
Jing Yan
· Assistant Professor of Molecular, Cellular and Developmental BiologyVerifiedYale University · Psychology
Active 2004–2026
About
Jing Yan is an assistant professor of molecular, cellular and developmental biology at Yale’s Faculty of Arts and Sciences. Her research focuses on understanding the biochemical and biophysical interactions within bacterial biofilm communities, particularly those formed by Vibrio cholerae, the bacterium responsible for cholera. Her work aims to uncover how bacteria recognize each other, adhere to surfaces, and then disperse to form new colonies, which is crucial for developing strategies to combat biofilm-related infections that are resistant to antibiotics. Yan's research employs a combination of genetics, microscopy, simulations, and biochemical analyses to investigate the molecular mechanisms underlying biofilm formation and dispersal. She has contributed to revealing that the extracellular matrix of biofilms, mainly composed of exopolysaccharides (EPS), is not inherently sticky but instead plays a role in excluding non-contributing cells, effectively acting as a membership marker. Her findings also show that as biofilms age, bacteria remodel their surfaces to switch interactions from attraction to repulsion, facilitating dispersal and colonization of new environments. Yan's work provides significant insights into the complex dynamics of bacterial communities and has implications for developing new approaches to treat biofilm-associated infections.
Research topics
- Biology
- Materials science
- Microbiology
- Genetics
- Nanotechnology
- Chemistry
- Physics
- Quantum mechanics
- Business
- Mathematics
- Cell biology
- Psychology
- Mechanics
- Paleontology
- Biochemical engineering
- Biophysics
- Cognitive science
- Optoelectronics
- Biochemistry
Selected publications
Journal of Tissue Viability · 2026-02-18
articleOpen accessTo explore nurses’ adherence and influencing factors to pressure injury (PI) prevention based on guidelines, and identify perceived barriers and facilitators to the evidence-based PI prevention practice in pediatric critical care units. A multi-site, quantitative, cross-sectional study spanning 16 provinces in China was conducted. Data were collected by a self-reported questionnaire, including three sections: demographic information, adherence to evidence-based PI prevention, and barriers to and facilitators of PI prevention practice. The data were analyzed using SPSS 27.0. In total, 574 nurses finished the online survey. The mean score of the evidence-based PI prevention compliance was 133.50 ± 15.10 (total score = 30-150), with a scoring rate of 89%. 54.9% of pediatric critical care nurses reported good adherence to PI prevention practice based on the guideline. The highest and lowest adherence mean score was observed in the “skin assessment and care” subscale (41.56±4.44, 92.36%) and “pressure injury risk assessment” (24.75 ± 5.10, 82.5%). Undergoing PI guideline training ( β = 0.096, P =0.039), smaller ward size (β = -0.127, P = 0.013), and hospital in eastern China ( β = 0.14, P = 0.042) were significantly associated with higher adherence. Low cooperation from patients and leadership support were identified as the top barriers and facilitators to the nurses’ adherence in practicing PI prevention. The adherence of nurses in pediatric critical units was relatively desirable. PI prevention adherence was influenced by several factors. There are some special barriers related to PI prevention adherence identified in pediatric critical care nurses. The findings may inform a theory and intervention to help the PI intervention in pediatric patients in critical care units. • Pediatric critical care nurses showed a high overall adherence rate (89%) to evidence-based pressure injury prevention. • Adherence was significantly higher among nurses who had received specific pressure injury guideline training and those working in smaller ward settings and hospitals in eastern China. • A major perceived barrier to prevention practices was low cooperation from pediatric patients, a challenge uniquely salient in the child and infant population. • Strong leadership and institutional support were identified as the top facilitators, suggesting that organizational culture is crucial for implementing evidence-based pressure injury prevention.
Biophysical Journal · 2025-02-01
articleSenior authormSystems · 2025-04-10 · 5 citations
articleOpen accessABSTRACT Vibrio cholerae pathogens cause cholera, an acute diarrheal disease resulting in significant morbidity and mortality worldwide. Biofilms in vibrios enhance their survival in natural ecosystems and facilitate transmission during cholera outbreaks. Critical components of the biofilm matrix include the Vibrio polysaccharides produced by the vps -1 and vps -2 gene clusters and the biofilm matrix proteins encoded in the rbm gene cluster, together comprising the biofilm matrix cluster. However, the biofilm matrix clusters and their evolutionary patterns in other Vibrio species remain underexplored. In this study, we systematically investigated the distribution, diversity, and evolution of biofilm matrix clusters and proteins across the Vibrio genus. Our findings reveal that these gene clusters are sporadically distributed throughout the genus, even appearing in species phylogenetically distant from Vibrio cholerae . Evolutionary analysis of the major biofilm matrix proteins RbmC and Bap1 shows that they are structurally and sequentially related, having undergone structural domain and modular alterations. Additionally, a novel loop-less Bap1 variant was identified, predominantly represented in two phylogenetically distant V. cholerae subspecies clades that share specific gene groups associated with the presence or absence of the protein. Furthermore, our analysis revealed that rbmB , a gene involved in biofilm dispersal, shares a recent common ancestor with Vibriophage tail proteins, suggesting that phages may mimic host functions to evade biofilm-associated defenses. Our study offers a foundational understanding of the diversity and evolution of biofilm matrix clusters in vibrios, laying the groundwork for future biofilm engineering through genetic modification. IMPORTANCE Biofilms help vibrios survive in nature and spread cholera. However, the genes that control biofilm formation in vibrios other than Vibrio cholerae are not well understood. In this study, we analyzed the biofilm matrix gene clusters and proteins across diverse Vibrio species to explore their patterns and evolution. We discovered that these genes are spread across different Vibrio species, including those not closely related to V. cholerae . We also found various forms of key biofilm proteins with different structures. Additionally, we identified genes involved in biofilm dispersal that are related to vibriophage genes, highlighting the role of phages in biofilm development. This study not only provides a foundational understanding of biofilm diversity and evolution in vibrios but also leads to new strategies for engineering biofilms through genetic modification, which is crucial for managing cholera outbreaks and improving the environmental resilience of these bacteria.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-02
articleAbstract The sheathed flagellum of Vibrio cholerae is a self-assembling membranous organelle that must coordinate axial assembly, sheath biogenesis, and rapid motor rotation. Here, we determine in-situ near-atomic structures of the sheathed flagellar motor inside intact cells. The motor anchors to the outer membrane through lipidated HL-rings without forming a membrane pore, thereby allowing axial assembly to drive sheath formation. Conserved LP-rings act as slide-rotary bushings that permit high-speed rotation within a dynamic envelope yet can constrict to seal the pore upon stress-induced ejection. We further show that stator activation requires a specific PomB-MotX interaction rather than peptidoglycan engagement. Together, these findings reveal how the distinctive architecture and dynamics of the sheathed flagellum promote V. cholerae motility, environmental survival, and persistent colonization of the human gut.
Single-cell imaging reveals spontaneous phenotypic sorting and bet-hedging in developing biofilms
bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-07
preprintOpen accessSenior authorCorrespondingSummary How phenotypic heterogeneity shapes biofilm architecture and development remains poorly understood. Motivated by this, we developed imaging tools to track intracellular levels of c-di-GMP, a key second messenger that controls the motile-to-sessile transition, in developing Vibrio cholerae biofilms at single-cell resolution. We show that c-di-GMP levels spontaneously bifurcate into a bimodal distribution that forms a spatially sorted pattern: High-c-di-GMP cells dominate the biofilm core while low-c-di-GMP cells localize to the periphery. Combining single-lineage tracing, mutant analysis, and agent-based modeling, we reveal that this pattern arises from differential viscosity and surface friction mediated by matrix-dependent interactions between cells and their microenvironments. We demonstrate that this heterogeneity and phenotypic sorting enable continuous emergence and shedding of planktonic cells, enhancing fitness in fluctuating environments. Our findings uncover a differential drag mechanism for pattern formation in multicellular systems, and expand the classical picture of biofilm lifecycle by highlighting the functional significance of phenotypic heterogeneity.
Dissecting the physics of bacterial biofilms with agent-based simulations
Current Opinion in Solid State and Materials Science · 2025-05-31 · 2 citations
articleSenior authorCorrespondingSoft Matter · 2025-01-01 · 3 citations
reviewOpen accessSenior authorCorrespondingadhesion and friction, and serves as the key feature that distinguishes biofilms from classical bacterial colonies. These studies lay the groundwork for many potential future directions, all of which will contribute to the establishment of a new "developmental biology" of biofilms.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-15 · 1 citations
preprintOpen accessSenior authorCorrespondingAbstract Surface adhesion is critical to the survival of pathogenic bacteria both in natural niches and during infections, often via forming matrix-embedded communities called biofilms. We previously identified a 57-amino acid peptide (Bap1-57aa) as a key contributor to biofilm adhesion of the pandemic pathogen Vibrio cholerae to various surfaces including lipid membranes. Here, we combine biophysical, computational, and genetic approaches to elucidate the molecular mechanism. A central aromatic-rich motif anchors the peptide to lipid bilayers while peripheral pseudo repeats enhance binding through avidity. Surprisingly, the core motif undergoes a lipid-induced conformational transition into a β-hairpin, enabling robust membrane insertion. Moreover, the biofilm-derived peptide, conserved in several other Vibrio species, can adhere to model host surfaces and is sensitive to membrane curvature. Our results provide molecular insight into biofilm adhesion and may lead to new strategies for targeted biofilm removal and the design of bioinspired underwater adhesives. Teaser A short peptide from Vibrio cholerae binds lipids using a unique β-hairpin motif and contributes to host colonization.
Complete chloroplast genome and phylogenetic analysis of <i>Iris confusa</i> (Iridaceae)
Mitochondrial DNA Part B · 2025-11-09 · 1 citations
articleOpen accessand contribute to further studies on phylogenetic analyses.
mBio · 2025-02-21 · 2 citations
articleOpen accessABSTRACT Bacteria form multicellular aggregates called biofilms. A crucial component of these aggregates is a protective matrix that holds the community together. Biofilm matrix composition varies depending upon bacterial species but typically includes exopolysaccharides (EPS), proteins, and extracellular DNA. Pseudomonas aeruginosa is a model organism for the study of biofilms, and in non-mucoid biofilms, it uses the structurally distinct EPS Psl and Pel, the EPS-binding protein CdrA, and eDNA as key matrix components. An interesting phenomenon that we and others have observed is that the periphery of a biofilm aggregate can be EPS-rich and contain very few cells. In this study, we investigated two possible models of assembly and dynamics of this EPS-rich peripheral region: (i) newly synthesized EPS is inserted and incorporated into the existing EPS-rich region at the periphery during biofilm aggregate growth or (ii) EPS is continuously turned over and newly synthesized EPS is deposited at the outermost edge of the aggregate. Our results support the latter model. Specifically, we observed that new EPS is continually deposited at the aggregate periphery, which is necessary for continued aggregate growth but not aggregate stability. We made similar observations in another paradigm biofilm-forming species, Vibrio cholerae . This pattern of deposition raises the question of how EPS is retained. Specifically, for P. aeruginosa biofilms, the matrix adhesin CdrA is thought to retain EPS. However, current thinking is that cell-associated CdrA is responsible for this retention, and it is not clear how CdrA might function in the relatively cell-free aggregate periphery. We observed that CdrA is enzymatically degraded during aggregate growth without negatively impacting biofilm stability and that cell-free CdrA can partially maintain aggregation and Psl retention. Overall, this study shows that the matrix of P. aeruginosa biofilms undergoes both continuous synthesis of matrix material and matrix turnover to accommodate biofilm aggregate growth and that cell-free matrix can at least partially maintain biofilm aggregation and EPS localization. Furthermore, our similar observations for V. cholerae biofilms suggest that our findings may represent basic principles of aggregate assembly in bacteria. IMPORTANCE Here, we show that, to accommodate growing cellular biomass, newly produced Psl is deposited over existing Psl at the periphery of biofilm aggregates. We demonstrated that V. cholerae employs a similar mechanism with its biofilm matrix EPS, VPS. In addition, we found that the protease LasB is present in the biofilm matrix, resulting in degradation of CdrA to lower molecular weight cell-free forms. We then show that the released forms of CdrA are retained in the matrix and remain functional. Together, our findings support that the P. aeruginosa biofilm matrix is dynamic during the course of aggregate growth and that other species may employ similar mechanisms to remodel their matrix.
Recent grants
Collaborative Research: Multiscale Analysis and Simulation of Biofilm Mechanics
NSF · $522k · 2022–2025
Frequent coauthors
- 29 shared
Japinder Nijjer
Yale University
- 28 shared
Steve Granick
University of Massachusetts Amherst
- 28 shared
Bonnie L. Bassler
Howard Hughes Medical Institute
- 25 shared
Howard A. Stone
- 20 shared
Qiuting Zhang
Fuzhou University
- 18 shared
Ned S. Wingreen
Princeton University
- 16 shared
Rich Olson
Wesleyan University
- 13 shared
Jung‐Shen B. Tai
University of Colorado Boulder
Labs
Yale Biofilm Research LabPI
Education
- 2014
Ph.D., Materials Science and Engineering
University of Illinois at Urbana-Champaign
- 2009
BS, Chemistry
Peking University
Awards & honors
- Breakthrough Prize in Fundamental Physics (2026)
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