conducted with US+MB had the lower level of hypoxia-inducible factor-1 (HIF-1) and Vimentin and the higher expression of E-cadherin than the other three groups. Finally, cells conducted with US+MB had less invadopodia formation. In conclusion, these results suggested that microbubble-mediated cavitation promoted apoptosis and suppressed invasion in AsPC-1 cells. SignificanceCancer cells have a high rate of cell division and a high rate of cell division can speed up the development of hypoxia which lead to promote cancer invasion and metastasis. Here we used microbubble-mediated cavitation to generate a mechanical shock wave which could effectively kill cancer cells through physical damage and intrinsic signaling pathway. Furthermore, effective killing of cancer cells could restrain the development of hypoxia and prevent invasion ability of cancer cells.

bioengineering↗

bioRxiv2020

Lineage Functional Types (LFTs): Characterizing functional diversity to enhance the representation of ecological behavior in Earth System Models

Process-based vegetation models attempt to represent the wide range of trait variation in biomes by grouping ecologically similar species into plant functional types (PFTs). This approach has been successful in representing many aspects of plant physiology and biophysics, but struggles to capture biogeographic history and ecological dynamics that determine biome boundaries and plant distributions. Grass dominated ecosystems are broadly distributed across all vegetated continents and harbor large functional diversity, yet most Earth System Models (ESMs) summarize grasses into two generic PFTs based primarily on differences between temperate C3 grasses and (sub)tropical C4 grasses. Incorporation of species-level trait variation is an active area of research to enhance the ecological realism of PFTs, which form the basis for vegetation processes and dynamics in ESMs. Using reported measurements, we developed grass functional trait values (physiological, structural, biochemical, anatomical, phenological, and disturbance-related) of dominant lineages to improve ESM representations. Our method is fundamentally different from previous efforts, as it uses phylogenetic relatedness to create lineage-based functional types (LFTs), situated between species-level trait data and PFT-level abstractions, thus providing a realistic representation of functional diversity and opening the door to the development of new vegetation models.

ecology↗