Biology subjects

Woo, S.

Publications and source records attributed to Woo, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Cpf1(Cas12a)-based genome editing in the filamentous cyanobacterium Nostoc punctiforme

The filamentous cyanobacterium Nostoc punctiforme is a key model organism used to study several aspects of cyanobacterial biology, including development, nitrogen-fixing symbioses with plants, and secondary metabolites, among others. While N. punctiforme is amenable to genetic manipulation, traditional approaches for the generation of mutant strains using homologous recombination are slow, requiring prolonged outgrowth under antibiotic selection to ensure isogenic mutant populations. CRISPR-based genome editing using Cpf1 (Cas12a) was recently shown to be an effective means of rapid generation of isogenic mutants in several cyanobacteria. In this study, Cpf1-based genome editing tools were developed for N. punctiforme. A total of 19 unmarked, in-frame deletion mutants were successfully constructed using Cpf1-targeted cleavage along with homology directed repair (HDR). The length of the homology arms (HAs) on the homologous repair template (HRT) used for HDR was found to be a critical factor for successful deletion of target genes, with some requiring up to 4 kb HAs to acquire mutant exconjugants. A strategy for allelic replacement was also developed by introducing an exogenous target site in place of the deleted genes, which could subsequently be targeted for cleavage and repaired with an HRT containing altered alleles of the genes of interest. Additionally, a single-step cloning strategy was devised, allowing for rapid assembly of editing plasmids, and improved conjugation protocols for genetic transfer from E. coli to N. punctiforme were implemented. Collectively, these tools and protocols should enhance the pace and ease of conducting genetic studies in this important model cyanobacterium.

microbiology↗

bioRxiv2026

Transcriptional divergence of the zebrafish sox17 lineage begins during gastrulation

The endoderm is specified at the onset of gastrulation and subsequently undergoes extensive migration before forming an epithelial sheet that gives rise to multiple organs, including the gut and respiratory tracts. Although the gene regulatory network underlying endoderm specification and the later processes that regionalize the gut are increasingly well understood, comparatively little is known about the intervening developmental events. Using single cell transcriptomics, we profiled the zebrafish sox17 lineage, comprising endoderm and dorsal forerunner cells, throughout and immediately after gastrulation. We found that dorsal forerunner cells remain transcriptionally homogeneous while undergoing coordinated temporal changes, associated with ciliogenesis and epithelial organization, during assembly of Kupffers vesicle. In contrast, endoderm cells transition from a migratory to an epithelial transcriptional state while progressively acquiring distinct regional identities. These findings indicate that endoderm regionalization emerges within the context of a broadly shared transcriptional program associated with migration and epithelialization.

Developmental Biology↗

bioRxiv2026

SenoQuant: One-stop AI software for senescence marker analysis and prediction

Senescent cells accumulate with age and contribute to tissue dysfunction, yet their identification in tissues is challenging due to low abundance, heterogeneous phenotypes, and the lack of specific markers. Senescence-associated features span multiple subcellular compartments, including nuclear DNA damage foci, cytosolic protein changes, and perinuclear alterations, each requiring tailored detection strategies. To overcome these challenges, we developed SenoQuant (https://github.com/HaamsRee/senoquant), a versatile software designed for comprehensive, accurate, and unbiased spatial quantification and prediction of senescence markers across diverse tissue contexts. Utilizing AI models, SenoQuant enables precise nuclear and cytoplasmic segmentation and detection of senescence markers across low- and high-plex imaging modalities, applicable to cultured cells and tissue sections from mice and humans. The platform also supports custom AI models; for example, we built SenCeption, a proof-of-concept predictor of single-cell p21 status from DAPI-stained nuclei in human skin. Available as a free napari plugin, SenoQuant is widely accessible to researchers. By providing a unified approach to senescence analysis and prediction, SenoQuant opens new opportunities for exploring the complex biology of senescence and its impacts on aging and disease.

Cell Biology↗

bioRxiv2026

A Modular T7 RNAP Expression Architecture for Orthogonal Multigene Expression in Yeast

Orthogonal gene expression systems based on bacteriophage-derived T7 RNA polymerase (T7 RNAP) offer a promising strategy for decoupling engineered transcription from host regulatory networks. Although recent advances have enabled productive T7 RNAP-mediated expression in Saccharomyces cerevisiae, strategies for independently controlling multiple genes within a shared T7 transcriptional framework remain limited. Here, we developed a modular pYTK-compatible T7 RNAP expression architecture that separates overall transcriptional capacity from gene-specific control of protein output. We established interchangeable T7 promoter, terminator, polyadenylation signal, and 5 untranslated region (UTR) parts for combinatorial assembly. Analysis of expression cassette dosage showed that transcript abundance and expression output scale with cassette copy number, with high-copy constructs producing transcript levels comparable to those driven by the GAL1 promoter. To enable gene-specific tuning, we constructed a library of fourteen 18 nt UTR elements that generated a [~]38-fold range of protein output from a common T7 promoter. Application of this library to a three-gene {beta}-carotene biosynthesis pathway enabled [~]20-fold variation in product titer through UTR assignment alone, without altering promoter identity or gene copy number. Together, these results establish a modular T7 RNAP expression framework in which cassette dosage defines overall transcriptional capacity while interchangeable UTR elements enable gene-specific tuning of expression output, providing a practical strategy for multigene expression control in yeast.

Synthetic Biology↗

bioRxiv2026

Met regulates endoderm migration in zebrafish

Cells can employ different modes of migration, switching between them depending on context. However, how migration modes are determined remains incompletely understood. The mode of migration depends not only on external signals and guidance cues but also on which cell surface receptors a cell expresses. Receptor tyrosine kinases (RTKs) are central mediators of many processes including cell migration, yet whether RTK signaling mediates shifts in migratory behavior in vivo remains unclear. Here, we show that the RTK Met promotes persistent, directional migration of endodermal cells during gastrulation in zebrafish. met is broadly expressed across migrating endoderm, and pharmacological inhibition or genetic loss of its function delays endoderm convergence. Quantitative live imaging and cell tracking reveal that loss of Met reduces displacement and persistence without substantially affecting velocity, indicating that Met promotes directional migration rather than motility per se. Although Met is canonically activated by hepatocyte growth factor (Hgf), expression of hgfa and hgfb during gastrulation is spatially restricted and temporally limited. Consistent with this, genetic loss of Hgf function indicates that it is dispensable for endoderm convergence and migration. Together, these findings identify Met as a regulator of migratory persistence during endoderm convergence and suggest a ligand-independent mode of RTK function in the regulation of cell behavior during development. HighlightsO_LIMet promotes directional migration of endoderm cells during convergence. C_LIO_LILoss of Met delays convergence by reducing cell displacement and persistence without affecting velocity. C_LIO_LIHgf signaling is dispensable for endoderm convergence despite being the canonical Met ligand. C_LI

developmental biology↗

bioRxiv2026

Tuned inhibitory control of neuronal firing thresholds explains predictive sensorimotor behavior

Prior expectations guide sensorimotor behavior when sensory information is uncertain, yet the cellular mechanisms underlying this integration remain elusive. Here, we investigate how priors in sensory motion direction shape neural population dynamics by combining recurrent neural network (RNN) modeling with macaque smooth pursuit behavior and middle temporal area (area MT) electrophysiology. Our RNN model reveals that prior expectations are implemented by elevating firing thresholds in neurons tuned away from the expected direction. This selective inhibition sharpens population tuning and reduces behavioral variability under weak sensory information conditions. We validated this prediction in vivo: delta-band local field potentials in area MT, where the phase reflects neural excitability states, exhibited direction-specific phase shifts that scaled with the deviation from the expected direction. These findings demonstrate that prior expectations enhance behavioral reliability through tuned inhibitory control of neuronal excitability, providing a mechanistic link between Bayesian inference and cortical circuit dynamics.

neuroscience↗

bioRxiv2026

Simultaneous optimization of lignocellulosic sugar catabolism via systematic laboratory evolution in dynamic conditions

Efficient co-utilization of hexose and pentose sugars from lignocellulose is essential for microbial production of bio-based chemicals, yet engineered non-native catabolic pathways can be suboptimal and evolutionarily unstable in complex resource environments. We used a Pseudomonas putida strain, previously engineered to catabolize xylose and arabinose to examine how resource abundance, temporal availability, and sub-culturing criteria shape evolutionary outcomes. Using an automated adaptive laboratory evolution (ALE) platform, we evolved the strain under static conditions with single selection pressures and dynamic regimes that imposed selection pressures on multiple sugars. These environments drove divergence between catabolic specialists and generalists. While selection regimes with weak or absent selection for xylose frequently resulted in loss of xylose catabolism, evolution under carbon-limited, mixed-sugar environments promoted stable retention and coordinated optimization of multiple catabolic pathways, increasing total sugar consumption in mixed-sugar conditions. Genomic, proteomic, and biochemical analyses showed that evolutionary stability was determined by pathway-specific fitness costs, leading to either pathway loss or cost-reducing refinement, depending on selection strength. An isolated generalist clone also exhibited improved indigoidine production from mixed sugars when compared to the parental strain. Together, these findings link resource dynamics to fitness landscapes that determine catabolic specialization, generalization, evolutionary trade-offs, and applicability to bioconversion.

bioengineering↗

bioRxiv2026

Kv11.1 (hERG) Protein Interaction Networks Connect Endocytic Trafficking to Polygenic Influences on Cardiac Repolarization

Polygenic scores (PGS) summarize the combined effects of common single-nucleotide polymorphisms and contribute to predictions of disease severity, but biological consequences linked to these common variants remain poorly defined. Here, we focused on polygenic liability for a measurable electrophysiologic trait (the QT interval). Prolonged QT interval, measured on patient electrocardiograms, is associated with an increased risk for cardiac arrhythmia. We investigated human induced pluripotent stem cell cardiomyocytes (hiPSC-CMs) from donors with extreme PGS (i.e., high and low) related to QT interval duration. We paired global proteomics with multiplexed affinity purification mass spectrometry (AP-MS) centered on Kv11.1 (hERG), a major determinant of QT-interval repolarization. Global proteomics indicated increased mitochondrial protein abundance in high-PGS cardiomyocytes, but this did not explain the Kv11.1 interactome. In high-PGS cells, Kv11.1 showed increased associations with myosin motor proteins and endosomal recycling machinery, consistent with altered (and potentially increased) recycling/trafficking dynamics rather than trafficking deficiency observed with most pathogenic Kv11.1 variants. This proof-of-concept study underscores a framework for linking polygenic factors to tractable biological consequences by combining patient-specific hiPSCs, proteomics and affinity-purification. Linking polygenic scores to changes in protein networks provides testable mechanisms that can be applied across many diseases. Significance StatementPolygenic scores (PGS) predict disease risk, but how biological pathways are influenced by these common variants remains difficult to define. We generated human induced pluripotent stem cells from individuals with extreme high- and low-PGS for QT interval, a key electrocardiographic measure linked to arrhythmia risk. By combining global proteomics and interactomics for a common ion channel involved in regulating the QT interval (Kv11.1) we found mechanisms that are influenced by common genetic traits in patients. Our work connects polygenic scores to pathway-level molecular mechanisms in human cells and provides a general framework for uncovering how complex genetic architecture drives disease-relevant biology. ClassificationBiological Sciences; Medical Sciences

genomics↗

bioRxiv2026

OmniDetect: a plant-produced universal IgG binder replacing secondary antibodies in immunoassays

High sensitivity in immunodetection technologies has long been a priority for both diagnostic kit development and routine laboratory research. We developed a recombinant fusion protein, OmniDetect-G3, as an alternative to conventional HRP-conjugated secondary antibodies, and successfully produced it in plants. OmniDetect-G3 binds to primary IgG antibodies regardless of host species, and also recognizes chicken IgY. In comparative analyses, OmniDetect-G3 exhibits 165-381% higher sensitivity than commercial secondary antibodies in western blot analysis and 30%-1145% higher sensitivity in ELISA, depending on commercial products tested. Moreover, OmniDetect-G3 showed robust performance when used with sera from vaccinated animals (porcine and bovine). The chemiluminescence signal generated by OmniDetect-G3 remained stable up to 30 minutes after reaction initiation. These findings indicate that plant-produced OmniDetect-G3 has strong potential as a universal mimetic to animal-derived HRP-conjugated secondary antibodies, offering simplified immunoassay workflows and improved detection efficiency.

immunology↗

bioRxiv2024

EFP Analyzer: A fast, accurate, and easy-to-teach program for analyzing Extracellular Field Potentials from iPSC-derived cardiomyocytes

RationaleInduced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) are an emerging model for determining drug effects and modeling disease. Specialized devices can generate Extracellular Field Potential (EFP) measurements from these cells, analogous to the ventricular complex of the electrocardiogram. ObjectiveThe objective of this study was to develop an easy-to-use, easy-to-teach, reproducible software tool to measure EFPs. Methods-ResultsWe present the EFP-Analyzer (EFPA), a semi-automized analyzer for EFP traces, which identifies and averages beats, identifies landmarks, and calculates intervals. We evaluated the tool in an analysis of 358 EFP traces from 22 patient-derived lines. We analyzed spontaneously beating iPSC-CMs, as well as optically paced iPSC-CMs through channelrhodopsin. We developed stringent quality criteria and measured EFP intervals, including Field Potential Duration (FPD). FPD from optically paced iPSC-CMs were shorter than those of spontaneously beating iPSC-CMs (283.7.0{+/-}54.2 vs. 293.0{+/-}47.5, p: 0.32, respectively). We further analyzed the usability and data replicability of EFPA through an inter-intra observer analysis. Correlation coefficient for inter-reader tangent and threshold measurements for these FPD ranged between r: 0.93-1.00. Bland-Altman plots comparing inter observer results for spontaneously beating and paced iPSC-CMs showed 95% limits of agreement (-13.6 to 19.4ms and -13.2 to 15.3ms, respectively). The EFP-analyzer could accurately detect FPD prolongation due to drug (moxifloxacin) or pathogenic loss of function mutations (CACNA1C N639T). This program is available for download at https://github.com/kroncke-lab/EFPA. The instructions will be available at the same listed website under the README section of the Github main page. ConclusionsThe EFP-Analyzer tool is a useful tool that enables the efficient use of iPSC-CMs as a model to study drug effects and disease.

pharmacology and toxicology↗

bioRxiv2024

A Nerve-Fibroblast Axis in Mammalian Lung Fibrosis

Fibrosis contributes to incurable pathologies in vital organs including the lung. Myofibroblasts are fibrogenic effector cells that accumulate via incompletely understood mechanisms. We discovered that 1-adrenoreceptor expressing myofibroblasts receive sympathetic nerve-derived noradrenergic inputs in fibrotic mouse and human lungs. We combined optical clearing, whole lung imaging, cell-specific gene deletion in sympathetic nerves and myofibroblasts, pharmacologic interventions, sympathetic nerve co-culture and precision-cut lung slices, with analysis of bronchoalveolar lavage fluid, lung tissues, single-cell RNA sequencing datasets, and isolated lung fibroblasts from patients with diverse forms of pulmonary fibrosis to characterize a fibrogenic unit comprised of aberrantly patterned sympathetic nerves and 1-adrenoreceptor subtype D expressing myofibroblasts. The discovery of this previously undefined nerve-fibroblast axis that is conserved across species demonstrates the pivotal contribution of nerves to tissue remodeling and heralds a novel paradigm in fibrosis research.

cell biology↗

bioRxiv2024

AP-1 Mediates Cellular Adaptation and Memory Formation During Therapy Resistance

Cellular responses to environmental stimuli are typically thought to be governed by genetically encoded programs. We demonstrate that melanoma cells can form and maintain cellular memories during the acquisition of therapy resistance that exhibit characteristics of cellular learning and are dependent on the transcription factor AP-1. We show that cells exposed to a low dose of therapy adapt to become resistant to a high dose, demonstrating that resistance was not purely selective. The application of therapy itself results in the encoding of transient gene expression into cellular memory and that this encoding occurs for both transiently induced and probabilistically arising expression. Chromatin accessibility showed concomitant persistence. A two-color AP-1 reporter system showed that these memories are encoded in cis, constituting an example of activating cis epigenetics. Our findings establish the formation and maintenance of cellular memories as a critical aspect of gene regulation during the development of therapy resistance.

systems biology↗

bioRxiv2024

Damage sensing through TLR9 Promotes Viral Clearance and Recovery During Influenza Infection

Host response aimed at eliminating the infecting pathogen, as well as the pathogen itself, can cause tissue injury. Tissue injury leads to the release of a myriad of cellular components including mitochondrial DNA, which the host senses through pattern recognition receptors. How the sensing of tissue injury by the host shapes the anti-pathogen response remains poorly understood. In this study, we utilized mice that are deficient in toll-like receptor-9 (TLR9), which binds to unmethylated CpG DNA sequences such as those present in bacterial and mitochondrial DNA. To avoid direct pathogen sensing by TLR9, we utilized the influenza virus, which lacks ligands for TLR9, to determine how damage sensing by TLR9 contributes to anti-influenza immunity. Our data show that TLR9-mediated sensing of tissue damage promotes an inflammatory response during early infection, driven by the epithelial and myeloid cells. Along with the diminished inflammatory response, the absence of TLR9 led to impaired viral clearance manifested as a higher and prolonged influenza components in myeloid cells including monocytes and macrophages rendering them highly inflammatory. The persistent inflammation driven by infected myeloid cells led to persistent lung injury and impaired recovery in influenza-infected TLR9-/-mice. Further, we show elevated TLR9 activation in the plasma samples of patients with influenza and its association with the disease severity in hospitalized patients, demonstrating its clinical relevance. Overall, we demonstrate an essential role of damage sensing through TLR9 in promoting anti-influenza immunity and inflammatory response. Author SummaryTissue damage is an inevitable outcome of clinically relevant lung infections, but the host mechanisms for detecting such damage during infection are not well understood. We investigated the role of Toll-like receptor 9 (TLR9) in sensing tissue damage caused by influenza. Since influenza lacks TLR9 ligands, we hypothesized that TLR9 signaling is driven by tissue damage molecules like mitochondrial DNA (mtDNA). Our data indicate that TLR9 reduces early inflammatory lung injury but impairs viral clearance, resulting in extensive immune cell infection, persistent inflammation, and delayed recovery. Myeloid-specific TLR9 deletion ameliorated late-stage inflammatory responses. In humans, influenza-infected individuals exhibited elevated TLR9 activity and mtDNA levels in plasma compared to healthy controls, with higher TLR9 activation potential correlating with severe disease requiring ICU admission. These findings suggest that TLR9-mediated damage sensing triggers both inflammatory tissue injury and viral clearance. These data indicate that TLR9 activity can serve as a crucial biomarker and therapeutic target to limit influenza induced tissue injury.

immunology↗

bioRxiv2024

Tissue-specific and endogenous protein labeling with split fluorescent proteins

The ability to label proteins by fusion with genetically encoded fluorescent proteins is a powerful tool for understanding dynamic biological processes. However, current approaches for expressing fluorescent protein fusions possess drawbacks, especially at the whole organism level. Expression by transgenesis risks potential overexpression artifacts while fluorescent protein insertion at endogenous loci is technically difficult and, more importantly, does not allow for tissue-specific study of broadly expressed proteins. To overcome these limitations, we have adopted the split fluorescent protein system mNeonGreen21-10/11 (split-mNG2) to achieve tissue-specific and endogenous protein labeling in zebrafish. In our approach, mNG21-10 is expressed under a tissue-specific promoter using standard transgenesis while mNG211 is inserted into protein-coding genes of interest using CRISPR/Cas-directed gene editing. Each mNG2 fragment on its own is not fluorescent, but when co-expressed the fragments self-assemble into a fluorescent complex. Here, we report successful use of split-mNG2 to achieve differential labeling of the cytoskeleton genes tubb4b and krt8 in various tissues. We also demonstrate that by anchoring the mNG21-10 component to specific cellular compartments, the split-mNG2 system can be used to manipulate protein function. Our approach should be broadly useful for a wide range of applications.

developmental biology↗

bioRxiv2023

KAT2 paralogs prevent dsRNA accumulation and interferon signaling to maintain intestinal stem cells

Histone acetyltransferases KAT2A and KAT2B are paralogs highly expressed in the intestinal epithelium, but their functions are not well understood. In this study, double knockout of murine Kat2 genes in the intestinal epithelium was lethal, resulting in robust activation of interferon signaling and interferon-associated phenotypes including the loss of intestinal stem cells. Use of pharmacological agents and sterile organoid cultures indicated a cell-intrinsic double-stranded RNA trigger for interferon signaling. Acetyl-proteomics and dsRIP-seq were employed to interrogate the mechanism behind this response, which identified mitochondria-encoded double-stranded RNA as the source of intrinsic interferon signaling. Kat2a and Kat2b therefore play an essential role in regulating mitochondrial functions as well as maintaining intestinal health. Highlights of the workO_LIKat2a and Kat2b double knockout in the murine intestinal epithelium triggers activation of the interferon signaling pathway C_LIO_LIKat2a/Kat2b knockout leads to intestinal stem cell loss and other mucosal phenotypes consistent with interferon activation C_LIO_LIHistone PTM mass spec profiling reveals the first in vivo study showing H3K9ac-specific loss with Kat2a and Kat2b double knockout, yet without correlation to interferon signaling pathway genes C_LIO_LIComprehensive proteomic analysis identifies non-histone acetyl-lysine targets of KAT2 in the mouse intestine in vivo, including mitochondrial proteins C_LIO_LIMitochondrial function is compromised upon Kat2 loss C_LIO_LIdsRIP-seq identifies double-stranded RNA from the mitochondria as a trigger for the intrinsic immune response upon Kat2 double knockout C_LI

molecular biology↗

bioRxiv2023

Endodermal cells use contact inhibition of locomotion to achieve uniform cell dispersal during zebrafish gastrulation

The endoderm is one of the three primary germ layers that ultimately gives rise to the gastrointestinal and respiratory epithelia and other tissues. In zebrafish and other vertebrates, endodermal cells are initially highly migratory with only transient interactions among one other, but later converge together to form an epithelial sheet. Here, we show that during their early, migratory phase, endodermal cells actively avoid each other through contact inhibition of locomotion (CIL), a characteristic response consisting of 1) actin depolymerization and membrane retraction at the site of contact, 2) preferential actin polymerization along a cell-free edge, and 3) reorientation of migration away from the other cell. We found that this response is dependent on the Rho GTPase RhoA. Expression of dominant-negative (DN) RhoA attenuated migration reorientation after cell-cell contact and increased the amount of time cells spent in contact with each other -- behaviors consistent with a loss of CIL. Computational modeling predicted that CIL is required to achieve the efficient and uniform dispersal characteristic of endodermal cells. Consistent with our model, we found that loss of CIL via DN RhoA expression resulted in irregular clustering of cells within the endoderm. Finally, using a combination of pharmacological and genetic perturbations, we identify EphA2 as the cell surface receptor mediating endodermal CIL. Together, our results suggest that endodermal cells use EphA2-and RhoA-dependent CIL as a cell dispersal and spacing mechanism, demonstrating how tissue-scale patterns can emerge from local cell-cell interactions.

developmental biology↗

bioRxiv2020

TAEL 2.0: An Improved Optogenetic Expression System for Zebrafish

Inducible gene expression systems are valuable tools for studying biological processes. We previously developed an optogenetic gene expression system called TAEL that is optimized for use in zebrafish. When illuminated with blue light, TAEL transcription factors dimerize and activate gene expression downstream of the TAEL-responsive C120 promoter. By using light as the inducing agent, the TAEL/C120 system overcomes limitations of traditional inducible expression systems by enabling fine spatial and temporal regulation of gene expression. Here, we describe ongoing efforts to improve the TAEL/C120 system. We made modifications to both the TAEL transcriptional activator and the C120 regulatory element, collectively referred to as TAEL 2.0. We demonstrate that TAEL 2.0 consistently induces higher levels of reporter gene expression and at a faster rate, but with comparable background and toxicity as the original TAEL system. With these improvements, we were able to create functional stable transgenic lines to express the TAEL 2.0 transcription factor either ubiquitously or with a tissue-specific promoter. We demonstrate that the ubiquitous line in particular can be used to induce expression at late embryonic and larval stages, addressing a major deficiency of the original TAEL system. This improved optogenetic expression system will be a broadly useful resource for the zebrafish community.

developmental biology↗

bioRxiv2018

The draft genome of an octocoral, Dendronephthya gigantea

BackgroundCoral reefs composed of stony corals are threatened by global marine environmental changes. However, soft coral communities composed of octocorallian species, appear more resilient. The genomes of several species of cnidarians have been published, including stony corals, sea anemones, and hydra, but as of yet no octocoral species. To fill this phylogenetic gap within the cnidarian, we sequenced the octocoral, Dendronephthya gigantea, a non-symbiotic soft coral, commonly known as the carnation coral.\n\nFindingsThe D. gigantea genome size is approximately 276 Mb. A high-quality genome assembly was constructed using 29.85Gb (108x coverage) of PacBio long reads and 35.54Gb (128x coverage) of Illumina short paired-end reads resulting in the largest N50 value reported among cnidarian of 1.4 Mb. About 12 % of the genome consisted of repetitive elements. We found 28,879 protein-coding genes. This gene set contained about 94% metazoan single-copy orthologs, indicating the gene models were predicted with high quality compared to other cnidarians. Based on molecular phylogenetic analysis, octocoral and hexacoral divergence occurred approximately 544 million years ago. Moreover, there is a clear difference in Hox gene composition: unlike in hexacorals, Antp superclass member Evx gene was absent in D. gigantea.\n\nConclusionsWe present the first genome assembly of a non-symbiotic octocoral, D. gigantea to aid in the comparative genomic analysis of cnidarians, including comparisons of stony and soft corals and symbiotic and non-symbiotic corals. In addition, the genome of this species may provide clues about differential genetic coping mechanisms between soft and stony coral regarding the global warming.

genomics↗