About

Ned S. Wingreen is a Professor of Molecular Biology at Princeton University and is affiliated with the Lewis-Sigler Institute. He is involved with the Center for the Physics of Biological Function, an NSF Physics Frontier Center. His research focuses on the biophysics of biological systems, contributing to the understanding of the physical principles underlying biological functions. Wingreen's work is characterized by a strong interdisciplinary approach, integrating physics and biology to explore complex biological phenomena.

Research topics

• Biology
• Physics
• Biophysics
• Cell biology
• Computer Science
• Genetics
• Ecology
• Chemistry
• Materials science
• Chemical physics
• Mechanics
• Biological system
• Microbiology
• Botany
• Statistical physics
• Psychology
• Nanotechnology
• Quantum mechanics
• Paleontology
• Engineering
• Biochemistry
• Environmental science
• Biochemical engineering
• Cognitive science

Selected publications

• <i>Pseudomonas aeruginosa</i> deploys competitor-specific antagonistic strategies

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-17

  articleOpen access

  1 Abstract Microbial competition shapes polymicrobial communities, yet it remains unclear whether bacteria deploy fixed or specific antagonistic strategies against different rivals. Here we show that Pseudomonas aeruginosa deploys distinct strategies to outcompete two clinically relevant species, Burkholderia cenocepacia and Staphylococcus aureus . Under matched conditions, competition with B. cenocepacia is mediated by contact-dependent Type VI secretion, whereas competition with S. aureus follows a staged diffusible program of alkyl quinolone-mediated growth inhibition followed by LasA-dependent lysis. Transcriptomic analysis supports a “Swiss Army knife” model of antagonism in which different competitive context triggers distinct subsets of P. aeruginosa ’s arsenal. Minimal dynamical models verify that contact-dependent killing is effective against slower-growing competitors, whereas a staged strategy of growth inhibition followed by killing via diffusible factors is preferable against faster-growing rivals. Together, these results show that the competitive success of P. aeruginosa depends on competitor-specific antagonistic strategies.

  PublisherOA PDFDOI

• Kinase KEY1 controls pyrenoid condensate size throughout the cell cycle by disrupting phase separation interactions

  Nature Cell Biology · 2026-03-17

  articleOpen access

  Abstract Biomolecular condensates spatially organize cellular functions, but the regulation of their size, number, dissolution and re-condensation is poorly understood. The pyrenoid, an algal biomolecular condensate that mediates one-third of global CO 2 fixation, typically exists as one large condensate per chloroplast, but during cell division it transiently dissolves and reconfigures into multiple smaller condensates. Here, we identify a kinase, KEY1, in the model alga Chlamydomonas reinhardtii that regulates pyrenoid condensate size and number dynamics throughout the cell cycle and is necessary for normal pyrenoid function and growth. Unlike the wild type, key1 mutant cells have multiple smaller condensates throughout the cell cycle that fail to dissolve during cell division. We show that KEY1 localizes to the condensates and promotes their dissolution by disrupting interactions between their core constituents, the CO 2 -fixing enzyme Rubisco and its linker protein EPYC1, through EPYC1 phosphorylation. We develop a biophysical model that recapitulates KEY1-mediated condensate size and number regulation and suggests a mechanism for controlling condensate position. These data provide a foundation for the mechanistic understanding of the regulation of size, number, position and dissolution in pyrenoids and other biomolecular condensates.

  PublisherDOI

• Virus-like antigen display delivers a stand–alone danger signal through the BCR that circumvents tolerance

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-24

  articleOpen access

  Abstract How B cells discriminate self from foreign antigens remains a central question, given inherent autoreactivity of the mature B cell receptor (BCR) repertoire. Soluble antigen (sAg) induces tolerance, whereas patterned antigen display on virus-like particles (pAg) triggers robust B cell responses that can proceed without T cell help. Here, we show how this divergence arises early in BCR signaling. Unlike sAg, pAg can bypass a Lyn-dependent negative feedback loop to trigger digital signaling, such that ultra-low concentrations of pAg produce strong and sustained Ca 2+ responses. Surprisingly, pAg drives maximal nuclear NF-κB but limited NFAT, whereas sAg does the opposite, reflecting differential production of diacylglycerol. Consequently, sAg induced an NFAT-dependent anergy program, whereas pAg evaded this state and instead engaged a cMyc-driven program that partially resembles a TLR-dependent danger response. Our findings reveal how proximal signaling directs distinct transcriptional fate to enable immunogenic B cell responses to virus-like antigen display.

  PublisherOA PDFDOI

• Roadmap for Condensates in Cell Biology

  arXiv (Cornell University) · 2026-01-07

  preprintOpen access

  Biomolecular condensates govern essential cellular processes yet elude description by traditional equilibrium models. This roadmap, distilled from structured discussions at a workshop and reflecting the consensus of its participants, clarifies key concepts for researchers, funding bodies, and journals. After unifying terminology that often separates disciplines, we outline the core physics of condensate formation, review their biological roles, and identify outstanding challenges in nonequilibrium theory, multiscale simulation, and quantitative in-cell measurements. We close with a forward-looking outlook to guide coordinated efforts toward predictive, experimentally anchored understanding and control of biomolecular condensates.

  PublisherDOI

• How do RNA molecules distinguish self from non-self?

  Proceedings of the National Academy of Sciences · 2026-04-03

  articleOpen access

  RNA molecules form homotypic clusters in a variety of contexts. mRNAs enriched in germ granules in Drosophila embryos are a canonical example, with polar granule component ( pgc ) mRNAs colocalized with other pgc mRNAs, and nanos mRNAs with other nanos mRNAs. The observation of homotypic clustering poses a conundrum: how can RNAs of a given sequence distinguish other RNAs of the same sequence from those with different sequences? Here we show in silico that RNAs can distinguish self from non-self through the presence of palindromic regions within RNA sequences, and that palindromes can mediate homotypic clustering. We further show that RNA–RNA interactions are unlikely to lead to homotypic clusters in the absence of palindromes due to a competition between intra- and intermolecular RNA structures. We explore the implications of the palindrome-based clustering hypothesis for nanos and pgc mRNAs, and suggest how it may clear up a surprising feature of nanos clusters. More broadly, our results indicate that the palindrome content of RNAs may be under evolutionary selection pressure across a range of contexts.

  PublisherOA PDFDOI

• Roadmap for Condensates in Cell Biology

  ArXiv.org · 2026-01-07

  articleOpen access

  Biomolecular condensates govern essential cellular processes yet elude description by traditional equilibrium models. This roadmap, distilled from structured discussions at a workshop and reflecting the consensus of its participants, clarifies key concepts for researchers, funding bodies, and journals. After unifying terminology that often separates disciplines, we outline the core physics of condensate formation, review their biological roles, and identify outstanding challenges in nonequilibrium theory, multiscale simulation, and quantitative in-cell measurements. We close with a forward-looking outlook to guide coordinated efforts toward predictive, experimentally anchored understanding and control of biomolecular condensates.

  PublisherOA PDF

• Author response: Nonequilibrium polysome dynamics promote chromosome segregation and its coupling to cell growth in Escherichia coli

  2025-06-24 · 2 citations

  peer-reviewOpen access

  Polysome formation within the nucleoid and repulsion between these major cytoplasmic components provide a self-organizing mechanism for chromosome segregation and modulation of its timing across growth rates in Escherichia coli.

  PublisherDOI

• Capillary interactions drive the self-organization of bacterial colonies

  Nature Physics · 2025-07-28 · 8 citations

  articleOpen access
  PublisherOA PDFDOI

• Author response: Nonequilibrium polysome dynamics promote chromosome segregation and its coupling to cell growth in Escherichia coli

  2025-05-19

  peer-reviewOpen access

  Chromosome segregation is essential for cellular proliferation. Unlike eukaryotes, bacteria lack cytoskeleton-based machinery to segregate their chromosomal DNA (nucleoid). The bacterial ParABS system segregates the duplicated chromosomal regions near the origin of replication. However, this function does not explain how bacterial cells partition the rest (bulk) of the chromosomal material. Furthermore, some bacteria, including Escherichia coli, lack a ParABS system. Yet, E. coli faithfully segregates nucleoids across various growth rates. Here, we provide theoretical and experimental evidence that polysome production during chromosomal gene expression helps compact, split, segregate, and position nucleoids in E. coli through out-of-equilibrium dynamics and polysome exclusion from the DNA meshwork, inherently coupling these processes to biomass growth across nutritional conditions. Halting chromosomal gene expression and thus polysome production immediately stops sister nucleoid migration while ensuing polysome depletion gradually reverses nucleoid segregation. Redirecting gene expression away from the chromosome and toward plasmids causes ectopic polysome accumulations that are sufficient to drive aberrant nucleoid dynamics. Cell width enlargement suggest that the proximity of the DNA to the membrane along the radial axis is important to limit the exchange of polysomes across DNA-free regions, ensuring nucleoid segregation along the cell length. Our findings suggest a self-organizing mechanism for coupling nucleoid segregation to cell growth.

  PublisherDOI

• Temporal Dynamics of Antigen-Specific T Cell Expansion in Primary SARS-CoV-2 Infection

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-11-05

  preprintOpen access

  Abstract Quantifying T cell response during primary infection in humans is crucial for understanding adaptive immunity. Leveraging a controlled human challenge to SARS-CoV-2, we characterized antigen-specific T cell response within and across individuals. Notably, individual clones reached similar maximum frequencies despite differences in the timing of their peak expansion. Mathematical modeling showed that this observation is consistent with precursor frequency, but not TCR signal strength, as the source of inter-clonal variability. Single-cell profiling revealed distinct temporal programs for CD4 + and CD8 + T cells, with CD4 + cells expanding earlier but contracting to a lower frequency. Clones with similar receptors, likely recognizing the same antigen, expanded at similar times. Together, these findings highlight how clone-intrinsic properties such as precursor frequency and lineage shape T cell clonal kinetics. These insights provide a quantitative framework for understanding T cell response in humans, with implications for vaccine design.

  PublisherDOI

Recent grants

• NIH Grant R01GM073186

  NIH · $1.1M · 2011

• Learning principles from the pyrenoid, a phase-separated organelle

  NIH · $1.0M · 2021–2025

• Learning principles from the pyrenoid, a phase-separated organelle

  NIH · $519k · 2021–2024

• INSPIRE Track 1: Resolving and optogenetically perturbing biofilms at the single-cell level

  NSF · $1.0M · 2014–2018

• Cell-cell interactions and the development of bacterial communities

  NIH · $5.5M · 2008–2026

Frequent coauthors

• Yigal Meir

  98 shared

• Bonnie L. Bassler

  Howard Hughes Medical Institute

  91 shared

• Yaojun Zhang

  Johns Hopkins University

  42 shared

• Howard A. Stone

  38 shared

• Chao Tang

  Center for Life Sciences

  34 shared

• Clifford P. Brangwynne

  Princeton University

  32 shared

• Ranjan Mukhopadhyay

  30 shared

• Kerwyn Casey Huang

  Stanford Medicine

  29 shared