Biology subjects

Fan, G.

Publications and source records attributed to Fan, G..

At least 19 recordsLinked to original sources

bioRxiv2026

Deletion of LRP1 in Smooth Muscle Cells Induces Infrarenal Aortic Aneurysms in Mice

Background: Low-density lipoprotein receptor-related protein 1 (LRP1) in smooth muscle cells (SMCs) is essential for maintaining aortic wall integrity. This study investigated whether deletion of LRP1 in SMCs induces region-specific aortic pathology and evaluated a potential therapeutic strategy. Methods: Lrp1-floxed mice were bred with Sm22-Cre+/0 mice to generate mice with SMC-LRP1 deletion (SMC-LRP1-/-) and wild-type littermates (SMC-LRP1+/+). Micro-computed tomography (micro-CT) was used to visualize the aorta, and aortic tissue sections were characterized histologically. To evaluate a potential therapeutic strategy, antisense oligonucleotides (ASOs) targeting hepatocyte-derived angiotensinogen (AGT) were administered to inhibit AGT synthesis. Results: Immunostaining and Western blotting confirmed LRP1 deletion in aortic SMCs. At 40 weeks of age, micro-CT revealed marked increases in aortic width and volume. Although dilatation occurred throughout the aorta, the infrarenal region exhibited the greatest expansion in both male and female SMC-LRP1-/- mice compared with SMC-LRP1+/+ littermates; subsequent analyses therefore focused on this region. LRP1 deletion in SMCs caused pronounced SMC loss and increased collagen deposition in the infrarenal aorta. Inhibition of hepatocyte-derived AGT with ASO attenuated infrarenal aortic dilatation and preserved aortic wall integrity in both male and female mice. Conclusions: Deletion of LRP1 in SMCs causes progressive aortic dilatation that includes the infrarenal aorta. Pharmacologic inhibition of hepatocyte-derived AGT attenuates infrarenal aortic dilatation.

pathology↗

bioRxiv2026

TFL1 homolog integrates temperature signals to control timing of developmental transitions in woodland strawberry

In overwintering plants of temperate climates, inflorescence and flower buds commonly form in autumn under cool temperatures, while flowering occurs the following spring. However, how cool temperatures regulate inflorescence and flower development remains poorly understood. We used woodland strawberry (Fragaria vesca L.), a perennial Rosaceae herb, to investigate the effects of cool temperature on reproductive development. We characterized temperature-dependent developmental patterns at macroscopic and microscopic scale and combined time- and stage-specific gene expression analyses. We show that cool temperature accelerates floral transition but subsequently slows inflorescence and flower development, causing increased inflorescence branching, higher floral organ numbers, and berry fasciation. These effects were restricted to the apical inflorescence and flower meristems, whereas higher-order meristems remained unaffected. Expression analyses revealed stage- and temperature-dependent changes in the abundance and spatial distribution of TERMINAL FLOWER1 (FvTFL1) encoding the floral repressor. Loss of functional FvTFL1 abolished temperature-dependent differences in floral transition, inflorescence branching, and floral organ numbers. Our results establish FvTFL1 as a major regulator of temperature-responsive reproductive development. The stage-specific activity of FvTFL1 provides a mechanism through which woodland strawberry integrates temperature signals to balance developmental plasticity of the primary growth axis with the robustness of lateral branches.

plant biology↗

bioRxiv2026

Diatoms maintain metabolic activity in deep ocean twilight zones

Phytoplankton are primarily confined to the sunlit epipelagic zone, yet intact algal cells persist in the oceans mesopelagic twilight zone where light is minimal. However, their survival strategies in the deeper ocean remain unknown. Here, we isolate Chaetoceros sp. DS1 from 1000 m depth and reveal its survival mechanisms under prolonged darkness and high pressure, including membrane lipid remodeling and enhanced antioxidant defenses. Importantly, DS1 maintains a latent photosynthetic reserve that activates upon exposure to dim blue light and higher pressure typical of the twilight zone, enabling photosynthesis and nutrient uptake. It exhibits metabolic flexibility by utilizing stored carbon in darkness and assimilating organic carbon under dim light. Global meta-omics data show widespread, transcriptionally active Chaetoceros-like diatoms in the twilight zone, expressing blue-light sensors and protein synthesis genes. These findings identify the ocean twilight zone as a previously overlooked niche for metabolically active phytoplankton, expanding understanding of deep-ocean microbial ecology and carbon cycling.

ecology↗

bioRxiv2026

Evolutionary Origins of Molecular Programs Underlying Brain Circuitry

The vertebrate pallium harbors independently evolved structures that, nevertheless, support strikingly similar sensory and cognitive circuit architectures. The mechanisms and evolutionary timing driving the emergence of these parallel pallial circuits remain unelucidated. Here, we integrated spatial transcriptomic and single-nucleus RNA-seq datasets from eight representative vertebrate species spanning approximately 500 million years of evolution to reconstruct the evolutionary assembly of the primary sensory-allocortical (Pr-Al) molecular axis, a conserved cortical hierarchical axis defined in our prior work. We uncovered that Pr- and Al-like neuronal identities are deeply conserved across sarcopterygians, encompassing all tetrapods and lobe-finned fishes. Intriguingly, this ancestral neuronal homology is uncoupled from spatially partitioned patterning: only tetrapods further compartmentalized these Pr- and Al- neurons into distinct pallium regions. Functional enrichment of Pr- and Al- gene programs uncovered a conserved tetrapod genetic core suite including MAPK signaling and axon guidance pathways. This core toolkit underwent sequential functional refinement from amphibians through mammals. Notably, mammals and birds convergently evolved association-cortical molecular profiles enriched for synaptic regulatory genes to support advanced cognitive functions. Collectively, this work delineates a stepwise vertebrate pallium evolutionary paradigm that explains how conserved molecular modules shape spatially organized brain circuitry across deep evolutionary time.

evolutionary biology↗

bioRxiv2026

Eleven deep-sea coral genome assemblies unveil insights into evolution, adaptation, and coral biodiversity

Deep-sea corals are vital in maintaining coral ecosystem biodiversity, yet their genetic characteristics remain largely unexplored. Here, we present 11 deep-sea coral genome assemblies, including four Hexacorallia and seven Octocorallia species, significantly contributing new genomic information across two orders. Our analysis reveals the historical dynamics of coral speciation and the influence of environmental factors on the evolution of coral reef ecosystems.Total of 126 horizontal gene transfer (HGT) events were detected, among which genes from the ancestor of symbiodiniaceae indicate that the ancestors of deep-sea corals may have inhabited shallow-sea environments. Notably, several of these HGTs are involved in phosphorus (PhnX/PhnW) and cholesterol (DHCR7) metabolisms within corals, indicating that HGTs may serve as an adaptive survival strategy for the coral holobionts. Deep-sea corals also rely on symbiotic bacteria to synthesize 10 essential amino acids (such as valine and tyrosine), retaining only partial amino acid synthesis capacity. In addition, we investigated the evolution of key biological rhythm genes and temperature adaptation in corals. The loss of key rhythm genes (e.g., clock and cry) in deep-sea corals and copy number difference of genes related to heat stress (e.g., Cbl-b and Rchy) revealed genetic difference between deep-sea and shallow-sea corals. Our new genome assemblies enhance the understanding of deep-sea coral evolution, biodiversity, and adaptation, providing a genetic foundation for coral conservation.

genomics↗

bioRxiv2026

FvTFL1 reverses the function of FvGI-FvCO-FvFT1 pathway in the photoperiodic flowering of woodland strawberry

O_LIPhotoperiod is a stable seasonal signal. Although the photoperiodic flowering is well understood in short-day (SD) and long-day (LD) annual plants, regulatory mechanisms in perennials remain elusive. In a perennial woodland strawberry (Fragaria vesca L.), flowering is induced in SDs in autumn and plants flower following spring, while in plants with mutated FvTERMINAL FLOWER1 (FvTFL1), LDs induce flowering. C_LIO_LIWe investigated photoperiodic flowering of F. vesca through phenotypic and molecular characterization of transgenic lines and their crosses. We studied natural variation in flowering time and gene expression in European accessions, and explored their correlations with climatic, geographical and genetic origins. C_LIO_LIWe showed that FvGIGANTEA (FvGI) and FvCONSTANS (FvCO) activate FvFLOWERING LOCUS T1 (FvFT1) in LDs resulting in early flowering in fvtfl1 mutant, while in SD F. vesca, activation of FvTFL1 by FvFT1 reverses the photoperiodic requirement of flowering. In natural accessions, decreasing expression of FvFT1 and FvTFL1 towards colder climates in the east and north correlated with earlier flowering. C_LIO_LIWe define a photoperiodic flowering mechanism controlling floral transition of perennial F. vesca in autumn that differs from known mechanisms in annual and perennial plants. Our findings open new avenues to understand how perennial plants cope with changing seasons across climatic and geographical ranges. C_LI

plant biology↗

bioRxiv2026

ExMODE: A Multi-Omics Repository for Extremophile Adaptation and Bioprospecting

Extreme environments, though hostile to most life forms, host specialized extremophile communities that have redefined biological cognition and emerged as vital biotechnological resources, with their unique adaptive traits and bioactive molecules driving advances in multiple scientific and industrial fields. However, research on extremophiles is hindered by limitations in culture-based methods, fragmented multi-omics data with non-uniform annotation standards across repositories, the lack of cross-extreme comparative research in existing resources, and the singularity of data dimensionality that neglects key structural information, all of which restrict the functional interpretation of extremophile microbes and the exploitation of their bioprospecting potential. To tackle these challenges, we developed ExMODE (https://db.genomics.cn/exmode/), a comprehensive multi-omics database platform dedicated to extremophiles. It centrally integrates multi-omics data from diverse extreme habitats with a standardized annotation framework, resolving data fragmentation and enabling systematic cross-environment comparative analyses to elucidate extremophile adaptive mechanisms. Moreover, ExMODE aggregates multi-dimensional datasets including genes, genomes, secondary metabolite sequences and protein structures, overcoming the constraints of single-dimensional data and significantly improving the efficiency of biotechnological resource discovery from extreme microorganisms.

microbiology↗

bioRxiv2026

Rewiring of 3D Enhancer-Promoter Interactome Underlies Diabetic Endothelial Dysfunction

BackgroundDiabetic vascular complications are driven by endothelial dysfunction, yet the role of 3D genome organization in this process is unknown. We sought to define the alterations in chromatin architecture in diabetic endothelium and identify the key regulators involved. MethodsWe generated a high-resolution 3D epigenomic atlas of diabetic endothelial cells from mouse models and human subjects using H3K27ac HiChIP, complemented by ChIP-seq, ATAC-seq, and RNA-seq. A human cohort was used to assess protein expression in diabetic versus non-diabetic endothelial cells. To identify JUNB-interacting proteins, we performed rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME), with protein-protein interaction validated by co-immunoprecipitation. Functional validation was performed using in vitro, ex vivo, and in vivo approaches, including endothelial-specific knockdown in a diabetic hindlimb ischemia model. ResultsMulti-omics profiling revealed extensive enhancer reprogramming in diabetic endothelium, with AP-1 binding motifs being consistently and selectively enriched in downregulated enhancers across three distinct diabetic models. Analysis of a human cohort confirmed significantly reduced JUNB protein levels in diabetic endothelial cells. We identified widespread disruption of JUNB-anchored enhancer-promoter interactions, which underlies transcriptional repression of key endothelial genes. RIME and co-immunoprecipitation established the E3 ubiquitin ligase RBBP6 as a direct JUNB interactor that promotes its polyubiquitination and proteasomal degradation in response to hyperglycemia. Human cohort analysis further showed reciprocal elevation of RBBP6 in diabetic endothelial cells. Either JUNB overexpression or RBBP6 knockdown restored enhancer-promoter connectivity, reactivated vasoprotective transcriptional programs, and rescued endothelial function. Critically, endothelial-specific knockdown of Rbbp6 in diabetic mice restored endothelium-dependent vasorelaxation and improved perfusion recovery after hindlimb ischemia, independent of systemic glucose levels. ConclusionsOur study unveils a novel mechanism whereby hyperglycemia induces enhancer reprogramming and disrupts endothelial 3D genome architecture through RBBP6-mediated degradation of JUNB. The RBBP6-JUNB axis is established as a crucial link between metabolic stress and epigenomic reprogramming in vascular disease, presenting a promising therapeutic target for diabetic vasculopathy.

genomics↗

bioRxiv2026

Cell Type Architecture and Positional Gene Gradients in an Adult Animal at Subcellular Resolution

The spatial organization of cell types and gene expression underlies tissue architecture and organismal physiology. However, resolving complete cellular and molecular landscapes within a three-dimensional context remains challenging, particularly in organisms with high cellular heterogeneity and complex geometry. Here, we developed a semi-supervised workflow to reconstruct high-resolution three-dimensional spatial transcriptomic models of the planarian Schmidtea mediterranea at single-cell resolution. Planarians are basal bilaterians capable of regenerating body structures after injury. Our reconstruction maps the distribution of cell types and spatially patterned gene expression across the intact organism and identifies 119 candidate positional control genes (PCGs). These genes are expressed across muscle, neural, and epidermal populations. Functional perturbation of selected candidates, including pitx3, ptpn11, pi4ka, upf3b, and cul1, revealed roles in regeneration following injury. In addition, we identify intestinal cells as prominent components of the microenvironment surrounding adult tgs1 pluripotent stem cells (neoblasts). Together, these results demonstrate the utility of three-dimensional spatial transcriptomic reconstruction for mapping cellular architecture and positional gene regulation in complex adult organisms.

developmental biology↗

bioRxiv2026

4D Single-Cell Spatial Transcriptomics Reveals Dynamic Morphogenetic Gradients and Regenerative Domains in Planarians

Regeneration relies on precise spatiotemporal gene expression and cellular responses to establish tissue identity and body patterning. Using high-resolution Stereo-seq (715 nm) on 353 sections from 16 whole animals at 8 regeneration timepoints, we constructed a 4D spatiotemporal transcriptomic map of planarian regeneration. Our analysis captured 36 refined cell types from 3,508,004 segmented cells, enabling genome-wide transcriptional imputation of gene expression dynamics across body axes at cellular, tissue, and organismal scales. We identified dynamic positional gradients and distinct spatially distributed cell types during regeneration, including an injury-induced Anterior Regenerative Zone (ARZ). The ARZ exhibited enriched positional signals in epidermal, muscle, and neural cells and was regulated by Mediator 8, which is crucial for polarity remodeling and blastema formation. This study provides a comprehensive spatial molecular and cellular map of regenerative processes, highlighting injury-induced spatial domains and key regulatory factors in planarian regeneration. We also provide an interactive web portal, offering a valuable resource for exploring and analyzing regeneration mechanisms in a spatiotemporal context.

developmental biology↗

bioRxiv2026

The genetic repertoire of the deep sea: from sequence to structure and function

The deep sea as the largest and maybe most hostile environment on Earth is still underexplored especially regarding its genetic repertoire. Yet, previous work has revealed significant habitat-specific deep-sea biodiversity. Here, we present an integrated deep-sea genetic dataset comprising 502 million nonredundant genes from 2,138 samples and 2.4 million predicted structures, and used it to link specific protein structures with genetic variants associated with life in the deep sea and to assess their biotechnology potential. Combining global sequence analysis with biophysical and biochemical measurements revealed unprecedented sequence diversity, yet substantial structural conservation of proteins. Especially proteins involved in replication, recombination, and repair were identified to be under rapid evolution and with specialized properties. Among these, a structurally divergent helicase exhibited advantages in controlling nanopore sequencing speed. Thus, our work positions the deep sea as a unique evolutionary engine that generates and hosts genetic diversity and bridges genetic knowledge with biotechnology.

bioinformatics↗

bioRxiv2025

Single-cell atlas reveals alveolar macrophage-specific Oncostatin-M drives pulmonary fibrosis via fibroblast activation in PCV2d infection

A hallmark of pulmonary fibrosis is the aberrant activation of lung fibroblasts into pathological fibroblasts that produce excessive extracellular matrix(1). Clarifying the cell-specific mechanisms by which viruses induce this process is crucial for developing effective strategies to intervene in disease progression. Here, we demonstrate that alveolar macrophage subsets specifically express tumor suppressor M (Osm) after infection by PCV2d infection and related intervention experiments in mice, combined with single-cell transcriptome sequencing (scRNA-seq). Through validation using histopathological analyses and an in vitro macrophage-fibroblast co-culture model, these alveolar macrophage-derived oncostatin M (Osm) were confirmed to specifically drive fibroblast activation. Vaccine intervention experiments further confirmed that targeted inhibition of oncostatin M (Osm) expression in alveolar macrophages significantly attenuated fibroblast activation and extracellular matrix deposition, thereby mitigating pulmonary fibrosis progression. Therefore, subgroup-specific secretion of oncostatin M (Osm) by alveolar macrophages represents a key driver mediating PCV2d infection-induced pulmonary fibrosis, and targeting this pathway offers a potential therapeutic strategy for viral-induced pulmonary fibrosis.

genomics↗

bioRxiv2025

NanoporeDB: A Structural Resource Of Multimeric Protein Nanopores In Single-Molecule Sensing

Protein nanopores are essential molecular gateways in biology and have inspired transformative technologies in biosensing and single-molecule sequencing. While this technology has transformed genomics and biosensing, the discovery of novel nanopore scaffolds remains limited due to the scarcity of experimentally resolved pore structures. Here, we present NanoporeDB, an open-access structural resource comprising over 6,600 high-confidence multimeric models across four representative pore types. Candidate proteins were systematically mined from large-scale datasets, including the AlphaFold Protein Structure Database, UniRef90, and MGnify90, and assembled using AlphaFold-Multimer and AlphaFold3. We performed membrane embedding, pore axis annotation, and constriction profiling to enable functional interpretation. NanoporeDB features an interactive web interface with 3D visualization and quantitative metrics such as insertion depth, tilt angle, and pore geometry. This resource provides a structural foundation for advancing nanopore-based molecular sensing, precision diagnostics, and synthetic biology.

bioinformatics↗

bioRxiv2025

Multimodal AI Decodes Extreme Environment Functional Dark Matter Beyond Homology

Functional annotation of proteins from extreme environments represents a major bottleneck for bioresource discovery, as a vast reservoir of functional dark matter defies existing homology-based methods. We demonstrate that environmental pressures impart conserved physicochemical energy signatures that co-determine protein function with sequence and structure. Here we developed ACCESS, a multimodal graph neural network employing hierarchical contrastive learning with a tailored label-sample co-embedding to fuse energy, sequence, and structural information and overcome homology scarcity. ACCESS surpasses state-of-the-art methods including BLASTp and CLEAN in annotating low-identity enzymes. Applied to extreme environmental metagenomics, we constructed a function map of extremophile enzymes to expand the biocatalyst library, pinpointed functionally critical residues to guide rational design, and enabled large-scale, function-based macro-evolutionary analyses. This paradigm transcends the limitations of homology, illuminating protein dark matter and accelerating the exploration of the biospheres functional diversity for applications in biotechnology and therapeutic development.

bioinformatics↗

bioRxiv2025

Inhibition of CGRP receptor ameliorates AD pathology by reprogramming lipid metabolism through HDAC11/LXRβ/ABCA1 signaling

The Calcitonin gene-related peptide (CGRP) receptor has gained attention in Alzheimers Disease (AD) research due to its involvement in regulating neuroinflammation. However, its role and mechanism in AD pathology remain unclear. Here, we demonstrate that CALCRL, a core component of the CGRP receptor, is upregulated in the hippocampus of AD dementia patients and 5xFAD mice. Knockout of the CGRP receptor ligand Calca or pharmacological blockade using Rimegepant (Rim), reduces soluble A{beta}1-42 oligomer-induced neuronal death and glial inflammation. Rim treatment also rescues neurobehavioral impairments, neurodegeneration, and lipid metabolism dysfunction in 5xFAD mice. Mechanistically, these effects are mediated through HDAC11 inhibition, which enhances LXR{beta} acetylation and ABCA1 expression, promoting the reprogramming of neuronal lipid metabolism. Importantly, this CALCRL/HDAC11/LXR{beta}/ABCA1 axis is conserved across both humans and mice. Our findings uncover a novel mechanism underlying AD pathogenesis and highlight the therapeutic potential of targeting CGRP signaling in AD. HIGHLIGHTSInhibition of CGRP receptor ameliorates disease pathology in models of AD HDAC11 mediates CGRP receptor function in AD HDAC11 is a pivotal regulator in lipid metabolism by LXR{beta}/ABCA1 signaling The HDAC11/LXR{beta}/ABCA1 axis is conserved in AD humans and mice

neuroscience↗

bioRxiv2025

Structural insights and engineering of deep-sea halophilic PET hydrolytic enzymes

Pervasive use of polyethylene terephthalate (PET) poses tremendous challenges for global waste management and environmental sustainability, fueling growing interests in enzymatic degradation as an eco-friendly solution. While PET hydrolases hold significant promise, their industrial deployment is hindered by insufficient performance, particularly under high-salinity conditions raised from high substrate loads. Building on our previous discovery of three deep-sea PET hydrolases (dsPETase01, dsPETase05 and dsPETase06) with exceptional halophilicity and PET-degrading activity, we here present their three-dimensional structures and mechanistic characterization. Structural comparison, site-directed mutagenesis, and domain swapping reveal key structural features and the essential role of C-terminal acidic residues in salt tolerance. Integrating semi-rational protein design, Transformer-based modeling, and disulfide bond engineering, we synergistically enhance the thermostability and catalytic efficiency of dsPETase05. These findings elucidate the unique structural features and salt adaptation mechanisms of deep-sea halophilic PET hydrolases, and inform the future engineering of biocatalysts for application in harsh industrial environments.

molecular biology↗

bioRxiv2025

Potent Efficacy of Computer-Aided Designed Peptide Degrader Drug on PCSK9-Mediated Hypercholesterolemia

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key regulator of low-density lipoprotein receptor (LDLR) degradation, which leads to increased levels of low-density lipoprotein cholesterol (LDL-C) and a heightened risk of hypercholesterolemia. Existing therapeutic strategies--such as monoclonal antibodies and gene-editing approaches--are limited by high production costs, potential safety concerns, and limited effectiveness in targeting intracellular PCSK9. Targeted protein degradation (TPD) represents a promising alternative capable of overcoming these limitations. In this study, we utilized computer-aided drug design (CADD) to develop a peptide-based degrader, Cadd4, aimed at selectively reducing PCSK9 levels. Through molecular docking and structural refinement, a peptide sequence with strong binding affinity to PCSK9 was identified. Functional evaluation was conducted both in vitro using human LX-2 cells and in vivo in high-fat diet (HFD)-induced hypercholesterolemic mouse models. Cellular uptake, PCSK9 degradation, and LDLR restoration were assessed via confocal microscopy, western blotting, and biochemical analysis. Safety was evaluated by monitoring liver enzyme levels and general physiological parameters. Cadd4 exhibited efficient intracellular delivery and selective PCSK9 degradation in LX-2 cell. In HFD-fed mice, hepatic PCSK9 expression was reduced by 38%, accompanied by a marked increase in LDLR levels. These changes translated into a 25% reduction in total plasma cholesterol and a 29% decrease in LDL-C concentrations. Biodistribution studies indicated liver-specific accumulation of Cadd4, consistent with its intended site of action. Experiments using human liver tissue further confirmed its ability to decrease PCSK9 and enhance LDLR levels. No signs of liver toxicity or adverse systemic effects were observed throughout the study. This work introduces Cadd4 as a CADD-designed peptide-based degrader capable of lowering plasma cholesterol by promoting LDLR recovery via PCSK9 degradation. Its intracellular mechanism of action addresses key gaps in current PCSK9-targeted therapies and supports the broader utility of TPD platforms in managing hypercholesterolemia. These findings offer a foundation for developing cost-effective, scalable therapies within the context of precision cardiovascular medicine.

pharmacology and toxicology↗

bioRxiv2025

FvFT1-FvTFL1 epistasis drives flowering time adaptation in woodland strawberry

Floral transition and flower bud development during autumn and winter are common in plants inhabiting temperate and cold climates. However, our understanding of the natural variation and underlying molecular mechanisms of such life-history strategy remain largely limited to Brassicaceae model species. To address this gap, we investigated flowering time variation across a broad geographical and bioclimatic range in Fragaria vesca (woodland strawberry), a perennial herb from the Rosaceae family. We found that the timing of floral transition and subsequent flowering in F. vesca populations is primarily shaped by population structure, reflecting postglacial colonization patterns from distinct refugia, and is further modulated by adaptations to winter temperatures. The association of increasing expression of FvFT1, the strawberry ortholog of FLOWERING LOCUS T, with delayed flowering in accessions from diverse climatic and genetic backgrounds suggested FvFT1 as a major candidate gene regulating flowering time variation. We further demonstrated how distinct florigen and antiflorigen roles of FvFT1 are dependent on functional alleles of F. vesca TERMINAL FLOWER1 (FvTFL1) and how the epistatic relationship between FvFT1 and FvTFL1 controls adaptive flowering time variation by adjusting sensitivity to floral inductive photoperiod and vernalization. Our findings reveal a major molecular basis of how timing of floral transition has adapted to temperature in a Rosaceae model inhabiting multiple climatic zones and highlight lineage-specific adaptive mechanisms underlying convergent life-history strategy. Significance statementMolecular mechanisms underlying flowering time adaptation have been primarily investigated in annual plants that transit to flowering in spring. However, many perennial plant species in temperate climates form flower buds in autumn and winter to flower in the following spring. We uncover wide geographical and climatic patterns of flowering time adaptation in the perennial model species woodland strawberry. We report that natural variation in the expression of strawberry FLOWERING LOCUS T (FvFT1) gene originating ice ages ago and further driven by local temperature adaptations control flowering time variation in this species. Finally, we show how FvFT1 may function as both flowering promoter and repressor depending on the genetic background, thus revealing a novel mechanism of flowering time adaptation.

plant biology↗