Biology subjects

Kundu, S.

Publications and source records attributed to Kundu, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Targeting TMPRSS2-ERG Fusion-Driven Prostate Cancer using Novel HBS-α-Helicomimics

Gene fusions between the androgen receptor (AR)-responsive gene TMPRSS2 and ERG occur in approximately 50% of prostate cancers (PCa), thereby promoting tumorigenesis through aberrant ERG expression. Therapeutic targeting of transcription factor-DNA interfaces remains a formidable challenge, largely owing to the entropic penalty associated with peptide folding during target engagement. Here, we describe the structure-guided design and preclinical evaluation of hydrogen-bond surrogate (HBS)-constrained alpha-helicomimics targeting the ERG-DNA recognition interface. Structural analysis of ERG-DNA complex revealed that DNA binding induces elongation of recognition helix H4 from approximately 2.5 to 4.0 helical turns. To stabilize the bioactive conformation, we incorporated an N-terminal HBS macrocycle, introduced D363E and S366E mutations to enhance DNA binding and structural stability, and added dual NLS-TAT tags to facilitate cellular delivery. Biochemical and cellular assays demonstrated that the lead compound, ERG helicomimics, competitively inhibited ERG binding to ETS motifs, disrupted ERG association with AR and other cofactors, leading to suppressed ERG transcriptional activity. Chromatin immunoprecipitation-qPCR confirmed reduced ERG occupancy at regulatory regions of canonical target genes, accompanied by downregulation of ERG-driven transcriptional programs. ERG helicomimics also reduced proliferation, migration, and invasion in ERG-positive PCa cells. In a murine xenograft model of TMPRSS2-ERG-positive PCa, systemic ERG helicomimics treatment suppressed tumor growth without overt toxicity and reduced Ki-67 expression compared with the designated control peptide. Collectively, our findings support HBS-constrained ERG helicomimics as a rational strategy for targeting ERG-driven PCa and warrant further therapeutic optimization.

cancer biology↗

bioRxiv2026

Scaling of structural variability of ecDNA polymer condensates with copy number boosts and stabilises oncogene regulatory contacts

Extrachromosomal DNAs (ecDNAs) form highly heterogeneous condensates in cancer cells that drive oncogene overexpression, yet how structural variability coexists with stable gene regulation remains unclear. Here, we develop a minimal polymer physics model of MYC-harbouring COLO320-DM ecDNAs, where BRD4-like complexes bind and bridge cognate sites along ecDNA rings. Above a critical binder concentration, ecDNAs phase separate into condensates exhibiting diverse conformations because of their thermodynamic folding degeneracy. Despite this variability, condensates retain conserved interaction scaffolds that give rise to reproducible contact patterns, including in-trans associated domains (I-TADs), genomic regions enriched in intermolecular regulatory contacts between distinct ecDNAs. We find that condensate 3D architecture follows universal scaling relations with ecDNA copy number, n, remaining robust to model parameter changes. Regulatory contacts within I TADs increase linearly with n, yet they are one order of magnitude stronger than in size matched control regions outside I TADs, whereas their relative fluctuations are markedly suppressed as n increases. This scaling produces enhanced, low-noise regulatory environments for oncogenes embedded within I-TADs, such as PVT1-MYC fusions, whereas the canonical MYC copy, located outside, is less amplified as experimentally observed. Our findings reveal universal polymer physics principles underlying ecDNA condensate organization, offering a mechanistic basis for selective oncogene amplification and potential advantages in cancer progression.

biophysics↗

bioRxiv2026

Clustered cytoneme interactions contribute to peripheral nervous system patterning in Drosophila

The formation of patterned adult tissues requires precise spatiotemporal communication between the cells that comprise the tissue during development. The dorsal thoracic sensory bristles of the peripheral nervous system (PNS) of the fruit fly Drosophila melanogaster relies on the activity of cell protrusions called cytonemes. Experimental studies have identified several of the mechanisms that govern individual cytoneme dynamics in the patterning PNS, and theoretical studies have considered the effects of their collective activity. However less is understood about how cytonemes in the developing PNS interact with each other to achieve wild type tissue patterning. Here, using in vivo and ex vivo imaging strategies combined with fly genetics, we show that cytonemes form clusters along the basal surface and that association with clusters promotes the dynamics of individual cytonemes. Clusters are dynamic and transient organizations of cytonemes, and we show that when their movement is perturbed ex vivo through locally aligned nanofibers wildtype PNS patterning is disrupted. We show evidence that cytoneme interactions via clusters is supported by the cell adhesion molecule E-cadherin, as reducing E-cadherin expression leads to changes in cluster dynamics, ability to promote cytoneme length, and overall patterning of the PNS. Taken together, our results support a model in which complex cytoneme interactions promote the dynamics of individual cytonemes. We propose that the enhanced dynamics and stability provided by increased cell-cell interactions may support both the range and strength of local signaling events.

developmental biology↗

bioRxiv2026

Retrieval uncertainty drives rapid consolidation of confabulated memories in retrosplenial cortex

Learning to make associations in the absence of direct reinforcement, based on previous memories of reward or punishment, is an evolutionary trait quintessential for survival. Little is known about if such higher order associations (HOA) can lead to fabrication of new memories for unreal events. We probed if uncertainty during retrieval of old memory representations can trigger such confabulation. Using chemogenetics, in vivo imaging, and behavior we show that uncertainty in memory perception can not only transfer conditioning to hitherto unexperienced novel context but also can get rapidly consolidated. We find while acquisition of HOA require dorsal-CA1 parvalbumin interneuron activity in intact hippocampus, retrieval requires retrosplenial cortex (RSc). We develop an automated Large-scale Brainwide Correlated Activity Mapping (LaBCAM) method to identify functional connectivity changes across different brain regions in such scenarios. LaBCAM finds that only uncertain remote retrieval engages canonical fear circuitry while regular retrieval does not. Longitudinal imaging of dendritic spines in RSc, a region involved in detection and context-dependent conflict resolution, reveals differential reorganization of spines during acquisition and rapid systems consolidation of HOA. Interestingly, we find HOA is implicated early in AD mice model (APP/PS1) and also in aged animals.

neuroscience↗

bioRxiv2026

Coral Guard substrates accelerate growth and fragment fusion for coral restoration

Coral reefs are declining globally, creating an urgent need for scalable technologies that improve the efficiency and effectiveness of active reef restoration. Coral reef restoration is increasingly constrained by algal overgrowth, which suppresses coral growth, survival, and restoration efficiency. Building on the recently developed Coral Guard platform, we evaluate its restoration performance under long-term in situ coral nursery conditions and introduce Fusion Guard Tiles, a geometry-optimized Coral Guard design that accelerates microfragment fusion. We evaluated Coral Guard Plugs using the branching coral Stylophora pistillata under complementary ex situ conditions and Fusion Guard Tiles using the massive reef-building coral Porites evermanni in in situ coral nurseries. In P. evermanni, Fusion Guard Tiles increased lateral tissue growth 2.6-fold and three-dimensional tissue surface area growth by >2.7-fold after 6 months compared with conventional substrates. After 12 months, colony height and volume were approximately 4.0-fold and 2.2-fold greater, respectively, while complete fragment fusion occurred only on Fusion Guard Tiles. In S. pistillata, Coral Guard Plugs increased lateral tissue growth by [~]1.7-fold. Microcomputed tomography revealed 10-13% higher skeletal density in both species. In P. evermanni, Fusion Guard Tiles also increased symbiont density by 70% and tissue protein content by [~]2.5-fold relative to controls. Together, these findings demonstrate that Coral Guard substrates suppress algal competition while accelerating coral growth, skeletal development, and microfragment fusion, providing a scalable, low-maintenance technology to enhance coral nursery productivity and reef restoration.

bioengineering↗

bioRxiv2026

ARL15 promotes inflammatory fibroblast activation and disease severity in rheumatoid arthritis: integrated transcriptomic and collagen-induced arthritis model analyses

BackgroundADP-ribosylation factor-like protein 15 (ARL15) is a rheumatoid arthritis (RA) susceptibility gene identified through GWAS. Previous studies suggested a role for ARL15 in synovial fibroblast (SF) pathogenicity, but its contribution to inflammatory arthritis remains unclear. We investigated the inflammatory role of ARL15 and its therapeutic potential in RA. MethodsARL15 was overexpressed in MH7A cells followed by bulk RNA sequencing and pathway enrichment analyses. Therapeutic relevance was evaluated in collagen-induced arthritis (CIA) mouse model using anti-ARL15 monoclonal antibodies, ARL15-targeting siRNA, or isoquinoline. Arthritis scores, histopathology, micro-CT and serum cytokines were assessed. Publicly available single-cell RNA sequencing (scRNA-seq) datasets were analyzed to determine ARL15 expression in RASF subsets. ResultsARL15 overexpression induced a pro-inflammatory transcriptional program characterized by upregulation of IL1A, IL1B, IL6, IL8, CXCL1, CXCL10, and CCL20. Gene set enrichment analysis revealed activation of IL6-JAK-STAT, TNF, interferon-response, and KRAS signaling pathways, with suppression of oxidative phosphorylation, lipid metabolism, and mTORC1 signaling. In CIA mice, ARL15 inhibition significantly reduced arthritis severity, inflammatory infiltrates, and joint destruction while preserving cartilage and bone integrity. Serum TNF-, IL-6, and IL-1{beta} levels were markedly decreased following ARL15 blockade. Combination monoclonal antibody treatment demonstrated the greatest therapeutic benefit. scRNA-seq analysis showed broad ARL15 expression across RA fibroblast populations, with enrichment in inflammatory lining and SF subsets. ConclusionsARL15 is a pro-inflammatory regulator of SF activation and arthritis progression. Integrated transcriptomic, single-cell, and in vivo analyses identify ARL15 as a therapeutic target for RA and support further translational development of ARL15 based therapies.

immunology↗

bioRxiv2026

A double-blinded, placebo-controlled field trial of an OspA-based oral reservoir targeted vaccine against Borrelia burgdorferi

Lyme disease, caused by Borrelia burgdorferi and transmitted by Ixodes scapularis ticks, remains a significant vector-borne illness in the United States. Small mammal reservoirs, particularly Peromyscus leucopus, play a critical role in B. burgdorferi maintenance. Here we conducted a five-year, randomized, double-blinded, placebo-controlled field trial deploying an oral OspA-based reservoir targeted vaccine (RTV) across seven Maryland sites. Bayesian modeling provided estimates of vaccine impact on mouse anti-OspA antibody levels, nymphal tick infection prevalence (NIP), mouse infection rates, and seroconversion to B. burgdorferi in hunting dogs. RTV sites exhibited an estimated 10.5% proportional increase in protective murine anti-OspA antibody levels and a 15.4% reduction in NIP by year five. We also found a lower infection prevalence in mouse blood fed nymphal ticks (9.8%). RTV sites exhibited modest decreases in mouse infection prevalence and dog seroconversion rates were similar between groups. Our results indicate that anti-OspA antibody in vaccinated-infected P. leucopus reduced B. burgdorferi summertime larval infection prevalence, measured as NIP reductions the following spring. This suggests that OspA-based oral RTV reduces B. burgdorferi transstadial transmission within tick populations. Our findings advance development of reservoir targeted solutions for Lyme disease prevention. Further evaluation of impacts on incidental hosts is needed.

microbiology↗

bioRxiv2026

Denatured Albumin Gains a Function of Regulating Platelet Activity

Platelets are blood cells that play a critical role in hemostasis and thrombosis. Serum albumin, which constitutes approximately 50% of plasma proteins, has traditionally been considered non-interactive with platelets and not involved in platelet function. Here, using a molecular force sensor and platelet adhesion and aggregation assays, we show that serum albumin, if denatured, specifically binds to integrin IIb{beta}3 in platelets and transmits platelet contractile forces, regulating platelet activation, adhesion and aggregation as effectively as fibrinogen (the clotting factor I). 0.1% ethanol or 10 {micro}M hydrogen peroxide, physiologically attainable in blood through alcohol intake or disease-elevated oxidative stress, are sufficient to denature albumin into a functional platelet ligand. These findings revealed albumin as a previously unrecognized but important regulator of platelet functions, with broad implications for the thrombotic risk in the context of physiological conditions that induce albumin denaturation.

cell biology↗

bioRxiv2026

RasG12V Oncogene-Induced Epithelial Senescence and Its Relay Promotes Host Metabolic Syndrome in Drosophila

Precancerous oncogenic activation in a target organ often induces senescence, a tumor-suppressive response known as oncogene-induced senescence (OIS). Clinical observations indicate a strong association of metabolic syndrome (MetS) with the precancerous and early-stage cancers. Notably, cells displaying OIS are characterized by a senescence-associated secretory phenotype (SASP), in which they secrete factors, including inflammatory cytokines. Thus, SASP from cells displaying OIS may trigger host MetS, which likely underpins its association with cancers, such as colorectal cancer (CRC). Here, we tested this hypothesis and show that, in Drosophila, the activated RasG12V oncogene, which is frequently implicated in human CRC, induces OIS in imaginal disc epithelium and systemically triggers host larval MetS via the conserved cytokine Upd1/IL6. Thus, the larval host with RasG12V-induced epithelial OIS displays MetS, characterized by obesity, increased lipid and glycogen accumulation in the fat body, and altered insulin signaling, marked by transition from hyperinsulinemia to insulin resistance--all at a precancerous stage. Further, we also noted hyperphagia and increased expression of insulin-like peptides (dILP2/3/5) in the brain of larvae displaying RasG12V-induced OIS. Notably, RasG12V-induced OIS is systemically relayed, leading to activation of a senescence-like program in the distant fat body. Genetic suppression of upd1 or pharmacological intervention with the senomorphic agent, Metformin, attenuated fat body senescence and mitigated MetS-associated phenotypes. Our findings thus identify a causal relationship between OIS and host MetS, suggesting its utility as an early biomarker for detecting cancers such as CRC and its potential as a prophylactic target.

cancer biology↗

bioRxiv2026

Homologous and Heterologous Immunization with a PIV5-Based Modified OspA Vaccine Confers Equivalent Protection Against Tick-Transmitted Borrelia burgdorferi

Vaccines targeting outer surface protein A (OspA) of Borrelia burgdorferi protect against Lyme disease by eliciting antibodies that neutralize spirochetes in the Ixodes scapularis tick midgut during engorgement before transmission occurs. We evaluated whether different delivery vehicles and administration routes for a modified OspA construct (OspABPBPk) differed in protective efficacy. Four groups of nine C3H-HeN mice were immunized with OspABPBPk delivered intranasally by live parainfluenza virus 5 (PIV5-OspABPBPk) or by subcutaneous administration of recombinant protein adjuvanted with aluminum hydroxide (rOspABPBPk) using three prime-boost regimens and a vector/adjuvant control: homologous intranasal PIV5-OspABPBPk (IN/IN), homologous subcutaneous rOspABPBPk (SC/SC), and heterologous intranasal PIV5-OspABPBPk prime/subcutaneous rOspABPBPk boost (IN/SC). Mice were challenged on day 90, approximately 2 months after the boost, with nymphal ticks infected with 19 strains of B. burgdorferi. All OspABPBPk-containing vaccines elicited high antigen-specific IgG antibody titers (geometric mean titers of 10^4-10^6, approximately 4 log10 higher than the control group), reduced B. burgdorferi loads in engorged nymphal ticks by 1.7-2 log10, neutralized B. burgdorferi motility in multi-strain cultures, and prevented recovery of viable spirochetes from tissues after tick challenge. While one mouse (1/9, 11%) in the heterologous IN/SC vaccinated group had detectable flaB DNA in tissues and seroreactivity to B. burgdorferi PepVF, culture of spirochetes from heart and bladder showed no evidence of active infection. Although homologous immunization produced the most consistent results in mice, different delivery vehicles and routes of immunization with OspABPBPk vaccines did not affect overall efficacy as assessed by recovery of viable B. burgdorferi from tissues.

microbiology↗

bioRxiv2026

Digest before Ingest: Early Recruitment of Membrane-bound DNaseX to Phagocytic Cups in Macrophages

Macrophages engulf and degrade pathogens and cellular debris through phagocytosis. The degradation process was generally believed to occur only after phagosome internalization and maturation. Here, we report an early DNase activity at the nascent phagocytic cup (PC) prior to its closure. Using a fluorescent DNase sensor, we revealed rapid and ubiquitous DNase activity upon PC formation across various macrophage types. We further identified the responsible enzyme as the membrane-bound DNaseX, which is constitutively recruited to the PC during PC formation. F-actin polymerization was found to correlate with DNase activity in the PC, likely by promoting physical engagement of DNaseX with solid DNA materials. Functionally, we show that macrophages degrade extracellular DNA (eDNA) within bacterial biofilms through direct physical contact, clearing the eDNA structures without internalization. These findings reveal a previously unrecognized DNA degradation mechanism operating at the macrophage membrane, suitable for degrading bulky eDNA materials which cannot be directly internalized by macrophages.

cell biology↗

bioRxiv2025

PDK1 and YAP1/TEAD signaling drive acquired KRAS inhibitor resistance in KRAS-mutant non-small cell lung cancer.

Mutations in KRAS are responsible for driving approximately 30% of NSCLC. While historically considered undruggable, recent breakthroughs have seen the FDA approval of two potent KRASG12C inhibitors, sotorasib (AMG510) and adagrasib (MRTX849). However, the efficacy of these inhibitors in the clinics has been limited by primary and acquired means of resistance. To elucidate mechanisms of acquired resistance, we generated a panel of resistant cell lines to the allele-specific KRAS inhibitors MRTX849 and MRTX1133 and observed an increased activation of the PDK1 and YAP1/TEAD signaling pathways. Pharmacological inhibition and genetic loss-of-function studies revealed a strong dependence on these pathways for the generation and maintenance of resistance to KRAS inhibition, which was then validated in vitro and in vivo. Furthermore, overexpression studies revealed that forced expression of either PDK1 or YAP1 led to increased resistance to KRAS inhibition in the sensitive lines. Taken together, our findings suggest that co-targeting PDK1 or YAP1/TEAD might be a potential approach to overcoming resistance to KRAS inhibition in NSCLC.

cancer biology↗

bioRxiv2025

Cardiolipin Remodeling as a Regulatory Switch in Osteogenesis: Insights from Multimodal Metabolic Imaging and Molecular Profiling

Cardiolipin (CL), a mitochondria-specific phospholipid, plays a fundamental role in respiratory chain organization and bioenergetic efficiency, yet its contribution to osteogenic differentiation is poorly defined. Here, we used a multimodal approach integrating untargeted LC-MS lipidomics, Raman spectroscopy, fluorescence lifetime imaging microscopy (FLIM), and structural imaging to investigate CL remodeling during human adipose-derived stem cell differentiation. Lipidomics revealed a selective enrichment of highly unsaturated CL species, accompanied by transcriptional upregulation of the cardiolipin biosynthetic and remodeling enzymes CDS1/2, PGS1, CRLS1, TAZ, and HADHA. Lipidomics also revealed a time-dependent increase in membrane-associated lipids including phosphatidylcholine (PC), serine, and phosphatidylinositol (PI). These lipids were implicated in supporting mitochondrial membrane expansion, oxidative phosphorylation, and signaling processes critical for osteoblast maturation. Spatial imaging techniques confirmed cardiolipin accumulation and redistribution in differentiated cells, while Raman-based direct classical least squares (DCLS) analysis provided label-free mapping of lipid species. Gene Ontology (GO) enrichment and protein-protein interaction network analysis further identified biological pathways related to bone remodeling, cardiolipin metabolism, and osteoblast-specific signaling. Fluorescence Lifetime Imaging Microscopy (FLIM) data revealed a metabolic shift from glycolysis to oxidative phosphorylation during differentiation, supported by structural and gene expression evidence. These changes temporally coincided with matrix mineralization and collagen organization, linking CL metabolism to both cellular bioenergetics and extracellular matrix production. Our findings identify cardiolipin remodeling as a metabolic checkpoint in osteogenesis and suggest that targeted modulation of CL pathways may provide new therapeutic strategies for enhancing bone regeneration.

cell biology↗

bioRxiv2025

Simulating C3-to-CAM transition under ancient atmospheric conditions

Crassulacean Acid Metabolism (CAM) plants have very low water demand and can survive in arid environment. It is hypothesized to evolve from C3 metabolism about 20 to 30 million years ago (MYA) when the Earth faced declining atmospheric CO2 concentration ([CO2]a), increasing aridity and decreasing temperature. Understanding whether and how these atmospheric changes favour C3-to-CAM transition will help in bioengineering CAM into crop plants to tackle the threat of global climate change and ensure food security. Our simulations of plant cellular metabolism under the changing atmospheric conditions of ancient times observe C3-to-CAM transition, capture possible temporal alterations of active metabolic pathways and further confirm that both the reduced [CO2]a and increased water scarcity associated with higher aridity, can act as evolutionary agents, driving the C3-to-CAM transition. Although the predicted elevated [CO2]a of future reveals a reversion towards C3-like behaviour, drought always favours CAM regardless of [CO2]a and temperature levels. Moreover, a minimum oxygen concentration is required to sustain elevated nocturnal respiration necessary for CAM, reflected by the increased activities of enzymes involved in the TCA cycle and the mitochondrial electron transport chain.

plant biology↗

bioRxiv2025

Interactions Between Dietary Metabolites and Regulatory Risk Variants for Human Colon Cancer

Interactions between genetic variants and environmental factors influence malignancy risk, including for colorectal cancer (CRC). Prevalent CRC susceptibility loci reside predominantly in noncoding regulatory DNA where they may interact with dietary influences to dysregulate expression of specific genes predisposing to neoplasia. The impacts of CRC protective and risk dietary metabolites, butyrate and deoxycholic acid, were thus studied on the transcription-directing activity of 3703 regulatory CRC-associated variants via massively parallel reporter assays (MPRA) in human colonic cells. 1595 variant-dietary metabolite interactions were identified, pointing to dysregulation of MED13L, NKD2, and several modulators of Wnt/{beta}-catenin signaling in potential CRC gene-environment interactions (GxE). Opposing impacts of butyrate and deoxycholic acid were also uncovered, indicating dietary influences may converge on common CRC risk loci and nominating FOSL1 and SP1 as mediators of these opposing responses. Coupling MPRA to relevant environmental factors offers an approach to extend insight into GxE in common human cancers.

genomics↗

bioRxiv2025

Epigenetic inheritance of complex learning abilities in the mammalian brain

For several decades, the question of whether cognitive and learning capacities can be inherited through non-genetic mechanisms has been the subject of ongoing debate. Here, we provide the first evidence of transgenerational inheritance of enhanced ability to learn complex tasks in the mammalian rodent brain. These inherited learning enhancements are not limited to specific stimuli, sensory modalities, or learning paradigms. Using behavioral, cellular biophysical, methylomics, genetics and molecular methods, we find that the inherited epigenetic modifications reflect an enhanced neuronal learning state, driven by increased intrinsic neuronal excitability in most pyramidal neurons in the relevant neuronal networks. This enhancement is mediated by persistent downregulation of the muscarinic M-current and is associated with widespread changes in DNA methylation, notably within coding genes associated with the M-current, the Kv7 pathway, in the hippocampi of trained F0 rats, as well as in non-coding RNAs in their sperm samples. Remarkably, a significant portion of these DNA methylation changes were also observed in the hippocampi of their untrained F1 offspring. These findings suggest that complex learning abilities can be inherited in the mammalian brain, as the offspring of trained rodents are born with the biophysical modifications that enable them to become super-learners, the exact change that occurs in their parents brains only after the rule learning.

neuroscience↗

bioRxiv2025

BIOPHYSICAL MECHANISMS UNDERLYING THE GENERATION AND MAINTENANCE OF RULE-LEARNING ENGRAM

Training rodents in a particularly difficult olfactory-discrimination task results with acquisition of high skill to perform the task superbly, termed rule-learning. We show that rule-learning occurs abruptly, in a "light bulb moment". Using whole-cell patch-clamp recordings in the piriform cortex of Fos2A-iCreER/TRAP2 mice, we targeted activated neurons, expressing immediate early genes (IEG). From the onset of training, IEG-positive neurons from trained animals display enhanced intrinsic excitability. Subsequently, synaptic excitation and inhibition is enhanced in these neurons, in a coordinated, cell-wide process. In parallel, the density of IEG-expressing neurons sharply declines. Double labeling with TRAP and c-Fos reveals that nearly two-thirds of the rule-memory engram neurons were engaged from the beginning of training. Silencing TRAP-expressing neurons using DREADDs leads to a complete loss of rule memory. We propose that rule learning occurs at a discrete moment, and is developed through a gradual process that stabilizes the memory of the rule.

neuroscience↗

bioRxiv2025

Genome sequencing, de novo assembly and annotation of the commercially important bamboo, Bambusa tulda Roxb.

Bambusa tulda Roxb., a member of the Bambusoideae subfamily, is an ecologically and commercially important plant resource widely distributed on the Indian subcontinent. Our study reports long-read PacBio HiFi sequencing and genome assembly of B. tulda. Flow cytometry analysis revealed its estimated genome size [~]3 Gb. The de novo genome assembly of B. tulda predicted 43 contigs, distributed across three subgenomes, with a total size of 1.37 Gb, contig N50 of 35.69 Mb, and BUSCO score 99%. Repetitive elements constitute 63.31% of the genome. Functional annotation predicted 56,890 protein-coding genes, constituting 19.44% of the genome. This high-quality draft genome assembly will serve as an invaluable resource for future studies on the life history traits, phylogenomic analysis, comparative genomics, and targeted genome modification for important trait improvement of B. tulda.

genomics↗