SLAMF1 as a novel molecule mediating the causal association between rheumatoid arthritis and interstitial lung disease: A Mendelian randomization study combined with transcriptomics and in vivo validation.

BACKGROUND: Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a common complication of rheumatoid arthritis (RA) that result in significant morbidity and mortality. Understanding the molecular mechanisms underlying RA-ILD is crucial for effective prevention. This study aims to identify the specific molecule that mediate the causal association between RA and ILD, as well as to explore its potential mechanisms in the pathogenesis of RA-ILD. METHODS: Using two-sample Mendelian randomization (MR) analyses, we investigated the causal relationship among 16,987 blood genes, RA and ILD. Subsequently, a two-step MR technique was employed to identify significant genes that mediate the association between RA and ILD, and to quantify their proportion of mediation effect. To validate the genes as mediators, the replication MR analysis was conducted and the in vivo experiment was performed using an established animal model of RA-ILD. Furthermore, integrated bioinformatic analyses were conducted to elucidate the specific biological functions of the determined mediator in pathogenesis of RA-ILD. RESULTS: Nine genes, namely MAPK8IP2, TAF11, SLAMF1, DAB2IP, GLUL, SLC4A10, PRSS35, NFX1, and PLK3, were identified as mediators. Among them, SLAMF1 was validated as the most significant mediator, accounting for 4.693% of the mediating effect on the causal relationship between RA and ILD. Upregulated mRNA expression of SLAMF1 was observed in the animal model of RA-ILD compared to controls. Bioinformatic analyses revealed that SLAMF1 was overexpressed in patients with lung fibrosis and correlated with a poor prognosis. Specifically, SLAMF1 was found to be predominantly overexpressed in T cells in lung tissues of patients with lung fibrosis. Additionally, the functional role of SLAMF1 was associated with multiple immune cell infiltrations and the biological process of extracellular matrix synthesis in pulmonary tissues from patients with lung fibrosis. CONCLUSION: SLAMF1 may play a crucial role as a molecular mediator in the causal association between RA and ILD, and participate in multiple mechanisms underlying the pathogenesis of RA-ILD. This research provides insights into how the development of RA influences the risk of ILD and offers potential interventional targets against RA-ILD.

Activation of an atypical plant NLR with an N-terminal deletion initiates cell death at the vacuole.

Plants evolve nucleotide-binding leucine-rich repeat receptors (NLRs) to induce immunity. Activated coiled-coil (CC) domain containing NLRs (CNLs) oligomerize and form apparent cation channels promoting calcium influx and cell death, with the alpha-1 helix of the individual CC domains penetrating the plasma membranes. Some CNLs are characterized by putative N-myristoylation and S-acylation sites in their CC domain, potentially mediating permanent membrane association. Whether activated Potentially Membrane Localized NLRs (PMLs) mediate cell death and calcium influx in a similar way is unknown. We uncovered the cell-death function at the vacuole of an atypical but conserved Arabidopsis PML, PML5, which has a significant deletion in its CCG10/GA domain. Active PML5 oligomers localize in Golgi membranes and the tonoplast, alter vacuolar morphology, and induce cell death, with the short N-terminus being sufficient. Mutant analysis supports a potential role of PMLs in plant immunity. PML5-like deletions are found in several Brassicales paralogs, pointing to the evolutionary importance of this innovation. PML5, with its minimal CC domain, represents the first identified CNL utilizing vacuolar-stored calcium for cell death induction.

Internal Thread Defect Generation Algorithm and Detection System Based on Generative Adversarial Networks and You Only Look Once.

In the field of industrial inspection, accurate detection of thread quality is crucial for ensuring mechanical performance. Existing machine-vision-based methods for internal thread defect detection often face challenges in efficient detection and sufficient model training samples due to the influence of mechanical geometric features. This paper introduces a novel image acquisition structure, proposes a data augmentation algorithm based on Generative Adversarial Networks (GANs) to effectively construct high-quality training sets, and employs a YOLO algorithm to achieve internal thread defect detection. Through multi-metric evaluation and comparison with external threads, high-similarity internal thread image generation is achieved. The detection accuracy for internal and external threads reached 94.27% and 93.92%, respectively, effectively detecting internal thread defects.

Industry 4.0-Compliant Occupational Chronic Obstructive Pulmonary Disease Prevention: Literature Review and Future Directions.

Chronic obstructive pulmonary disease (COPD) is among prevalent occupational diseases, causing early retirement and disabilities. This paper looks into occupational-related COPD prevention and intervention in the workplace for Industry 4.0-compliant occupation health and safety management. The economic burden and other severe problems caused by COPD are introduced. Subsequently, seminal research in relevant areas is reviewed. The prospects and challenges are introduced and discussed based on critical management approaches. An initial design of an Industry 4.0-compliant occupational COPD prevention system is presented at the end.

A new species of the newt genus Hypselotriton (Amphibia, Urodela, Salamandridae) from Jiangxi Province, southeastern China.

A new newt species, Hypselotritonhuanggangensis sp. nov., is described based on nine specimens collected from Huanggangshan Mountains, Yanshan County, Jiangxi, China. Morphologically, the new species is characterized by the combination of nine external characters: (1) obvious black patches with clear boundaries on the whole body; (2) ground color of the dorsal body tan; (3) ground color of venter bright orange; (4) skin rough; (5) vertebral ridge weak; (6) fingers and toes overlapping when forelimb and hindlimb adpressed towards each other along body; (7) postocular orange spot absent; (8) small white warty glands around the eye; (9) two discontinuous longitudinal lines formed by white warty glands from neck to lateral parts of tail. Molecularly, the new species forms an independent clade with strong support in the phylogenetic trees of the genus based on the mitochondrial locus of NADH dehydrogenase subunit 2 (ND2) gene fragments. The new species distinctly differs from H.fudingensis by differences in its body measurements, vertebral ridge, dorsal black patches, and ventral black patches. Furthermore, the new species and H.fudingensis are geographically isolated by a series of high mountain ranges, including the Wuyishan and Jiufengshan Mountains. The number of Hypselotriton species is now 11.

GSK3ß Substrate-competitive Inhibitors Regulate the gut Homeostasis and Barrier Function to Inhibit Neuroinflammation in Scopolamine-induced Alzheimer's Disease Model Mice.

Alzheimer's disease (AD) is a neurodegenerative disease mainly characterized by cognitive impairment. Glycogen synthase kinase 3 (GSK3ß) is a potential therapeutic target against AD. Isoorientin (ISO), a GSK3ß substrate competitive inhibitor, plays anti-AD effects in in vitro and in vivo AD model. TFGF-18 is an ISO synthetic analog with improved potency, but its neuroprotective effect in vivo remains to be elucidated, and the underlying mechanisms of GSK3ß inhibitor against AD need to be clarified. This study investigated the TFGF-18 and ISO effects on gut homeostasis and neuroinflammation in scopolamine (SCOP)-induced AD mice. And the protection on barrier function was observed in in vitro blood-brain barrier (BBB) model of mouse brain microvascular endothelial cells (bEnd.3). The results show that TFGF-18 and ISO improved cognitive function in SCOP-induced mice, and inhibited cholinergic system disorders and inflammation in the brain and intestine, decreased the level of lipopolysaccharides (LPS) in serum and intestine, protected the diversity and balance of intestinal microbiome, increased the expressions of tight junction protein (ZO-1, occludin), brain derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF) in the mouse brain and intestine. In addition, TFGF-18 and ISO protected against barrier damage in LPS-stimulated BBB model of bEnd.3 cells in vitro. TFGF-18 and ISO increased the ratio of p-GSK3ß/GSK3ß, suppressed toll-like receptors 4 (TLR-4) expression and nuclear factor kappa-B (NF-κB) activation in vivo and in vitro, and increased the expressions of ß-catenin, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in vitro. In conclusion, The GSK3ß inhibitors TFGF-18 and ISO modulate the gut homeostasis and barrier function to inhibit neuroinflammation and attenuate cognitive impairment by regulating NF-κB, ß-catenin and Nrf2/HO-1 pathways.

An order-disorder core-shell strategy for enhanced work-hardening capability and ductility in nanostructured alloys.

Nanocrystalline metallic materials have the merit of high strength but usually suffer from poor ductility and rapid grain coarsening, limiting their practical application. Here, we introduce a core-shell nanostructure in a multicomponent alloy to address these challenges simultaneously, achieving a high tensile strength of 2.65 GPa, a large uniform elongation of 17%, and a high thermal stability of 1173 K. Our strategy relies on an ordered superlattice structure that excels in dislocation accumulation, encased by a ≈3 nm disordered face-centered-cubic nanolayer acting as dislocation sources. The ordered superlattice with high anti-phase boundary energy retards dislocation motions, promoting their interaction and storage within the nanograins. The disordered interfacial nanolayer promotes dislocation emission and effectively accommodates the plastic strain at grain boundaries, preventing intergranular cracking. Consequently, the order-disorder core-shell nanostructure exhibits enhanced work-hardening capability and large ductility. Moreover, such core-shell nanostructure exhibits high coarsening resistance at elevated temperatures, enabling it high thermal stability. Such a design strategy holds promise for developing high-performance materials.

A new record and a novel morph description of Boigastoliczkae (Squamata, Colubridae) from China.

Background: The Asian Cat Snake genus Boiga Fitzinger, 1826 includes 37 species, with high species diversity. Five species of Boiga have been recorded in China including B.multomaculata (Boie, 1827), B.kraepelini (Stejneger, 1902), B.cyanea (Duméril, Bibron & Duméril, 1854), B.guangxiensis (Wen, 1998) and B.siamensis (Nutaphand, 1971). Previously, the validity of the species Boigastoliczkae (Wall, 1909) was controversial. B.stoliczkae was considered in synonymy with B.ochracea. Currently, the taxonomy of B.multomaculata and B.ochracea (Theobald, 1868) was revised so that B.multomaculata and B.ochracea actually represent a single species and B.stoliczkae was recognised as a valid species. B.stoliczkae was previously known to be found in the west from central Nepal through Darjeeling, Sikkim and Bhutan to Arunachal Pradesh and Assam in north-eastern India. New information: One adult female specimen of the Asian Cat Snake was collected from Gyirong County, near the China-Nepal border, Tibet, China during fieldwork on August 2023. We compared morphology and mitochondrial DNA sequence data with all the species of the genus Boiga. Both datasets strongly supported referring the Chinese specimens to B.stoliczkae (Wall, 1909) due to the 21 mid-dorsal scale rows and the uncorrected p-distance (mitochondrial DNA gene cytochrome b) between this specimen and B.stoliczkae which is 1.7%. We further described morphological characters of the Chinese specimen in detail and compared these with the specimens that had been previously described. The dorsal ground colour of the Chinese specimen is dark brown, with a black stripe distributed almost evenly across the tail. This is a novel morph of the species B.stoliczkae. The newly-collected Chinese specimen expands the distribution of the species on the Himalaya range.

Zn2+-dependent association of cysteine-rich protein with virion orchestrates morphogenesis of rod-shaped viruses.

The majority of rod-shaped and some filamentous plant viruses encode a cysteine-rich protein (CRP) that functions in viral virulence; however, the roles of these CRPs in viral infection remain largely unknown. Here, we used barley stripe mosaic virus (BSMV) as a model to investigate the essential role of its CRP in virus morphogenesis. The CRP protein γb directly interacts with BSMV coat protein (CP), the mutations either on the His-85 site in γb predicted to generate a potential CCCH motif or on the His-13 site in CP exposed to the surface of the virions abolish the zinc-binding activity and their interaction. Immunogold-labeling assays show that γb binds to the surface of rod-shaped BSMV virions in a Zn2+-dependent manner, which enhances the RNA binding activity of CP and facilitates virion assembly and stability, suggesting that the Zn2+-dependent physical association of γb with the virion is crucial for BSMV morphogenesis. Intriguingly, the tightly binding of diverse CRPs to their rod-shaped virions is a general feature employed by the members in the families Virgaviridae (excluding the genus Tobamovirus) and Benyviridae. Together, these results reveal a hitherto unknown role of CRPs in the assembly and stability of virus particles, and expand our understanding of the molecular mechanism underlying virus morphogenesis.

Internal thread defect detection system based on multi-vision.

In the realm of industrial inspection, the precise assessment of internal thread quality is crucial for ensuring mechanical integrity and safety. However, challenges such as limited internal space, inadequate lighting, and complex geometry significantly hinder high-precision inspection. In this study, we propose an innovative automated internal thread detection scheme based on machine vision, aimed at addressing the time-consuming and inefficient issues of traditional manual inspection methods. Compared with other existing technologies, this research significantly improves the speed of internal thread image acquisition through the optimization of lighting and image capturing devices. To effectively tackle the challenge of image stitching for complex thread textures, an internal thread image stitching technique based on a cylindrical model is proposed, generating a full-view thread image. The use of the YOLOv8 model for precise defect localization in threads enhances the accuracy and efficiency of detection. This system provides an efficient and intuitive artificial intelligence solution for detecting surface defects on geometric bodies in confined spaces.

Radiating blood flow signal: A new ultrasound feature of thyroid carcinoma.

OBJECTIVE: To summary radiating blood flow signals and evaluate their diagnostic value in differentiating benign and malignant thyroid nodules. MATERIALS AND METHODS: We retrospectively recruited consecutive patients undergoing US at 4 hospitals from 2018 to 2022. In a training dataset, the correlations of US features with malignant thyroid nodules were assessed by multivariate logistic analysis. Multivariate logistic regression models involving the ACR TI-RADS score, radiating blood flow signals and their combination were built and validated internally and externally. The AUC with 95% asymptotic normal confidence interval as well as sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) with 95% exact binomial confidence intervals were calculated. RESULTS: Among 2475 patients (1818 women, age: 42.47 ± 11.57; 657 men, age: 42.16 ± 11.69), there were 3187 nodules (2342 malignant nodules and 845 benign nodules). Radiating blood flow signals were an independent risk factor for diagnosing thyroid carcinoma. In the training set, the AUC of the model using the combination of radiating blood flow signals and the ACR TI-RADS score (0.95 95 % CI: [0.94, 0.97]; P < 0.001) was significantly higher than that of the ACR TI-RADS model (0.91 [0.89, 0.93]). In the two internal validation sets and the external validation set, the AUCs of the combination model were 0.97 [0.96, 0.98], 0.92 [0.88, 0.96], and 0.91 [0.86, 0.95], respectively, and were all significantly higher than that of the ACR TI-RADS score (0.92 [0.90, 0.95], 0.86 [0.81, 0.91], 0.84 [0.79, 0.89]; P < 0.001). CONCLUSION: Radiating blood flow is a new US feature of thyroid carcinomas that can significantly improve the diagnostic performance vs. the ACR TI-RADS score.

Synergistic effect of genistein and adiponectin reduces fat deposition in chicken hepatocytes by activating the ERß-mediated SIRT1-AMPK signaling pathway.

Dietary supplementation with bioactive substances that can regulate lipid metabolism is an effective approach for reducing excessive fat deposition in chickens. Genistein (GEN) has the potential to alleviate fat deposition; however, the underlying mechanism of GEN's fat-reduction action in chickens remains unclear. Therefore, the present study aimed to explore the underlying mechanism of GEN on the reduction of fat deposition from a novel perspective: intercellular transmission of adipokine between adipocytes and hepatocytes. The findings showed that GEN enhanced the secretion of adiponectin (APN) in chicken adipocytes, and the enhancement effect of GEN was completely blocked when the cells were pretreated with inhibitors targeting estrogen receptor ß (ERß) or proliferator-activated receptor γ (PPARγ) signals, respectively. Furthermore, the results demonstrated that both co-treatment with GEN and APN or treatment with the medium supernatant (Med SUP) derived from chicken adipocytes treated with GEN significantly decreased the content of triglyceride and increased the protein levels of ERß, Sirtuin 1 (SIRT1) and phosphor-AMP-activated protein kinase (p-AMPK) in chicken hepatocytes compared to the cells treated with GEN or APN alone. Moreover, the increase in the protein levels of SIRT1 and p-AMPK induced by GEN and APN co-treatment or Med SUP treatment were blocked in chicken hepatocytes pretreated with the inhibitor of ERß signals. Importantly, the up-regulatory effect of GEN and APN co-treatment or Med SUP treatment on the protein level of p-AMPK was also blocked in chicken hepatocytes pretreated with a SIRT1 inhibitor; however, the increase in the protein level of SIRT1 induced by GEN and APN co-treatment or Med SUP treatment was not reversed when the hepatocytes were pretreated with an AMPK inhibitor. In conclusion, the present study demonstrated that GEN enhanced APN secretion by activating the ERß-Erk-PPARγ signaling pathway in chicken adipocytes. Subsequently, adipocyte-derived APN synergized with GEN to activate the ERß-mediated SIRT1-AMPK signaling pathway in chicken hepatocytes, ultimately reducing fat deposition. These findings provide substantial evidence from a novel perspective, supporting the potential use of GEN as a dietary supplement to prevent excessive fat deposition in poultry.

Structure and Activity of Reconstructed Pseudo-Ancestral Cyclotides.

Cyclotides are cyclic peptides that are promising scaffolds for the design of drug candidates and chemical tools. However, despite there being hundreds of reported cyclotides, drug design studies have commonly focussed on a select few prototypic examples. Here, we explored whether ancestral sequence reconstruction could be used to generate new cyclotides for further optimization. We show that the reconstructed 'pseudo-ancestral' sequences, named Ancy-m (for the ancestral cyclotide of the Möbius sub-family) and Ancy-b (for the bracelet sub-family), have well-defined structures like their extant members, comprising the core structural feature of a cyclic cystine knot. This motif underpins efforts to re-engineer cyclotides for agrochemical and therapeutic applications. We further show that the reconstructed sequences are resistant to temperatures approaching boiling, bind to phosphatidyl-ethanolamine lipid bilayers at micromolar affinity, and inhibit the growth of insect cells at inhibitory concentrations in the micromolar range. Interestingly, the Ancy-b cyclotide had a higher oxidative folding yield than its comparator cyclotide cyO2, which belongs to the bracelet cyclotide subfamily known to be notoriously difficult to fold. Overall, this study provides new cyclotide sequences not yet found naturally that could be valuable starting points for the understanding of cyclotide evolution and for further optimization as drug leads.

Choriocapillaris flow features in children with myopic anisometropia.

AIMS: To examine differences between the eyes in choriocapillaris perfusion and choroidal thickness in children with myopic anisometropia. METHODS: In this observational and prospective study, 46 children with myopic anisometropia were enrolled. Choriocapillaris perfusion parameters, including the percentage of flow voids, the total number of flow voids and the average flow void area were obtained by optical coherence tomography angiography (OCTA). The OCTA image was divided into a 1 mm-diameter central circle (C1) and a 2.5 mm-diameter annulus (without the inner central 1 mm circle, C1-2.5). Both C1 and C1-2.5 are centred on the foveola. The C1-2.5 was divided into nasal (N1-2.5), temporal (T1-2.5), inferior (I1-2.5) and superior (S1-2.5) areas. Differences in these parameters in different regions between eyes were analysed. RESULTS: There were no significant differences in the percentage of flow voids and the average flow void area between the fellow eyes. The total number of signal voids was significantly higher in the less myopic eyes in C1-2.5 (p=0.032), S1-2.5 (p=0.008) and N1-2.5 (p=0.019). Changes in spherical equivalent refraction and axial length were both correlated with the changes in the total number of flow voids in N1-2.5 (R=-0.431, p=0.03; R=-0.297, p=0.047). CONCLUSIONS: The choroid in the macular region becomes thinner and the total number of flow voids in the nasal macular region decreased with the amplitude of myopia. This suggests that a decrease in total number of flow voids may indicate an early change in myopia.

HMGA1 drives chemoresistance in esophageal squamous cell carcinoma by suppressing ferroptosis.

Chemotherapy is a primary treatment for esophageal squamous cell carcinoma (ESCC). Resistance to chemotherapeutic drugs is an important hurdle to effective treatment. Understanding the mechanisms underlying chemotherapy resistance in ESCC is an unmet medical need to improve the survival of ESCC. Herein, we demonstrate that ferroptosis triggered by inhibiting high mobility group AT-hook 1 (HMGA1) may provide a novel opportunity to gain an effective therapeutic strategy against chemoresistance in ESCC. HMGA1 is upregulated in ESCC and works as a key driver for cisplatin (DDP) resistance in ESCC by repressing ferroptosis. Inhibition of HMGA1 enhances the sensitivity of ESCC to ferroptosis. With a transcriptome analysis and following-up assays, we demonstrated that HMGA1 upregulates the expression of solute carrier family 7 member 11 (SLC7A11), a key transporter maintaining intracellular glutathione homeostasis and inhibiting the accumulation of malondialdehyde (MDA), thereby suppressing cell ferroptosis. HMGA1 acts as a chromatin remodeling factor promoting the binding of activating transcription factor 4 (ATF4) to the promoter of SLC7A11, and hence enhancing the transcription of SLC7A11 and maintaining the redox balance. We characterized that the enhanced chemosensitivity of ESCC is primarily attributed to the increased susceptibility of ferroptosis resulting from the depletion of HMGA1. Moreover, we utilized syngeneic allograft tumor models and genetically engineered mice of HMGA1 to induce ESCC and validated that depletion of HMGA1 promotes ferroptosis and restores the sensitivity of ESCC to DDP, and hence enhances the therapeutic efficacy. Our finding uncovers a critical role of HMGA1 in the repression of ferroptosis and thus in the establishment of DDP resistance in ESCC, highlighting HMGA1-based rewiring strategies as potential approaches to overcome ESCC chemotherapy resistance. Schematic depicting that HMGA1 maintains intracellular redox homeostasis against ferroptosis by assisting ATF4 to activate SLC7A11 transcription, resulting in ESCC resistance to chemotherapy.

Scanning mutagenesis identifies residues that improve the long-term stability and insecticidal activity of cyclotide kalata B1.

Cyclotides are plant-derived disulfide-rich cyclic peptides that have a natural function in plant defense and potential for use as agricultural pesticides. Because of their highly constrained topology, they are highly resistant to thermal, chemical, or enzymatic degradation. However, the stability of cyclotides at alkaline pH for incubation times of longer than a few days is poorly studied but important since these conditions could be encountered in the environment, during storage or field application as insecticides. In this study, kalata B1 (kB1), the prototypical cyclotide, was engineered to improve its long-term stability and retain its insecticidal activity via point mutations. We found that substituting either Asn29 or Gly1 to lysine or leucine increased the stability of kB1 by twofold when incubated in an alkaline buffer (pH = 9.0) for 7 days, while retaining its insecticidal activity. In addition, when Gly1 was replaced with lysine or leucine, the mutants could be cyclized using an asparaginyl endopeptidase, in vitro with a yield of ∼90% within 5 min. These results demonstrate the potential to manufacture kB1 mutants with increased stability and insecticidal activity recombinantly or in planta. Overall, the discovery of mutants of kB1 that have enhanced stability could be useful in leading to longer term activity in the field as bioinsecticides.

G protein-coupled estrogen receptor 1 ameliorates nonalcoholic steatohepatitis through targeting AMPK-dependent signaling.

Nonalcoholic fatty liver disease (NAFLD), especially nonalcoholic steatohepatitis (NASH), has emerged as a prevalent cause of liver cirrhosis and hepatocellular carcinoma, posing severe public health challenges worldwide. The incidence of NASH is highly correlated with an increased prevalence of obesity, insulin resistance, diabetes, and other metabolic diseases. Currently, no approved drugs specifically targeted for the therapies of NASH partially due to the unclear pathophysiological mechanisms. G protein-coupled estrogen receptor 1 (GPER1) is a membrane estrogen receptor involved in the development of metabolic diseases such as obesity and diabetes. However, the function of GPER1 in NAFLD/NASH progression remains unknown. Here, we show that GPER1 exerts a beneficial role in insulin resistance, hepatic lipid accumulation, oxidative stress, or inflammation in vivo and in vitro. In particular, we observed that the lipid accumulation, inflammatory response, fibrosis, or insulin resistance in mouse NAFLD/NASH models were exacerbated by hepatocyte-specific GPER1 knockout but obviously mitigated by hepatic GPER1 activation in female and male mice. Mechanistically, hepatic GPER1 activates AMP-activated protein kinase signaling by inducing cyclic AMP release, thereby exerting its protective effect. These data suggest that GPER1 may be a promising therapeutic target for NASH.

Genome assembly and annotation of the king ratsnake, Elaphe carinata.

The king ratsnake (Elaphe carinata) of the genus Elaphe is a common large, non-venomous snake widely distributed in Southeast and East Asia. It is an economically important farmed species. As a non-venomous snake, the king ratsnake predates venomous snakes, such as cobras and pit vipers. However, the immune and digestive mechanisms of the king ratsnake remain unclear. Despite their economic and research importance, we lack genomic resources that would benefit toxicology, phylogeography, and immunogenetics studies. Here, we used single-tube long fragment read sequencing to generate the first contiguous genome of a king ratsnake from Huangshan City, Anhui province, China. The genome size is 1.56 GB with a scaffold N50 of 6.53M. The total length of the genome is approximately 621 Mb, while the repeat content is 42.26%. Additionally, we predicted 22,339 protein-coding genes, including 22,065 with functional annotations. Our genome is a potentially useful addition to those available for snakes.