Biology subjects

Ruan, X.

Publications and source records attributed to Ruan, X..

At least 19 recordsLinked to original sources

bioRxiv2026

DNA methylation reveals molecular heterogeneity and urate excretion-associated subtypes of gout

Background: The molecular heterogeneity among gout patients remains largely unexplored, hindered the precise treatment for gout. Common indices for gout subtyping are cumbersome to measure, resulting in poor patient compliance. Methods: We elucidated the molecular heterogeneity of gout and developed a simple, reliable classification method for gout subtypes based on genome-wide DNA methylation, to facilitate individualized treatment. Genome-wide DNA methylation profiling was conducted in two independent cohorts, comprising a discovery cohort (n = 108) and a validation cohort (n = 100) representing four clinical gout subtypes. Results: We identified two gout subgroups associated with the fractional excretion of uric acid (FEUA) but not with 24-hour urinary uric acid levels (UUE) based on unsupervised clustering of whole-genome DNA methylation profiles, highlighting the contribution of epigenetic regulation to molecular heterogeneity in urate metabolism. Enrichment analysis links FEUA-associated subtypes to renal cell types, calcium related pathways and extended to the circulating immune compartment, with neutrophil- versus memory B cell-skewed leukocyte composition. A methylation-based classification model using 18 LASSO-selected CpGs with an XGBoost classifier effectively distinguished patients with high and low uric acid excretion, achieving excellent predictive performance (training cohort: AUC = 0.96, AP = 0.91; validation cohort: AUC = 0.86, AP = 0.85), outperforming the published model with clinical characteristics and SNPs. The signature site-associated genes NEK1 and TRPS1 display significant expression differences among urate-stratified patients and immune cells groups. TRPS1 may affect the AP-1/NF-{kappa}B inflammatory programme. Conclusions: These findings reveal distinct DNA methylation signatures underlying gout heterogeneity and demonstrate the feasibility of DNA methylation markers for gout subtype classification. The proposed methylation-based model provides a promising approach for personalized management of gout.

bioinformatics↗

bioRxiv2026

The BraALA3 Homologs Mediate Propiconazole-Modulated Plant Growth in flowering Chinese cabbage

In agriculture, propiconazole (PCZ) controls excessive growth in flowering Chinese cabbage but poses dietary safety risks due to residue accumulation. Therefore, identifying novel PCZ targets and breeding PCZ-free cultivars is critical for the safe production of flowering Chinese cabbage. Here, we identified three P4-ATPase flippase homologs aminophospholipid ATPase 3 (BraALA3a/b/c) in flowering Chinese cabbage that function as sensitive targets for PCZ. These proteins exhibit high binding affinity for PCZ, which directly inhibits their ATPase activity. Overexpression of the BraALA3 homologs enhanced plant growth and increased sensitivity to PCZ, whereas knockdown led to dwarfism and reduced sensitivity. Based on these findings, we identified editable active sites via protoplast-based screening. Genetic transformation of one such site yielded BraALA3a/braala3aK200T mutant lines, which displayed a dwarf and compact architecture. These findings provide a precise molecular target for developing PCZ-free germplasm in flowering Chinese cabbage through gene editing.

plant biology↗

bioRxiv2025

Reciprocal Homoeologous Replacement of MYB Factors Drives the Evolutionary Trade-off between Yield and Fiber Quality in Cotton

The long-standing phenotypic trade-off between Upland cotton (Gossypium hirsutum, high yield) and Sea Island cotton (G. barbadense, high quality) represents a major bottleneck in cotton breeding and industrialization. Despite rapid advances in genomics, the genomic structural variations driving the divergence of these two domestication strategies, and their subsequent impact on downstream transcriptional networks, remain unclear. This study integrates multi-tissue transcriptomic atlases spanning the full growth period with pan-genomic analyses of both Upland and Sea Island cotton, proposing a "Reciprocal Selective Retention (RSR)" strategy adopted by the two species during evolution. Transcriptomic analysis revealed that while the transcriptional chassis of the two species is highly conserved, a drastic "phase inversion" occurs during fiber development. Sea Island cotton appears to trade off for quality by specifically activating a "delayed elongation" module (at 20 DPA), whereas Upland cotton initiates a "precocious filling" program to pursue yield. Further Weighted Gene Co-expression Network Analysis (WGCNA), combined with genomic Presence/Absence Variation (PAV) analysis, identified a set of key transcription factors exhibiting a "3-vs-3" reciprocal loss pattern. Upland cotton specifically retained CRF10, WIND1, and MYB93, constructing a genetic foundation of "robust root system and strong regeneration" to support high yield. Conversely, Sea Island cotton specifically retained MYB111 and ERF105/017 to maintain long-staple characteristics and environmental buffering. Whole-genome structural variation and microsynteny analyses confirmed that these differences stem from asymmetric physical deletions (e.g., a 5 kb deletion in MYB111) or fragment sequence collapse (e.g., a 15.9 kb sequence divergence in MYB93) on homologous chromosomes. The RSR model proposed in this study not only offers a novel insight into the genetic roots of the negative correlation between yield and quality but also provides clear genomic targets for precision improvement using gene-editing technologies such as CRISPR.

genomics↗

bioRxiv2025

Suppression of hepatic amino acid catabolism by the human-specific lncRNA hLMR1

Amino acid (AA) catabolism and ureagenesis in the liver are essential for maintaining systemic nitrogen homeostasis. Patients with metabolic-associated fatty liver disease (MAFLD) exhibit impaired hepatic AA catabolism and urea production, accompanied by repression of genes governing these pathways. The molecular basis of this repression remains unknown. Here, we identify the hepatocyte-specific long noncoding RNA hLMR1 as a key suppressor of hepatic AA catabolism. Using a humanized liver mouse model, we show that hLMR1 knockdown broadly upregulates genes involved in AA degradation and ureagenesis. Chromatin isolation by RNA purification (ChIRP) coupled with RNA-seq reveals extensive interactions between hLMR1 and the pre-mRNAs of AA catabolism genes, mediated by a conserved complementary motif within hLMR1 (nucleotides 587-598). In primary human hepatocytes, hLMR1 overexpression inhibits glucagon-induced activation of AA catabolic genes, whereas deletion of the 587-598 region abrogates this effect. Analysis of human liver RNA-seq datasets demonstrates a negative correlation between hLMR1 expression and AA catabolic gene programs in MAFLD. Together, these findings uncover hLMR1 as a previously unrecognized regulator of hepatic nitrogen metabolism, linking lncRNA dysregulation to metabolic dysfunction in MAFLD.

molecular biology↗

bioRxiv2025

A Multimodal Adaptive Optical Microscope For In Vivo Imaging from Molecules to Organisms

Understanding biological systems requires observing features and processes across vast spatial and temporal scales, spanning nanometers to centimeters and milliseconds to days, often using multiple imaging modalities within complex native microenvironments. Yet, achieving this comprehensive view is challenging because microscopes optimized for specific tasks typically lack versatility due to inherent optical and sample handling trade-offs, and frequently suffer performance degradation from sample-induced optical aberrations in multicellular contexts. Here, we present MOSAIC, a reconfigurable microscope that integrates multiple advanced imaging techniques including light-sheet, label-free, super-resolution, and multi-photon, all equipped with adaptive optics. MOSAIC enables non-invasive imaging of subcellular dynamics in both cultured cells and live multicellular organisms, nanoscale mapping of molecular architectures across millimeter-scale expanded tissues, and structural/functional neural imaging within live mice. MOSAIC facilitates correlative studies across biological scales within the same specimen, providing an integrated platform for broad biological investigation.

cell biology↗

bioRxiv2025

LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance

Chronic myeloid leukemia (CML) resistance to BCR-ABL tyrosine kinase inhibitors (TKIs) can arise from ABL kinase domain mutations, BCR-ABL fusion gene amplification, or kinase-independent mechanisms. To investigate imatinib-resistance, we performed quantitative mass spectrometry comparing the proteome and phosphoproteome of K562 cells (a standard CML model) and ImR cells, an imatinib-resistant K562 derivative that also exhibits cross-resistance to second- and third-generation BCR-ABL TKIs. In addition to revealing global proteome and phosphoproteome changes associated with drug resistance, we identified LIN28A--a multi-functional RNA-binding protein--as a critical mediator of imatinib resistance. LIN28A was significantly overexpressed and hyperphosphorylated in ImR cells. Depleting LIN28A via shRNA restored imatinib sensitivity, while its ectopic expression in parental K562 cells induced imatinib resistance. Mechanistically, LIN28A coordinates an extensive kinase-substrate network regulating proliferation, survival, and metabolism to drive resistance. Notably, pharmacological inhibition of LIN28A-dependent kinases (PKC, AKT, SGK1, and RPS6K) suppressed ImR proliferation. Midostaurin, a clinical PKC/FLT3 inhibitor used in FLT3-ITD--positive AML, potently re-sensitized ImR cells to imatinib. Our findings suggest that targeting LIN28A and its downstream effectors, particularly PKC, could overcome resistance to imatinib and next-generation BCR-ABL inhibitors.

cancer biology↗

bioRxiv2025

Human-Specific Suppression of Hepatic Fatty Acid Catabolism by RNA-Binding Protein HuR

RNA binding proteins (RBPs) play essential roles in all major steps of RNA processing. Genetic studies in human and mouse models support that many RBPs are crucial for maintaining homeostasis in key tissues/organs, but to what extent the function of RBPs is conserved between humans and mice is not clear. Our recent study using a chimeric humanized liver mouse model found that knocking down human HuR in human hepatocytes resulted in a broad upregulation of human genes involved in fatty acid catabolism. This regulation is human-specific, as the knocking down of mouse HuR in the liver of traditional mouse models did not show these effects. To further study this human-specific role of HuR, we co-overexpressed HuR with PPAR, a master transcription factor that promotes fatty acid catabolism, in cultured cells. We found that HuR suppressed the expression of PPAR induced fatty acid catabolism genes in human cells but not in mouse cells. We provide evidence supporting that the human-specific suppressive effect of HuR is independent of PPAR expression or location. The regulatory effects of HuR are also independent of its role in regulating mRNA stability. Using the human HMGCS2 gene as an example, we found that the suppressive effect of HuR cannot be explained by decreased promoter activity. We further provide evidence supporting that HuR suppresses the pre-mRNA processing of HMGCS2 gene, leading to accumulated intron/pre-mRNA expression of HMGCS2 gene. Furthermore, overexpression of HuR blocked and knocking down of HuR sensitized PPAR agonist-induced gene expression. By analyzing published RNA-seq data, we found compromised pre-mRNA processing for fatty acid catabolism genes in patients with fatty liver diseases, which was not observed in mouse fatty liver disease models. Our study supports the model that HuR suppresses the expression of fatty acid catabolism genes by blocking their pre-mRNA processing, which may partially explain the mild effects of PPAR agonists in treating fatty liver diseases in humans as compared with studies in mice.

molecular biology↗

bioRxiv2025

Tibicos differentially affects faecal microbiota composition and short-chain fatty acid production in prediabetic and healthy adults in a simulated digestive tract

Prediabetes and obesity are increasingly prevalent chronic pro-inflammatory conditions driven by gut microbiota dysfunction. To assist in the management of such diseases, researchers are interested in gut-microbiota targeted dietary interventions. Tibicos is a plant-based fermented beverage shown to modulate gut microbiota, with anti-hyperglycaemic and anti-inflammatory effects in in vitro and in vivo human and animal studies. We investigated the effects of ginger-cayenne tibicos on healthy and prediabetic pooled faecal microbiota, with a static in vitro digestion/ colonic fermentation model using faeces from adult overweight/ obese donors with prediabetes, and healthy donors (n=3 per group). Changes in faecal microbiota composition and short-chain fatty acid (SCFA) production were determined. Baseline prediabetic faeces was less abundant in butyrate-producing bacterial taxa and SCFAs. In vitro colonic fermentation Time and Status (prediabetic vs. healthy) were the major determinants of shifts in faecal microbial community abundance and diversity. Tibicos reduced beneficial bacterial taxa loss in prediabetic faecal microbiota. However, tibicos improved the functional capacity of healthy faecal microbiota to a larger extent, with increased SCFA production and significant correlations between bacterial species and SCFAs. The differential shifts in composition and SCFAs observed during simulated gastrointestinal transit suggest that ginger-cayenne tibicos has the potential to beneficially modulate human faecal microbiota in both healthy and prediabetic participants. This study indicates that ginger-cayenne tibicos may be a useful tool in the management of prediabetes and obesity in humans and provides pilot data for the development of larger clinical trials.

microbiology↗

bioRxiv2024

NOLC1 Suppresses Immuno-chemotherapy by Inhibiting p53-mediated Ferroptosis in Gastric Cancer

Gastric cancer (GC) is one of the most malignant cancers, and cisplatin (Cis)-based chemotherapy remains the main clinical treatment for GC. However, Cis resistance often occurs, largely limiting its therapeutic efficacy in tumors. Therefore, a better understanding of the drug resistance mechanism could reveal new approaches for improving GC treatment efficacy. Here, we define the integrative role of nucleolar and coiled-body phosphoprotein 1 (NOLC1), a molecular chaperone that is significantly upregulated in GC tissues and Cis-resistant GC cells. Knocking down NOLC1 increased GC sensitivity to Cis by regulating ferroptosis. Mechanistically, NOLC1 binds to the p53 DNA binding domain (DBD), decreasing p53 nuclear accumulation stimulated by Cis and suppressing p53 transcriptional functions. Then, the p53-mediated ferroptosis is suppressed. Furthermore, the silence of NOLC1 promoted ferroptosis-induced immunogenic cell death (ICD) and reprogrammed the immunosuppressive tumor microenvironment, thereby increasing sensitivity to anti-programmed cell death-1 (PD-1) therapy plus Cis. The combination of anti-PD-1 plus Cis effectively inhibited GC growth without significant side effects. In summary, our findings reveal that targeting NOLC1 may be a novel therapeutic strategy for GC and may increase the efficacy of chemotherapy combined with immune checkpoint inhibitor (ICI) therapy.

cancer biology↗

bioRxiv2024

Insecticide resistance in Myzus persicae collected from sweet pepper

Populations of the green peach aphid, Myzus persicae, rapidly develop resistance to insecticides applied in agriculture, necessitating regular resistance monitoring of pest populations. Previous research identified two dominant multilocus genotypes (MLGs) in conventional (using insecticides + biological control agents) Dutch sweet pepper greenhouses: MLG-A under pymetrozine application and MLG-R under flonicamid application. This suggests positive selection for the genotypes by the application of these insecticides. However, no resistance of M. persicae to these insecticides has been reported yet. To investigate whether the insecticides were selectively driving the emergence of these specific MLGs, we compared the sensitivity of MLG-A and MLG-R to pymetrozine and flonicamid to that of six other genotypes from the same crop system. Additionally, we screened the M. persicae populations from Dutch sweet pepper greenhouses for known mutations conferring resistance to carbamates, pyrethroids, neonicotinoids, and tetronic and tetramic acid derivatives. Our results show that both MLG-A and MLG-R are less sensitive to pymetrozine compared to the other genotypes investigated. Furthermore, full mortality for MLG-R, the genotype least sensitive to flonicamid, was not achieved at the recommended field dose for this insecticide. Resistance mutations for carbamates and pyrethroids were prevalent among the MLGs, including MLG-A and MLG-R, while mutation A2226V, which is linked to resistance to tetronic and tetramic acid derivatives, was absent. Notably, the neonicotinoid resistance mutation R81T was found only in MLG-R, making this the northernmost detection of R81T in M. persicae to date. This study shows that various resistance mechanisms can accumulate in a single aphid genotype and that insecticides likely play a role in selecting for the dominant genotypes of M. persicae in conventional greenhouses.

genetics↗

bioRxiv2024

Cell-type-specific splicing of transcription regulators and Ptbp1 by Rbfox1/2/3 in the developing neocortex

How master splicing regulators crosstalk with each other and to what extent transcription regulators are differentially spliced remain unclear in the developing brain. Here, cell-type-specific RNA-Seq of the developing neocortex uncover that transcription regulators are enriched for differential splicing, altering protein isoforms or inducing nonsense-mediated mRNA decay. Transient expression of Rbfox proteins in radial glia progenitors induces neuronal splicing events preferentially in transcription regulators such as Meis2 and Tead1. Surprisingly, Rbfox proteins promote the inclusion of a mammal-specific alternative exon and a previously undescribed poison exon in Ptbp1. Simultaneous ablation of Rbfox1/2/3 in the neocortex downregulates neuronal isoforms and disrupts radial neuronal migration. Furthermore, the progenitor isoform of Meis2 promotes Tgfb3 transcription, while the Meis2 neuron isoform promotes neuronal differentiation. These observations indicate that transcription regulators are differentially spliced between cell types in the developing neocortex.

developmental biology↗

bioRxiv2024

Disrupted Post-Transcriptional Regulation of Gene Expression as A Hallmark of Fatty Liver Progression

It is known that both transcriptional and post-transcriptional mechanisms control the messenger RNA (mRNA) levels. Compared to transcriptional regulations, our understanding of how post-transcriptional regulations adapt during fatty liver progression at the whole transcriptome level is unclear. While traditional RNA-seq analysis uses only reads mapped to exons to determine gene expression, recent studies support that intron-mapped reads can be reliably used to estimate gene transcription. In this study, we analyzed differential gene expression at both exon and intron levels using two liver RNA-seq datasets from mice that were fed a high-fat diet for seven weeks (mild fatty liver) or thirty weeks (severe fatty liver). We found the correlation between gene transcription and mature mRNA levels was much lower in mice with mild fatty liver as compared with mice with severe fatty liver. This result indicates broad post-transcriptional regulations for early fatty liver and such regulations are comprised for severe fatty liver. Specifically, Gene Ontology analysis revealed that genes involved in synapse organization and cell adhesion were transcriptionally upregulated, while their mature mRNAs were unaffected in the mild fatty liver. Further characterization of post-transcriptionally suppressed genes at early fatty liver revealed that their mRNAs harbor significantly longer 3 UTR, one of the major features that may subject RNA transcripts to non-sense mediated RNA decay (NMD). We further show that the expression of representative genes that were post-transcriptionally suppressed were upregulated in mice with hepatocyte-specific defect of NMD. Finally, we provide data supporting a time-dependent decrease in NMD activity in the liver of a diet-induced metabolic dysfunction-associated fatty liver disease mouse model. In summary, our study supports that NMD is essential in preventing unwanted/harmful gene expression at the early stage of fatty liver and such a mechanism is lost due to decreased NMD activity in mice with severe fatty liver.

bioinformatics↗

bioRxiv2024

YTHDF1 mediates translational control by m6A mRNA methylation in adaptation to environmental challenges

Animals adapt to environmental challenges with long-term changes at the behavioral, circuit, cellular, and synaptic levels which often require new protein synthesis. The discovery of reversible N6-methyladenosine (m6A) modifications of mRNA has revealed an important layer of post-transcriptional regulation which affects almost every phase of mRNA metabolism and therefore translational control. Many in vitro and in vivo studies have demonstrated the significant role of m6A in cell differentiation and survival, but its role in adult neurons is understudied. We used cell-type specific gene deletion of Mettl14, which encodes one of the subunits of the m6A methyltransferase, and Ythdf1, which encodes one of the cytoplasmic m6A reader proteins, in dopamine D1 receptor expressing or D2 receptor expressing neurons. Mettl14 or Ythdf1 deficiency blunted responses to environmental challenges at the behavioral, cellular, and molecular levels. In three different behavioral paradigms, gene deletion of either Mettl14 or Ythdf1 in D1 neurons impaired D1-dependent learning, whereas gene deletion of either Mettl14 or Ythdf1 in D2 neurons impaired D2-dependent learning. At the cellular level, modulation of D1 and D2 neuron firing in response to changes in environments was blunted in all three behavioral paradigms in mutant mice. Ythdf1 deletion resembled impairment caused by Mettl14 deletion in a cell type-specific manner, suggesting YTHDF1 is the main mediator of the functional consequences of m6A mRNA methylation in the striatum. At the molecular level, while striatal neurons in control mice responded to elevated cAMP by increasing de novo protein synthesis, striatal neurons in Ythdf1 knockout mice didnt. Finally, boosting dopamine release by cocaine drastically increased YTHDF1 binding to many mRNA targets in the striatum, especially those that encode structural proteins, suggesting the initiation of long-term neuronal and/or synaptic structural changes. While the m6A-YTHDF1 pathway has similar functional significance at cellular level, its cell type specific deficiency in D1 and D2 neurons often resulted in contrasting behavioral phenotypes, allowing us to cleanly dissociate the opposing yet cooperative roles of D1 and D2 neurons.

neuroscience↗

bioRxiv2024

Nanoscale volumetric fluorescence imaging via photochemical sectioning

Optical nanoscopy of intact biological specimens has been transformed by recent advancements in hydrogel-based tissue clearing and expansion, enabling the imaging of cellular and subcellular structures with molecular contrast. However, existing high-resolution fluorescence microscopes have limited imaging depth, which prevents the study of whole-mount specimens without physical sectioning. To address this challenge, we developed "photochemical sectioning," a spatially precise, light-based sample sectioning process. By combining photochemical sectioning with volumetric lattice light-sheet imaging and petabyte-scale computation, we imaged and reconstructed axons and myelination sheaths across entire mouse olfactory bulbs at nanoscale resolution. An olfactory-bulb-wide analysis of myelinated and unmyelinated axons revealed distinctive patterns of axon degeneration and de-/dysmyelination in the neurodegenerative mouse, highlighting the potential for peta- to exabyte-scale super-resolution studies using this approach.

neuroscience↗

bioRxiv2024

The cGAS-STING Pathway Is Essential in Acute Ischemia-Induced Neutropoiesis and Neutrophil Priming in the Bone Marrow

Acute myocardial ischemia triggers a rapid mobilization of neutrophils from the bone marrow to peripheral blood, facilitating their infiltration into the infarcted myocardium. These cells are critical for inducing inflammation and contributing to myocardial repair. While neutrophils in infarcted tissue are better characterized, our understanding of whether and how ischemia regulates neutrophil production, differentiation, and functionality in the bone marrow remains limited. This study investigates these processes and the influence of the cGAS-STING pathway in the context of myocardial infarction. The cGAS-STING pathway detects aberrant DNA within cells, activates STING, and initiates downstream signaling cascades involving NFKB and IRF3. We analyzed neutrophils from bone marrow, peripheral blood, and infarct tissues using MI models generated from wild-type, Cgas-/-, and Sting-/- mice. These models are essential for studying neutropoiesis (neutrophil production and differentiation), as it involves multiple cell types. RNA sequencing analysis revealed that ischemia not only increased neutrophil production but also promoted cytokine signaling, phagocytosis, chemotaxis, and degranulation in the bone marrow before their release into the peripheral blood. Inhibition of the cGAS-STING pathway decreased neutrophil production after MI and down-regulated the same pathways activated by ischemia. Neutrophils lacking cGAS or STING were less mature, exhibited reduced activation, and decreased degranulation. Deletion of cGAS and STING decreased the expression of a large group of IFN-stimulated genes and IFIT1+ neutrophils from peripheral blood and the infarct tissue, suggesting that cGAS-STING plays an essential role in neutrophils with the IFN-stimulated gene signature. Importantly, transcriptomic analysis of Cgas-/- and Sting-/- neutrophils from bone marrow and MI tissues showed downregulation of similar pathways, indicating that the functionality developed in the bone marrow was maintained despite infarct-induced stimulation. These findings highlight the importance of neutropoiesis in dictating neutrophil function in target tissues, underscoring the critical role of the cGAS-STING pathway in neutrophil-mediated myocardial repair post-ischemia.

immunology↗

bioRxiv2024

The forgotten wine: understanding the fermentation and composition of palm wine

Palm wine is an alcoholic beverage that has existed for centuries and has important economic and socio-culture values in many tropical and sub-tropical countries. Lesser known than other types of wines, palm wine is made by spontaneous fermentation of palm sap by naturally occurring microbial communities. The palm sap ecosystem has unique microbial composition and diversity, which determines the composition of the eventual wine and is likely affected by geographical distinctiveness. While these features are well understood in grape and rice wine, these features have not been understood in palm wine. In this review, we gather information of microbial communities and metabolite profiles from published studies, covering a wide range of methodologies and regions, to better understand the causal links between the principal microbial species and major metabolites of palm wine. We assess palm wine quality across production regions and local practices to provide general characteristics of palm wine and identify specific regional information. These will provide better understandings to the function of microbial communities and metabolite diversity, the contribution of regional variations and to ensure product quality in this important and widespread, yet overlooked, fermented beverage. One sentence summaryreview and synthesis of microbial ecology and metabolites in palm wine fermentation across geography and their contribution to cultural food systems

microbiology↗

bioRxiv2024

Stimulated saliva has a distinct composition that influences release of volatiles from wine

Saliva influences the release of aroma in the oral cavity. The composition of human saliva varies depending on stimulation and hosts origin; however, the compositional differences of saliva and their influences on aroma release have not been fully evaluated. In this study, we recruited 30 healthy adults (15 Australians and 15 Chinese) and collected saliva samples at three stages: before, during, and after stimulation. Salivary samples were characterised by flow rate, total protein concentration, esterase activity, microbiome composition by full-length 16S rRNA gene sequencing, and the ability to release aroma from wine by headspace solid-phase microextraction gas chromatography-mass spectrometry (HS-SPME-GC-MS). Differences in salivary composition and specific wine volatiles were found between Australian and Chinese participants, and amongst the three stimulation stages. Significant correlations between the relative abundance of 3 bacterial species and 10 wine volatiles were observed. Our results confirm the influence of participants geographic origin and stimulation on salivary composition, highlighting the role of salivary components, especially salivary bacteria, on the release of aroma from wine.

microbiology↗

bioRxiv2024

Image processing tools for petabyte-scale light sheet microscopy data

Light sheet microscopy is a powerful technique for high-speed 3D imaging of subcellular dynamics and large biological specimens. However, it often generates datasets ranging from hundreds of gigabytes to petabytes in size for a single experiment. Conventional computational tools process such images far slower than the time to acquire them and often fail outright due to memory limitations. To address these challenges, we present PetaKit5D, a scalable software solution for efficient petabyte-scale light sheet image processing. This software incorporates a suite of commonly used processing tools that are memory and performance-optimized. Notable advancements include rapid image readers and writers, fast and memory-efficient geometric transformations, high-performance Richardson-Lucy deconvolution, and scalable Zarr-based stitching. These features outperform state-of-the-art methods by over one order of magnitude, enabling the processing of petabyte-scale image data at the full teravoxel rates of modern imaging cameras. The software opens new avenues for biological discoveries through large-scale imaging experiments.

bioinformatics↗