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Xiong, Z.

Publications and source records attributed to Xiong, Z..

At least 37 records · Page 2Linked to original sources

Integrating 12 Spatial and Single Cell Technologies to Characterise Tumour Neighbourhoods and Cellular Interactions in three Skin Cancer Types

Cutaneous squamous cell carcinoma (cSCC), basal cell carcinoma (BCC), and melanoma - the three major skin cancers - collectively comprise over 70% of all cancer cases. Despite their prevalence, much understanding of cellular interactions in the skin cancer microenvironment is needed, both in the outer skin layer where the cancer originates and at the deeper junctional and dermal layers into which it progresses. To address this gap, we integrated 12 complementary spatial and single-cell technologies to generate orthogonally-validated cell signatures, spatial maps, and interactomes for cSCC, BCC, and melanoma. Through comprehensive comparisons and integrating these spatial methods, we provided practical benchmarking guidelines for experimental design and analysis. By identifying keratinocyte cancer cells and melanomas, we found distinct signatures of these cells compared to non-cancer keratinocytes and melanocytes. Spatial integration of transcriptomics, proteomics and glycomics uncovered cancer niches enriched for cancer initiating cells (melanocytes or keratinocytes) and fibroblast and T-cell (MKFT) clusters, with altered tyrosine and pyrimidine metabolism. Ligand-receptor analysis across >700 cell-type combinations and >1.5 million interactions highlighted key roles for CD44, integrins, and collagens, with CD44-FGF2 emerging as a potential therapeutic target. Consistently, melanoma showed strong MFT interactions, validated by Opal Polaris, RNAScope, Proximal Ligation Assay and two additional single-cell spatial platforms (making a total of 14 technologies). For population-scale generalisation, genetic associations from >500,000 individuals were mapped onto spatial skin tissues, identifying SNPs enriched in domains containing melanocytes and T cells and their ligand-receptor pairs, shedding light on functional mechanisms linking genetic heritability to cells within cancer tissue. We built an interactive multiomics resource for exploring spatially-resolved molecular signatures and cellular crosstalk in skin cancer, available at https://skincanceratlas.com.

cancer biology↗

Isoliensinine Ameliorates Pathological Cardiac Hypertrophy After Aerobic Exercise by Activating Cytochrome c Oxidase Subunit 6A2

Pathological cardiac hypertrophy is an abnormal remodeling process of the heart under chronic pressure overload, characterized by myocardial fibrosis, apoptosis, and progressive decline in cardiac function, ultimately leading to heart failure or death. Although aerobic exercise, particularly swimming, has been shown to alleviate pathological cardiac hypertrophy, its molecular mechanisms remain incompletely understood. In this study, metabolomic and transcriptomic analyses revealed the molecular mechanisms underlying swimming-induced improvement of pathological cardiac hypertrophy. Results showed that swimming training significantly altered the level of isoliensinine in animals. Further studies demonstrated that isoliensinine exerts cardioprotective effects by regulating the expression of Cytochrome C Oxidase Subunit 6A2 (COX6A2), establishing for the first time the critical role of the Isoliensinine-COX6A2 signaling axis in cardiac function regulation. To validate this axis, a pathological cardiac hypertrophy model was constructed in mice through transverse aortic constriction (TAC). Both swimming training and isoliensinine intervention significantly improved cardiac structure and function. In vitro experiments using isoproterenol (ISO)-induced hypertrophy in H9C2 cells further confirmed the essential role of this signaling axis in suppressing pathological hypertrophy and maintaining mitochondrial homeostasis. Our findings demonstrate that swimming mitigates pathological cardiac hypertrophy by enhancing COX6A2 expression by isoliensinine, thereby improving mitochondrial function. This study not only expands the understanding of exercise-mediated mechanisms in pathological cardiac remodeling but also highlights the cardioprotective potential of isoliensinine and COX6A2 as therapeutic targets for preventing and treating heart failure.

molecular biology↗

Bridging 3D Molecular Structures and Artificial Intelligence by a Conformation Description Language

Artificial intelligence, particularly language models (LMs), is reshaping research paradigms across scientific domains. In the fields of chemistry and pharmacy, chemical language models (CLMs) have achieved remarkable success in two-dimensional (2D) molecular modeling tasks by leveraging one-dimensional (1D) representations of molecules, such as SMILES and SELFIES. However, extending these successes to three-dimensional (3D) molecular modeling remains a significant challenge, largely due to the absence of effective 1D representations for capturing 3D molecular structures. To address this gap, we introduce ConfSeq, a novel molecular conformation description language that integrates SMILES with internal coordinates including dihedral angles, bond angles, and pseudo-chirality. This design naturally ensures SE(3) invariance, while preserving the human readability and conciseness characteristic of SMILES. ConfSeq enables the reformulation of a range of 3D molecular modeling tasks, such as molecular conformation prediction, 3D molecular generation, and 3D molecular representation, into sequence modeling problems. Then, by simply employing a standard Transformer architecture, we achieve state-of-the-art performance on various benchmark sets. Furthermore, compared to widely used diffusion-based approaches in 3D molecular modeling, the ConfSeq-based method offers unique advantages in inference efficiency, generation controllability, and enables scoring of generated molecules. We believe that ConfSeq can serve as a foundational tool, advancing the development of sequence-based 3D molecular modeling methods.

bioinformatics↗

Caspase-1 self-terminates protease activity to enforce homeostasis and prevent inflammasome-driven diseases

Signal shutdown mechanisms must exist to silence the potent inflammatory programs initiated by the caspase-1 (CASP1) protease, to allow inflammation to resolve and reinstate tissue homeostasis. It is unknown how CASP1 terminates its activity in vivo. Here, we use a knock-in mouse model in which the CASP1 CARD domain linker (CDL) is mutated to prevent self-cleavage (Casp1.CDL mice) to show that CASP1 CDL autoproteolysis terminates CASP1 activity in vivo. We examined these mice under homeostatic conditions and in response to major physiological challenges. In the brain, CASP1 CDL mutation caused anxiety-like behaviour under homeostatic conditions, and exacerbated hippocampal spatial learning deficits in the APP23 genetic model of amyloid-induced neurodegeneration. In the bone marrow, CASP1 CDL mutation promoted steady-state granulopoiesis. In a model of diet-induced liver disease, CASP1 CDL mutation accelerated liver steatosis and promoted liver immune cell infiltration, inflammation and damage. In a liver healing model, CASP1 CDL mutation delayed disease resolution, indicating that CASP1 autocleavage is required to restore homeostasis after a major challenge to organ function. Our data reveal that CASP1 CDL self-cleavage terminates CASP1 inflammatory programs in vivo to maintain homeostasis in steady-state, restore homeostasis after a major challenge to organ function, and suppress inflammasome-driven diseases. These data identify CASP1 as a prime anti-inflammatory drug target, as CASP1 inhibitors may enforce homeostasis and prevent inflammasome-driven diseases.

immunology↗

Spatial Transcriptomic Signature of Progressive Fibrosis in Human MASLD: Role of Senescence and Metabolic Reprogramming.

Granular detail about the location and nature of liver cell interactions and the metabolic, inflammatory and fibrogenic pathways driving progressive fibrosis in metabolic dysfunction-associated steatotic liver disease (MASLD) is needed to deliver novel therapeutic targets. Here we used spatial transcriptomic data from human MASLD liver biopsies to identify the major cell types and their potential interconnected activities within specific tissue regions across the spectrum of MASLD. Gene expression data were generated using 10X Genomics Visium technology from 33 formalin-fixed paraffin-embedded liver biopsy samples and overlaid with annotated anatomical regions. Differential gene expression (DEG) and pathway analyses, cellular deconvolution and ligand-receptor interactions were conducted for each annotated anatomical category, with specific protein expression validated using CODEX spatial proteomics and immunohistochemistry staining. Unsupervised gene expression data grouped the annotated spots into 2 main clusters enriched for early/intermediate vs late fibrosis and transcriptome-based cellular deconvolution was well aligned with annotated histopathological features. In addition to extracellular matrix/receptor interactions and immune cell recruitment and trafficking, several genes encoding immunoglobulins were highly upregulated in late-stage fibrosis and were spatially associated with a senescence signature. Upregulated DEGs for early/intermediate-stage fibrosis were significantly enriched for metabolic pathways, oxidative phosphorylation and fatty acid metabolism. In contrast glycolysis genes were strongly co-expressed with late stage fibrosis. MASLD progression is accompanied by a decline in normal liver metabolic function and significant reprogramming of metabolic fuel utilisation. The spatial association of a senescence signature with expression of genes encoding immunoglobulins and complement has been linked to aging and is associated with progressive fibrosis. This work provides a valuable discovery dataset spanning different stages of human liver fibrosis and highlights the complex crosstalk between metabolic perturbations and inflammation underpinning fibrosis progression.

genomics↗

S100a4+ alveolar macrophages accelerate the progression of precancerous atypical adenomatous hyperplasia by promoting fatty acid metabolism

Lung cancer is preceded by premalignant lesions, and what factors drive this transformation and the potential regulatory mode in the context of tumor initiation remain to be elucidated. In the course of precancerous lesions, we found a phasic shift in metabolic patterns. Macrophages are a heterogeneous cell population with high plasticity in the tumor microenvironment. Single-cell interaction and metabolic analyses highlighted a cellular state, S100a4+ alveolar macrophages, which exhibited distinct fatty acid metabolic activity, such as palmitic acid metabolism, at the atypical adenomatous hyperplasia stage, accompanied by an angiogenic-promoting function in a pre-neoplastic setting. These findings were reproducible in human single-cell transcriptomes and had been confirmed by histopathological staining and in vitro cell coculture assays. Taken together, the results from this study demonstrated that the S100a4+ alveolar macrophage subset contributes to tumorigenesis by altering its metabolic state, suggesting that metabolic interventions targeting this cell state in the early stage of disease may delay neoplastic transformation of the lung epithelium.

cancer biology↗

Spatial analysis of HPV associated cervical intraepithelial neoplastic tissues demonstrate distinct immune signatures associated with cervical cancer progression

Cervical cancer remains the fourth most common cancer affecting women worldwide, and incidences of other HPV-related cancers continue to rise. For the development of effective prevention strategies in high-risk patients, we aimed to better understand the roles of inflammatory pathways and the tumour microenvironment as the main driver of progression to malignancy in HPV-infected tissues. We analysed the spatial organisation of seven samples of HPV+ high-grade squamous intraepithelial lesion (HSIL) and cervical intraepithelial neoplasia 3 (CIN3), comparing tumour heterogeneity and immune microenvironments between pre-malignant (neoplastic) and adjacent cervical tissues. We observed evidence of immune suppression within the neoplastic regions across all samples and identified distinct immune clusters for each dysplastic lesion. Previous single-cell data analyses in an HPV16 E7 oncoprotein-driven transgenic mouse model suggested a potential role for IL34-CSF1R signalling in immune modulation, where low IL34 expression was associated with Langerhans cell dysfunction, and, in cervical cancer, with poor patient outcome. Here, we observed that IL34-CSF1R co-expression was absent within HPV-associated neoplastic tissues but present in adjacent normal tissue regions. Additionally, we identified enrichment of an M2 gene signature in neoplastic tissue, while adjacent tissue was enriched with a pro-inflammatory M1 gene signature. Our findings provide bio-pathological insights into the spatial cellular and molecular mechanisms underlying HPV-associated cervical cancer immune regulation and suggest a strategy to modulate the immune system in HPV-positive neoplastic cervical and other tissues.

genomics↗

SciMind: A Multimodal Mixture-of-Experts Model for Advancing Pharmaceutical Sciences

Large language models (LLMs) have made substantial strides, but their use in reliably tackling issues within specialized domains, particularly in interdisciplinary areas like pharmaceutical sciences, is hindered by data heterogeneity, knowledge complexity, unique objectives, and a spectrum of constraint conditions. In this area, diverse modalities such as nucleic acids, proteins, molecular structures, and natural language are often involved. We designed a specialized token set and introduced a new Mixture-of-Experts (MoEs) pre-training and fine-tuning strategy to unify these modalities in one model. With this strategy, weve created a multi-modal mixture-of-experts foundational model for pharmaceutical sciences, named SciMind. This model has undergone extensive pre-training on publicly accessible datasets including nucleic acid sequences, protein sequences, molecular structure strings, and biomedical texts, and delivers good performance on biomedical text comprehension, promoter prediction, protein function prediction, molecular description, and molecular generation.

bioinformatics↗

Multipath projection stereolithography (MPS) for 3D printing microfluidic devices

Although many lab-on-chip applications require inch-sized devices with microscale feature resolution, achieving this via current 3D printing methods remains challenging due to inherent tradeoffs between print resolution, design complexity, and build sizes. Inspired by microscopes that can switch objectives to achieve multiscale imaging, we report a new optical printer coined as Multipath Projection Stereolithography (MPS) specifically designed for printing microfluidic devices. MPS is designed to switch between high-resolution (1xmode, [~]10{micro}m) and low-resolution (3x mode, [~]30{micro}m) optical paths to generate centimeter sized constructs (3cm x 6cm) with a feature resolution of [~]10{micro}m. Illumination and projection systems were designed, resin formulations were optimized, and slicing software was integrated with hardware with the goal of ease of use. Using a test-case of micromixers, we show user-defined CAD models can be directly input to an automated slicing software to define printing of low-resolution features via the 3x mode with embedded microscale fins via 1x mode. A new computational model, validated using experimental results, was used to simulate various fin designs and experiments were conducted to verify simulated mixing efficiencies. New 3D out-of-plane micromixer designs were simulated and tested. To show broad applications of MPS, multi-chambered chips and microfluidic devices with microtraps were also printed. Overall, MPS can be a new fabrication tool to rapidly print a range of lab-on-chip applications.

bioinformatics↗

Unveiling the mechanisms of black phosphorus nanosheets-induced viable but non-culturable state in Bacillus tropicus

The release of black phosphorus (BP) nanosheets has raised concerns regarding potential ecological risks. Previous studies have confirmed their toxicity to bacteria, but discrepancies were observed between results obtained from the growth curve and colony forming unit (CFU) methods, indicating the possibility of bacterial cells entering a viable but non-culturable (VBNC) state induced by BP nanosheets. To accurately assess the risks, it is crucial to understand the underlying mechanisms. In this study, we investigated the effect of BP nanosheets on Bacillus tropicus, a gram-positive bacterium, using transcriptome sequencing and biological assays. Our findings revealed that BP nanosheets caused minimal cell death but predominately induced the VBNC state in most cells. At the transcriptional level, we observed significant down-regulation of pathways associated with cellular metabolism and respiratory chain in response to BP nanosheet treatment. Bacterial cells in the VBNC state exhibited depressed respiration to maintain basal cellular activity. Additionally, the reduced cellular respiration and metabolic activity were associated with a decrease in antibiotic susceptibility of the bacteria. These results provide new insights into the antibacterial mechanisms of BP nanosheets and emphasize the necessity of employing appropriate approaches, beyond the traditional CFU method, to assess the bacterial toxicity of nanomaterials. Environmental implicationBacteria play a crucial role as indicators in ecological risk assessment. Although numerous studies have highlighted the exceptional antibacterial properties of black phosphorus (BP) nanosheets, the unique viable but non-culturable (VBNC) state of bacteria is often overlooked when evaluating the ecological risks of nanomaterial, including BP nanosheets. In our study, we found that BP nanosheets can induce Bacillus tropicus into a VBNC state by suppressing cellular metabolism- and respiratory chain-related pathways, shedding light on their ecological risk assessment implications. This finding underscores the importance of utilizing appropriate approaches in evaluating the bacterial toxicity of nanomaterials.

pharmacology and toxicology↗

Production of four-gene (GTKO/hCD55/hTBM/hCD39)-edited donor pigs and kidney xenotransplantation

BackgroundThe number of multigene-modified donor pigs for xenotransplantation is increasing with the advent of gene editing technologies. However, which gene combination is suitable for which organ transplantation remains unclear. MethodsIn this study, we utilized CRISPR/Cas9 gene editing technology, PiggyBac transposon system and somatic cell cloning to construct GTKO/hCD55/hTBM/hCD39 four-gene-edited cloned (GEC) pigs and performed kidney transplantation from pig to rhesus monkey to evaluate the effectiveness of these GEC pigs. ResultsFirst, 107 cell colonies were obtained through drug selection, of which 7 were 4-GE colonies. Two colonies were selected for somatic cell nuclear transfer, resulting in 7 fetuses, of which 4 were GGTA1 biallelic knockout. Both fetuses had higher expression of hCD55, hTBM and hCD39. Therefore, these two fetuses were selected for two consecutive rounds of cloning, resulting in a total of 97 live piglets. After phenotype identification, the GGTA1 gene of these pigs was inactivated, and hCD55, hTBM and hCD39 were expressed in cells and multiple tissues. Furthermore, the numbers of monkey IgM and IgG binding to the peripheral blood mononuclear cells (PBMCs) of the 4-GEC pigs were markedly reduced. Moreover, 4-GEC porcine PBMCs had greater survival rates than those from wild-type pigs through complement-mediated cytolysis assays. In pig-to-monkey kidney xenotransplantation, the kidney xenograft successfully survived for 11 days. All physiological and biochemical indicators were normal, and no hyperacute rejection or coagulation abnormalities were found after transplantation. ConclusionThese results indicate that the GTKO/hCD55/hTBM/hCD39 four-gene modification effectively alleviates immune rejection, and the pig kidney can functionally support the recipient monkeys life.

genetics↗

FAPM: Functional Annotation of Proteins using Multi-Modal Models Beyond Structural Modeling

Assigning accurate property labels to proteins, like functional terms and catalytic activity, is challenging, especially for proteins without homologs and "tail labels" with few known examples. Unlike previous methods that mainly focused on protein sequence features, we use a pretrained large natural language model to understand the semantic meaning of protein labels. Specifically, we introduce FAPM, a contrastive multi-modal model that links natural language with protein sequence language. This model combines a pretrained protein sequence model with a pretrained large language model to generate labels, such as Gene Ontology (GO) functional terms and catalytic activity predictions, in natural language. Our results show that FAPM excels in understanding protein properties, outperforming models based solely on protein sequences or structures. It achieves state-of-the-art performance on public benchmarks and in-house experimentally annotated phage proteins, which often have few known homologs. Additionally, FAPMs flexibility allows it to incorporate extra text prompts, like taxonomy information, enhancing both its predictive performance and explainability. This novel approach offers a promising alternative to current methods that rely on multiple sequence alignment for protein annotation. The online demo is at: https://huggingface.co/spaces/wenkai/FAPM_demo.

bioinformatics↗

MMCCI: Multimodal Cell-Cell Interaction Integrative Analysis of Single Cell and Spatial Data

Cell-cell interaction (CCI) analyses are an indispensable tool for harnessing the detail and depth of spatial and single-cell transcriptomics datasets by inferring inter-cellular communications, but no methods to integrate CCI results across samples exist currently. To address this, we have developed a computational pipeline, Multimodal CCI (MMCCI), to statistically integrate and analyze CCI results from existing popular CCI tools. We benchmarked MMCCIs integration on single-cell spatial datasets and found it to be highly accurate compared to simpler methods. We utilized MMCCIs integration and downstream biological analyses to uncover global and differential interaction patterns in multimodal aging brain and melanoma spatial datasets.

bioinformatics↗

Queen loss fails to elicit physiological and transcriptional responses in workers of the invasive garden ant Lasius neglectus

Insect colonies with morphologically distinct castes have been called superorganisms because their queens and workers are functionally analogous to the germline and soma in metazoan bodies. In the haplodiploid ants, workers typically lost the sperm storage organ but retained ovaries so they can lay unfertilized eggs. Worker reproduction often occurs after queen loss and is accompanied by a number of physiological changes. However, in some evolutionarily derived ants, workers have become functionally sterile and in many of these species colonies contain multiple queens and can readily raise replacement queens - a syndrome characteristic for invasive ants. We hypothesized that the combination of full worker sterility and regular queen replacement should have eliminated important aspects of the physiological interdependence between queens and workers. We tested this hypothesis by analysing fat body gene expression and worker resistance to oxidative stress in colonies of the invasive ant Lasius neglectus with and without queens. We found age-related transcriptional shifts between young and old queens and young and old workers, suggesting rapid ageing in all castes. However, the removal of any queens in controlled experiments failed to elicit changes in the transcriptional activity and oxidative stress resistance of workers, consistent with our hypothesis. The invasive syndrome of this ant may thus have led to a somatic work force that evolved to be physiologically independent of queen presence.

evolutionary biology↗

Bacillus velezensis HBXN2020 alleviates Salmonella Typhimurium-induced colitis by improving intestinal barrier integrity and reducing inflammation

Bacillus velezensis is a species of Bacillus that has been widely investigated because of its broad-spectrum antimicrobial activity. However, most studies on Bacillus velezensis have focused on the biocontrol of plant diseases, with few reports on antagonizing Salmonella Typhimurium infections. In this investigation, it was discovered that Bacillus velezensis HBXN2020, which was isolated from healthy black pigs, possessed strong anti-stress and broad-spectrum antibacterial activity. Importantly, Bacillus velezensis HBXN2020 did not cause any adverse side effects in mice when administered at various doses (1 x 107, 1 x 108, and 1 x 109 CFU) for 14 d. Supplementing Bacillus velezensis HBXN2020 spores, either as a curative or preventive measure, dramatically reduced the levels of Salmonella Typhimurium ATCC14028 in the mices feces, ileum, cecum, and colon, as well as the disease activity index (DAI), in a model of infection caused by this pathogen in mice. Additionally, supplementing Bacillus velezensis HBXN2020 spores significantly regulated cytokine levels (TNF-, IL-1{beta}, IL-6, and IL-10) and maintained the expression of tight junction proteins and mucin protein. Most importantly, adding Bacillus velezensis HBXN2020 spores to the colonic microbiota improved its stability and increased the amount of beneficial bacteria (Lactobacillus and Akkermansia). All together, Bacillus velezensis HBXN2020 can improve intestinal microbiota stability and barrier integrity and reduce inflammation to help treat infection by Salmonella Typhimurium.

microbiology↗

Molecular mechanism of NAD+ binding to the Nudix homology domains of DBC1

DBC1 (deleted in breast cancer 1) is a human nuclear protein that modulates the activities of various proteins. NAD+ (oxidized form of nicotinamide adenine dinucleotide) is thought to potentially bind to the Nudix homology domains (NHDs) of DBC1, thereby regulating DBC1-PARP1 [poly (adenosine diphosphate-ribose) polymerase] interactions, the modulation of which may restore DNA repair to protect against cancer, radiation, and aging. Therefore, our study comprehensively employed methods including NMR (Nuclear Magnetic Resonance), ITC (isothermal titration calorimetry), genetic mutation, and computer biology to thoroughly investigate the molecular mechanism of the binding interaction between NAD+ and its precursor NMN with the NHD domain of DBC1 (DBC1354-396). The results from NMR and ITC indicate that NAD+ likely interacts with DBC1354-396 through hydrogen bonding, with a binding affinity nearly twice that of NMN. The key binding sites are primarily E363 and D372. Molecular Docking further revealed the importance of conventional hydrogen bonds and carbon-hydrogen bonds in the binding process. These findings may lead to a better understanding of how NAD+ regulates the physiological functions of DBC1, thereby offering guiding principles for the development of targeted therapies and drug research focused on tumor diseases associated with DBC1.

biochemistry↗

Chromosome-Level Genome Assembly of Navel orange cv. Gannanzao (Citrus sinensis Osbeck cv. Gannanzao)

Navel orange cv. Gannanzao is a variant of the navel orange cv. Newhall (C. sinensis Osbeck cv. Newhall) that exhibits an earlier maturation, making it commercially valuable. However, the underlying mechanism underneath its early maturation remains unknown. To address this question, we conducted genome sequencing and de novo assembly of navel orange cv. Gannanzao. The assembled genome sequence is 334.57 Mb in length with a GC content of 31.48%. It comprises 318 contigs (N50 = 3.23 Mb) and 187 scaffolds (N50 = 31.86 Mb). The BUSCO test demonstrates 94.6% completeness. The annotation revealed 23,037 gene models, 164.95 Mb of repetitive sequences, and 2,554 ncRNA. Comparative analysis identified 323 fruit ripening-related genes in navel orange cv. Gannanzao genome, while navel orange cv. Newhall genome contained 345 such genes. These genes were organized into 320 orthologous gene families, with 30.3% of them exhibiting differences in gene copy numbers between the two genomes. Additionally, we identified 15 fruit ripening-related genes that have undergone adaptive evolution, suggesting their potential role in advancing fruit maturation in navel orange cv. Gannanzao. Whole genome sequencing and annotation of navel orange cv. Gannanzao provides a valuable resource to unravel the early maturation mechanism of citrus and enriches the genomic resources for citrus research.

genomics↗

Chromosome-Level Genome Assembly of Navel orange cv. Gannanzao (Citrus sinensis Osbeck cv. Gannanzao)

Navel orange cv. Gannanzao is a variant of the navel orange cv. Newhall (C. sinensis Osbeck cv. Newhall) that exhibits an earlier maturation, making it commercially valuable. However, the underlying mechanism underneath its early maturation remains unknown. To address this question, we conducted genome sequencing and de novo assembly of navel orange cv. Gannanzao. The assembled genome sequence is 334.57 Mb in length with a GC content of 31.48%. It comprises 318 contigs (N50 = 3.23 Mb) and 187 scaffolds (N50 = 31.86 Mb). The BUSCO test demonstrates 94.6% completeness. The annotation revealed 23,037 gene models, 164.95 Mb of repetitive sequences, and 2,554 ncRNA. Comparative analysis identified 323 fruit ripening-related genes in navel orange cv. Gannanzao genome, while navel orange cv. Newhall genome contained 345 such genes. These genes were organized into 320 orthologous gene families, with 30.3% of them exhibiting differences in gene copy numbers between the two genomes. Additionally, we identified 15 fruit ripening-related genes that have undergone adaptive evolution, suggesting their potential role in advancing fruit maturation in navel orange cv. Gannanzao. Whole genome sequencing and annotation of navel orange cv. Gannanzao provides a valuable resource to unravel the early maturation mechanism of citrus and enriches the genomic resources for citrus research.

genomics↗