Biology subjects

Su, J.

Publications and source records attributed to Su, J..

At least 127 records · Page 7Linked to original sources

bioRxiv2022

Single-cell multi-omics defines the cell-type specific impact of splicing aberrations in human hematopoietic clonal outgrowths

RNA splicing factors are recurrently affected by alteration-of-function mutations in clonal blood disorders, highlighting the importance of splicing regulation in hematopoiesis. However, our understanding of the impact of dysregulated RNA splicing has been hampered by the inability to distinguish mutant and wildtype cells in primary patient samples, the cell-type complexity of the hematopoietic system, and the sparse and biased coverage of splice junctions by short-read sequencing typically used in single-cell RNA sequencing. To overcome these limitations, we developed GoT-Splice by integrating Genotyping of Transcriptomes (GoT) with enhanced efficiency long-read single-cell transcriptome profiling, as well as proteogenomics (with CITE-seq). This allowed for the simultaneous single-cell profiling of gene expression, cell surface protein markers, somatic mutation status, and RNA splicing. We applied GoT-Splice to bone marrow progenitors from patients with myelodysplastic syndrome (MDS) affected by mutations in the most prevalent mutated RNA splicing factor - the core RNA splicing factor SF3B1. High-resolution mapping of SF3B1mut vs. SF3B1wt hematopoietic progenitors revealed a fitness advantage of SF3B1mut cells in the megakaryocytic-erythroid lineage, resulting in an expansion of SF3B1mut erythroid progenitor (EP) cells. SF3B1mut EP cells exhibited upregulation of genes involved in regulation of cell cycle and mRNA translation. Long-read single-cell transcriptomes revealed the previously reported increase of aberrant 3 splicing site usage in SF3B1mut cells. However, the ability to profile splicing within individual cell populations uncovered distinct cryptic 3 splice site usage across different progenitor populations, as well as stage-specific aberrant splicing during erythroid maturation. Lastly, as splice factor mutations occur in clonal hematopoiesis (CH) with increased risk of neoplastic transformation, we applied GoT-Splice to CH samples. These data revealed that the erythroid lineage bias, as well as cell-type specific cryptic 3 splice site usage in SF3B1mut cells, precede overt MDS. Collectively, we present an expanded multi-omics single-cell toolkit to define the cell-type specific impact of somatic mutations on RNA splicing, from the earliest phases of clonal outgrowths to overt neoplasia, directly in human samples.

cancer biology↗

bioRxiv2022

On How, and Why, and When, We Grow Old

Growth and aging are fundamental features of animal life. The march from fertilization to oblivion comes in enormous variety: days and hundreds of cells for nematodes, decades and trillions of cells for humans.1-4 Since Verhulst (18385) proposed the Logistic Equation - exponential growth with countervailing linear decline in rate - biologists have searched for ever better density dependent growth equations,6-12 none which accurately capture the relationship between size and time for real animals.13-15 Furthermore, while growth and aging run in parallel, whether the relationship is causal has been unknown. Here we show, by examining growth and lifespan in units of numbers of cells, N, (Cellular Phylodynamics6), that both processes are linked to the same reduction in the fraction of cells dividing, occurring by a simple expression, the Universal Mitotic Fraction Equation. Lifespan is correlated with an age when fewer than one-in-a-thousand cells are dividing, quantifying the long-appreciated mechanism of aging, the failure of cells to be rejuvenated by dilution with new materials made, and DNA repaired, at mitosis.24-26 These observations provide practical mathematical expressions for comprehending, and managing, the challenges of growth and aging, for such tasks as improving the effectiveness of COVID-19 vaccination in the elderly.

developmental biology↗

bioRxiv2022

Clair3-Trio: high-performance Nanopore long-read variant calling in family trios with Trio-to-Trio deep neural networks

Accurate identification of genetic variants from family child-mother-father trio sequencing data is important in genomics. However, state-of-the-art approaches treat variant calling from trios as three independent tasks, which limits their calling accuracy for Nanopore long-read sequencing data. For better trio variant calling, we introduce Clair3-Trio, the first variant caller tailored for family trio data from Nanopore long-reads. Clair3-Trio employs a Trio-to-Trio deep neural network model, which allows it to input the trio sequencing information and output all of the trios predicted variants within a single model to improve variant calling. We also present MCVLoss, a novel loss function tailor-made for variant calling in trios, leveraging the explicit encoding of the Mendelian inheritance. Clair3-Trio showed comprehensive improvement in experiments. It predicted far fewer Mendelian inheritance violation variations than current state-of-the-art methods. We also demonstrated that our Trio-to-Trio model is more accurate than competing architectures. Clair3-Trio is accessible as a free, open-source project at https://github.com/HKU-BAL/Clair3-Trio.

bioinformatics↗

bioRxiv2022

Additive and Dominant Loci Jointly Pyramiding the Grain Quality of Hybrid Rice

Hybrid rice has an advantage in its heterosis, resulting in high yield and resistance to biotic and abiotic stress. However, genetic improvement of grain quality is more challenging in hybrid rice than in inbred rice due to additional complexity, such as the dominant effect. It is critical to identify a path to efficiently develop inbreds and identify their superior crosses for hybrid production. Here, we developed a pipeline for joint analysis of phenotypes, effects, and generations (JPEG) and analysed 113 inbred varieties as male parents, five tester varieties as female parents, and their 565 (113x5) hybrid testcrosses for 12 grain quality traits, including grain length and width, chalkiness, and amylose content. A total of 1,619,588 single nucleotide polymorphisms were obtained for the parent varieties and inferred for the hybrids using whole-genome sequencing with an average sequencing depth of 11x. Genome-wide association studies with JPEG identified 128 loci associated with at least one of the 12 traits. There were 44 and 97 loci with additive and dominant effects, respectively, including 13 overlaps. Among the 128 associated loci, 42 loci are located in or near (<200 kb) 17 known genes. Pyramiding genetic loci with additive and/or dominant effects in genomic selection dramatically improves the accuracy of predicting hybrid performances. More than 45% of genetic variation was explained by the identified markers for all traits except one (30%). These results demonstrate that pyramiding genetically identified additive and dominant loci can afford substantial power for predicting hybrid performances, presenting opportunities to identify superior crosses from existing phenotypes and genotypes of inbreds and hybrids.

plant biology↗

bioRxiv2022

Single-cell RNA-sequencing analysis reveals the molecular mechanism of subchondral bone cell heterogeneity in the development of osteoarthritis

The cellular composition and underlying spatiotemporal transformation processes of subchondral bone in osteoarthritis (OA) remain unknown. Herein, various cell subsets from tibial plateau of OA patients are identified, and the mechanism of subchondral microstructure alteration is elaborated using single-cell RNA sequencing technique. We identified two novel endothelial cell (EC) populations characterized by either exosome synthesis and inflammation response, or vascular function and angiogenesis. Three osteoblast (OB) subtypes are introduced, separately related to vascularization, matrix manufacturing and matrix mineralization. The distinct roles and functions of these novel phenotypes in OA development are further discussed, as well as interaction network between these subpopulations. The variation tendency of each population is testified in a DMM mouse model. The identification of cell types demonstrates a novel taxonomy and mechanism for ECs and OBs inside subchondral bone area, provides new insights into the physiological and pathological behaviors of subchondral bone in OA pathogenesis.

pathology↗

bioRxiv2022

Maintaining hypoxia environment of subchondral bone alleviates osteoarthritis progression

Abnormal subchondral bone remodeling featured by over-activated osteoclastogenesis leads to articular cartilage degeneration and osteoarthritis (OA) progression, but the mechanism is still unclear. In this study, we used lymphocyte cytosolic protein 1 (Lcp1) knock-out mice to suppress subchondral osteoclast formation in mice OA model with anterior cruciate ligament transection (ACLT) and Lcp1-/- mice showed decreased bone remodeling and sensory innervation in subchondral bone accompanied by retarded cartilage degeneration. For mechanisms, in wildtype mice with ACLT the activated osteoclasts in subchondral bone induced type-H vessels and elevated oxygen concentration which ubiquitylated hypoxia-inducible factor 1 (HIF-1), vital for maintaining chondrocyte homeostasis in articular chondrocytes and led to cartilage degeneration. Deletion of Lcp1 impeded osteoclast-mediated angiogenesis, which maintained the low levels of oxygen partial pressure (pO2) in subchondral bone as well as the whole joint and delayed the OA progression. Stabilization of HIF-1 delayed cartilage degeneration and knockdown of Hif1a abolished the protective effects of Lcp1 knockout. Notably, we identified a novel subgroup of hypertrophic chondrocytes highly associated with OA by single cell sequencing analysis of human articular chondrocytes. Lastly, we showed that Oroxylin A, an Lcp1-encoded protein L-plastin (LPL) inhibitor, could alleviate OA progression. In conclusion, maintaining hypoxic environment in subchondral bone is an attractive strategy for OA treatment. TeaserInhibiting subchondral osteoclastogenesis alleviates OA progression via maintaining joint hypoxia environment.

biochemistry↗

bioRxiv2022

OncoPubMiner: A platform for oncology publication mining

Knowledge bases that are up-to-date and of expert quality are fundamental in biomedical research fields. A knowledge base established with human participation and subjected to multiple inspections is crucial for supporting clinical decision-making, especially in the exponentially growing field of precision oncology. The number of original publications in the field has skyrocketed with the advancement of technology and in-depth research evolved. It has become an increasingly pressing issue that researchers need to consider how to gather and mine these articles accurately and efficiently. In this paper, we present OncoPubMiner (https://oncopubminer.chosenmedinfo.com), a free and powerful system that combines text mining, data structure customization, publication search with online reading, project-centered and team-based data collection to realize a one-stop "keyword in, knowledge out" oncology publication mining platform. It was built by integrating all the open-access abstracts from PubMed and full-text articles from PubMed Central, and is updated on a daily basis. The system makes it straightforward to obtain precision oncology knowledge from scientific articles. OncoPubMiner will assist researchers in developing professional structured knowledge base systems efficiently, and bringing the oncology community closer to achieving precision oncology goals. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=150 SRC="FIGDIR/small/483968v1_ufig1.gif" ALT="Figure 1"> View larger version (64K): org.highwire.dtl.DTLVardef@68235aorg.highwire.dtl.DTLVardef@e9256aorg.highwire.dtl.DTLVardef@9783daorg.highwire.dtl.DTLVardef@15193e2_HPS_FORMAT_FIGEXP M_FIG OncoPubMiners one-stop "keyword in, knowledge out" workflow (A) is built on key features such as text mining (B), publication search (C), form customization (D), and team-based curation (E). C_FIG

bioinformatics↗

bioRxiv2022

Mucins form a nanoscale material barrier against immune cell attack

The cancer cell glycocalyx serves as a major line of defense against immune surveillance. However, how specific physical properties of the glycocalyx contribute to immune evasion and how these properties are regulated are not well understood. Here, we uncover how the surface density, glycosylation, and crosslinking of cancer-associated mucins contribute to the nanoscale material thickness of the glycocalyx, and further analyze the effect of the glycocalyx thickness on resistance to effector cell attack. Natural Killer (NK) cell-mediated cytotoxicity exhibits a near perfect inverse correlation with the glycocalyx thickness of target cells regardless of the specific glycan structures present. NK cells expressing a chimeric antigen receptor (CAR) have an enhanced ability to breach the glycocalyx and kill target cells. Equipping the NK cell surface with a mucin-digesting enzyme also improves killing with a performance enhancement that rivals or exceeds CARs in some cases. Together, our results provide new considerations for improving cancer immunotherapies.

biophysics↗

bioRxiv2022

m6A-TSHub: unveiling the context-specific m6A methylation and m6A-affecting mutations in 23 human tissues

As the most pervasive epigenetic marker present on mRNA and lncRNA, N6-methyladenosine (m6A) RNA methylation has been shown to participate in essential biological processes. Recent studies revealed the distinct patterns of m6A methylome across human tissues, and a major challenge remains in elucidating the tissue-specific presence and circuitry of m6A methylation. We present here a comprehensive online platform m6A-TSHub for unveiling the context-specific m6A methylation and genetic mutations that potentially regulate m6A epigenetic mark. m6A-TSHub consists of four core components, including (1) m6A-TSDB: a comprehensive database of 184,554 functionally annotated m6A sites derived from 23 human tissues and 499,369 m6A sites from 25 tumor conditions, respectively; (2) m6A-TSFinder: a web server for high-accuracy prediction of m6A methylation sites within a specific tissue from RNA sequences, which was constructed using multi-instance deep neural networks with gated attention; (3) m6A-TSVar: a web server for assessing the impact of genetic variants on tissue-specific m6A RNA modification; and (4) m6A-CAVar: a database of 587,983 TCGA cancer mutations (derived from 27 cancer types) that were predicted to affect m6A modifications in the primary tissue of cancers. The database should make a useful resource for studying the m6A methylome and genetic factor of epitranscriptome disturbance in a specific tissue (or cancer type). m6A-TSHub is accessible at: www.xjtlu.edu.cn/biologicalsciences/m6ats.

bioinformatics↗

bioRxiv2022

Hypoxia Dynamically Regulates DBC1 Ubiquitination and Stability by SIAH2 and OTUD5 in Breast Cancer Progression

DBC1 has been characterized as a key regulator of physiological and pathophysiological activities, such as DNA damage, senescence and tumorigenesis. However, the mechanism by which the functional stability of DBC1 is regulated has yet to be elucidated. Here, we report that the ubiquitination-mediated degradation of DBC1 is dynamically regulated by the E3 ubiquitin ligase SIAH2 and deubiquitinase OTUD5 under hypoxic stress. Mechanistically, hypoxia promoted the competitive binding of SIAH2 with OTUD5 to DBC1, resulting in the ubiquitination and subsequent degradation of DBC1 through the ubiquitin-proteasome pathway. Siah2 knockout inhibited tumor cell proliferation and migration, which could be rescued by double knockout of Siah2/DBC1. Human tissue microarray analysis further revealed that the SIAH2/DBC1 axis was responsible for tumor progression under hypoxic stress. These findings define a key role of the hypoxia-mediated SIAH2-DBC1 pathway in the progression of human breast cancer and provide novel insights into the metastatic mechanism of breast cancer.

cell biology↗

bioRxiv2022

Isolated Grauer's gorilla populations differ in diet and gut microbiome

The animal gut microbiome has been implicated in a number of key biological processes, ranging from digestion to behavior, and has also been suggested to facilitate local adaptation. However, studies in wild animals rarely compare multiple populations that differ ecologically, which is the level at which local adaptation may occur. Further, few studies simultaneously characterize diet and the gut microbiome from the same sample, despite the likely presence of co-dependencies. Here, we investigate the interplay between diet and gut microbiome in three geographically isolated populations of the critically endangered Grauers gorilla, which we show to be genetically differentiated. We find population- and social group-specific dietary and gut microbial profiles and co-variation between diet and gut microbiome, despite the presence of core microbial taxa. There was no detectable effect of age, sex, or genetic relatedness on the microbiome. Diet differed considerably across populations, with the high-altitude population consuming a lower diversity of plants compared to low-altitude populations, consistent with food plant availability constraining diet. The observed pattern of covariation between diet and gut microbiome is likely a result of long-term social and ecological factors. Our study suggests that the gut microbiome is sufficiently plastic to support flexible food selection and hence contribute to local adaptation.

ecology↗

bioRxiv2022

An integrated approach to protein discovery and detection from complex biofluids

Ovarian cancer, a leading cause of cancer related deaths among women, has been notoriously difficult to routinely screen for and diagnose early. Researchers and clinicians continue to seek routinely usable, non-invasive, screening methods as early detection significantly improves survival. Biomarker screening is ideal; however, currently available ovarian cancer biomarkers lack desirable sensitivity and specificity. Furthermore, the most fatal forms, high grade serous cancers often originate in the fallopian tube; therefore, sampling from the vaginal environment provides more proximal sources for tumor detection. To address these shortcomings and leverage proximal sampling, we developed an untargeted mass spectrometry microprotein profiling method and identified a signature of cystatin A, validated this protein in an animal model, and sought to overcome the limits of detection inherent to mass spectrometry by demonstrating that cystatin A is present at 100 pM concentrations using a label-free microtoroid resonator. The findings highlight the potential utility for early-stage detection where cystatin A levels would be low. Significance StatementIt is now clear that high-grade serous ovarian cancer can originate in the fallopian tube epithelium. These tumors colonize the ovary and then metastasize throughout the peritoneum. This discovery has raised important, and yet unaddressed, questions how we might be able to detect and screen for this deadly disease for which there is no routine screening. We have leveraged vaginal lavages from a murine model of the disease as a complex biological fluid for untargeted discovery of microproteins using mass. We improved our limits of detection by conjugating a cystatin A antibody to the surface of a microtoroid resonator to allow us to specifically detect cystatin A from vaginal lavages at early time points across biological replicates.

cancer biology↗

bioRxiv2021

Symphonizing pileup and full-alignment for deep learning-based long-read variant calling

Deep learning-based variant callers are becoming the standard and have achieved superior SNP calling performance using long reads. In this paper, we present Clair3, which leveraged the best of two major method categories: pile-up calling handles most variant candidates with speed, and full-alignment tackles complicated candidates to maximize precision and recall. Clair3 ran faster than any of the other state-of-the-art variant callers and performed the best, especially at lower coverage.

bioinformatics↗

bioRxiv2021

The class I TCP transcription factor AtTCP8 is a modulator of phytohormone-responsive signaling networks

The plant-specific TEOSINTE BRANCHED1/ CYCLOIDEA/ PROLIFERATING CELL FACTOR (TCP) transcription factor family is most closely associated with regulating plant developmental programs. Recently, TCPs were also shown to mediate host immune signaling, both as targets of pathogen virulence factors and regulators of plant defense genes. However, any comprehensive characterization of TCP gene targets is still lacking. Loss of the class I TCP AtTCP8 attenuates early immune signaling, and when combined with mutations in AtTCP14 and AtTCP15, additional layers of defense signaling in Arabidopsis thaliana. Here we focus on TCP8, the most poorly characterized of the three to date. We use chIP and RNA-sequencing to identify TCP8-bound gene promoters and differentially regulated genes in the tcp8 mutant, data sets that are heavily enriched in signaling components for multiple phytohormone pathways, including brassinosteroids (BRs), auxin, and jasmonic acid (JA). Using BR signaling as a representative example, we show that TCP8 directly binds and activates the promoters of the key BR transcriptional regulators BZR1 and BZR2/BES1. Furthermore, tcp8 mutant seedlings exhibit altered BR-responsive growth patterns and complementary reductions in BZR2 transcript levels, while the expressed protein demonstrates BR-responsive changes in subnuclear localization and transcriptional activity. We conclude that one explanation for the significant targeting of TCP8 alongside other TCP family members by pathogen effectors may lie in its role as a modulator of brassinosteroid and other plant hormone signaling pathways. One Sentence SummaryOne member of a pathogen-targeted transcription factor family modulates phytohormone response networks and displays brassinosteroid-dependent cellular location and activity.

plant biology↗

bioRxiv2021

In vivo adenine base editing corrects newborn murine model of Hurler syndrome

Mucopolysaccharidosis type I (MPS I) is a severe disease caused by loss-of-function mutations variants in the -L-iduronidase (IDUA) gene. In vivo genome editing represents a promising strategy to correct IDUA mutations, and has the potential to permanently restore IDUA function over the lifespan of the patients. Here, we used adenine base editing to directly convert A>G (TAG>TGG) in newborn murine model harboring Idua-W392X mutation, which recapitulates the human condition and is analogous to the highly prevalent human W402X mutation. We engineered a split-intein dual-adeno-associated virus (AAV) 9 in vivo adenine base editor to circumvent the package size limit of AAV vectors. Intravenous injection of AAV9-base editor system into MPS I newborn mice led to sustained enzyme expression sufficient for correction of metabolic disease (GAGs substrate accumulation) and prevention of neurobehavioral deficits. We observed a reversion of the W392X mutation in 22.46{+/-}6.74% of hepatocytes, 11.18{+/-}5.25% of heart and 0.34{+/-}0.12% of brain, along with decreased GAGs storage in peripheral organs (liver, spleen, lung and kidney). Collectively, these data showed the promise of a base editing approach to precisely correct a common genetic cause of MPS I in vivo and could be broadly applicable to the treatment of a wide array of monogenic diseases.

genetics↗

bioRxiv2021

Lin28a rejuvenates muscle stem cells via mitochondrial optimization

The well-conserved correlation between juvenility and tissue regeneration was first discussed by Charles Darwin. Ectopic Lin28 is known to play an important role in somatic reprogramming and tissue regeneration, but endogenous Lin28s role in tissue homeostasis and juvenility had remained unclear. Through lineage tracing, we found that a rare subset of muscle stem cells (MuSCs) expressing Lin28a can respond to acute injury by proliferating as Pax3+ or Pax7+ MuSCs, and contribute to all types of myofibers during muscle regeneration. Compared with conventional Pax7+ MuSCs, Lin28a+ MuSCs express more Pax3 and show enhanced myogenicity in vitro. In terms of the epigenetic clock, adult Lin28a+ MuSCs lie between adult Pax7+ MuSCs and embryonic Pax7+ myoblasts according to their DNA methylation profiles. We found that Lin28a+ MuSCs upregulate several embryonic limb bud mesoderm transcription factors and could maintain a juvenile state with enhanced stem cell self-renewal and stress-responsiveness in vitro and in vivo. When combined with telomerase and TP53 inhibition to biomimic mouse Lin28a+ MuSCs, we found that Lin28a can rejuvenate and dedifferentiate aged human primary myoblasts into engraftable, self-renewing MuSCs. Mechanistic studies revealed that Lin28a activated the HIF1A pathway by optimizing mitochondrial ROS (mtROS), thereby rejuvenating MuSC self-renewal and muscle regeneration. Our findings connect the stem cell factor Lin28, mtROS metabolism and stress response pathways to the process of stem cell rejuvenation and tissue regeneration.

cell biology↗

bioRxiv2021

How Our Cells Become Our Selves: The Cellular Phylodynamic Biology of Growth and Development

Our lives begin with 1 cell, then 2, then 4, then the trillion cell adult, comprised of cell lineages, tissues, organs. How does this occur? Examination in numbers of cells, N, Cellular Phylodynamics, revealed two previously unappreciated processes: UNI-GROWTH, the slowing of growth that occurs as we become larger, caused by fewer cells dividing, captured by the Universal Mitotic Fraction and Universal Growth Equations, with accuracy confirmed for 13 species, including nematodes, mollusks, and vertebrates; and ALLO-GROWTH, the creation of body parts from Founder Cells, captured by the Cellular Allometric Growth Equation, which describes mitotic expansion by Cell-Heritable change in the Cell Cycle Time. These equations can generate cell lineage approximations, bringing the power of coalescent theory to developmental biology.

developmental biology↗

bioRxiv2021

Comparative genomic and pan-genomic characteristion of Staphylococcus epidermidis from different sources unveils the molecular basis and potential biomarkers of pathogenic strains

Coagulase-negative Staphylococcus (CoNS) is the most common pathogen causing traumatic endophthalmitis, Staphylococcus epidermidis is the most common species which colonizes human skin, eye surfaces and nasal cavity and is the main cause of nosocomial infection, specially foreign body-related bloodstream infections (FBR-BSIs). Although some studies have reported the genome characteristics of S. epidermidis, a comprehensive understanding of its pathogenicity and the genome of ocular trauma-sourced strains is still lacking. In this study, we sequenced, analyzed and reported the whole genomes of 11 ocular trauma-sourced samples of S. epidermidis that caused traumatic endophthalmitis. By integrating publicly available genomes, we obtained a total of 187 S. epidermidis samples from healthy and diseased eyes, skin, respiratory tract and blood. Combined with pangenome, phylogenetic and comparative genomic analyses, our study supported that S. epidermidis, regardless of niche source, exhibits two founder lineages with different pathogenicities. Moreover, we identified potential biomarkers associated with the virulence of S. epidermidis, namely, essD, uhpt, sdrF, sdrG, fbe and icaABCDR. The essD and uhpt genes have high homology with esaD and hpt in Staphylococcus aureus, showing that the genomes of S. epidermidis and S. aureus may have communicated during evolution, while the sdrF, sdrG, fbe, and icaABCDR genes are related to biofilm formation. Compared to S. epidermidis from blood sources, ocular-sourced strains causing intraocular infection had no direct relationship with biofilm formation. In conclusion, this study not only provided additional data resources for studies on S. epidermidisis, but also improved understanding of the evolution and pathogenicity of different source strains. ImportantsIn this study, we comprehensively analysied and reported the whole genome sequence (WGS) of the strains that caused traumatic endophthalmitis. Through comparative genomic analyses among 187 S. epidermidis samples from healthy and diseased eyes, skin, respiratory tract and blood, we identified 10 potential biomarkers of pathogenic strains. Finally, we revealed S. epidermidis-induced traumatic endophthalmitis may be independent of biofilm formation. Overall, our data may facilitate comparative research of S. epidermidis and provide clinical value for identifying pathogenic or contaminating strains.

microbiology↗