<?xml version='1.0' encoding='UTF-8'?>
<rss xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:webfeeds="http://webfeeds.org/rss/1.0" xmlns:atom="http://www.w3.org/2005/Atom" xmlns:content="http://purl.org/rss/1.0/modules/content/" version="2.0">
  <channel>
    <title>eLife: latest articles by subject</title>
    <link>https://elifesciences.org</link>
    <description>Articles published by eLife, filtered by given subjects</description>
    <atom:link href="https://observer.elifesciences.org/report/latest-articles-by-subject" rel="self"/>
    <docs>http://www.rssboard.org/rss-specification</docs>
    <generator>observer (using python-feedgen)</generator>
    <language>en</language>
    <lastBuildDate>Thu, 10 Sep 2026 17:17:36 +0000</lastBuildDate>
    <webfeeds:analytics id="G-TZ0BM7CV5E" engine="GoogleAnalytics"/>
    <item>
      <title>Viral commitment to infection depends on host metabolism</title>
      <link>https://elifesciences.org/articles/107825</link>
      <description>Viral infection begins with attachment to host surface structures such as receptors, pili, or porins. While prior research has focused on structural compatibility and recognition, the role of host physiology, particularly metabolic state, on viral commitment to infection remains underexplored. Here, we measured the adsorption rates (&lt;i&gt;η&lt;/i&gt;) of five &lt;i&gt;Escherichia coli&lt;/i&gt; phages representing various life cycles and entry pathways under controlled metabolic conditions. Four phages showed significantly reduced adsorption under energy-limited states, with weaker-binding phages being more sensitive. Using &lt;i&gt;E. coli&lt;/i&gt; and its phages allowed us to institute a number of control infections that would be difficult with other organisms. Our findings support a two-step infection model where bound phages may disengage under unfavorable conditions, reducing commitment to non-productive infections. We observed a correlation between adsorption rates under energy-competent conditions and sensitivity to host metabolic state. Our results highlight host physiology as a key factor in virus–host interactions under energy-limited conditions.</description>
      <author>anmaran@protonmail.com (Anastasios Marantos)</author>
      <author>anmaran@protonmail.com (Kim Sneppen)</author>
      <author>anmaran@protonmail.com (Namiko Mitarai)</author>
      <author>anmaran@protonmail.com (Stanley Brown)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107825</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Thu, 20 Aug 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-08-20T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>A unifying model of T-cell signaling protein condensates in reconstitution experiments</title>
      <link>https://elifesciences.org/articles/109567</link>
      <description>The formation of condensates by the Linker for the Activation of T-cells (LAT) is a key signal gating and amplification step in the T-cell receptor signaling pathway. LAT condensation is challenging to study in-vivo and is therefore often investigated using reconstitution experiments. While these experiments recapitulate key aspects of LAT condensation, they also exhibit some puzzling features. Here, we describe the mechanisms underlying these observations using two complementary models. First, we employ a Smoluchowski aggregation model to show that the delay time before condensation is observed arises from a low effective binding probability between LAT monomers. Second, we propose a field-theoretic model that reproduces all condensate morphologies observed in experiments, showing that they can arise from common underlying dynamics modulated by variations in experimental conditions. This result unifies different experimental observations reported previously. While this article addresses open questions regarding the formation of LAT condensates, our results also provide a common framework for understanding condensation of other multivalent membrane proteins such as EGFR, FGFR2, and nephrin.</description>
      <author>yadomar@mit.edu (Arup K Chakraborty)</author>
      <author>yadomar@mit.edu (Jay T Groves)</author>
      <author>yadomar@mit.edu (Mehran Kardar)</author>
      <author>yadomar@mit.edu (Simou Sun)</author>
      <author>yadomar@mit.edu (Yannick Azhri Din Omar)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.109567</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Mon, 10 Aug 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-08-10T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>The titin N2A-MARP signalosome constrains muscle longitudinal hypertrophy in response to stretch</title>
      <link>https://elifesciences.org/articles/107597</link>
      <description>Titin-based mechanosensing is a key driver of trophic signaling in muscle, yet the downstream pathways linking titin sensing to muscle remodeling remain poorly understood. To investigate these signaling mechanisms, we utilized unilateral diaphragm denervation (UDD), an in vivo model that induces titin-stiffness-dependent hypertrophy via mechanical stretch. Using UDD in rats and mice, we characterized the longitudinal hypertrophic response and distinguished stretch-induced signaling from denervation effects by performing global transcriptomic and proteomic analyses following UDD and bilateral diaphragm denervation (BDD) in rats. Our findings identified upregulation of titin-associated muscle ankyrin repeat proteins (MARPs). Subsequent phosphorylation enrichment mass spectrometry in mouse diaphragm highlighted the involvement of the N2A-element. UDD in MARP knockout (KO) mice resulted in enhanced longitudinal hypertrophy, with Western blot analysis revealing activation of the mTOR pathway. Furthermore, pharmacological inhibition of mTORC1 with rapamycin suppressed longitudinal hypertrophy, demonstrating that mTOR signaling regulates titin-mediated hypertrophic growth in a MARP-dependent manner. These findings establish MARPs as key modulators of titin-based mechanotransduction and highlight mTORC1 as a central regulator of longitudinal muscle hypertrophy.</description>
      <author>coeno@arizona.edu (Coen Ottenheijm)</author>
      <author>coeno@arizona.edu (Eva Peters)</author>
      <author>coeno@arizona.edu (Henk L Granzier)</author>
      <author>coeno@arizona.edu (Jochen Gohlke)</author>
      <author>coeno@arizona.edu (Joshua Strom)</author>
      <author>coeno@arizona.edu (Ju Chen)</author>
      <author>coeno@arizona.edu (Paul Langlais)</author>
      <author>coeno@arizona.edu (Robbert van der Pijl)</author>
      <author>coeno@arizona.edu (Shengyi Shen)</author>
      <author>coeno@arizona.edu (Siegfried Labeit)</author>
      <author>coeno@arizona.edu (Stefan Conijn)</author>
      <author>coeno@arizona.edu (Stephan Lange)</author>
      <author>coeno@arizona.edu (Zaynab Hourani)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107597</guid>
      <category>Cell Biology</category>
      <category>Physics of Living Systems</category>
      <pubDate>Thu, 30 Jul 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-07-30T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Cluster size determines internal structure of transcription factories in human cells</title>
      <link>https://elifesciences.org/articles/103955</link>
      <description>Transcription is a fundamental cellular process and the first step of gene expression. In human cells, it depends on the binding to chromatin of various proteins, including RNA polymerases and numerous transcription factors (TFs). Observations indicate that these proteins tend to form macromolecular clusters, known as &lt;i&gt;transcription factories&lt;/i&gt;, whose morphology and composition are still debated. While some microscopy experiments have revealed the presence of &lt;i&gt;specialised factories&lt;/i&gt;, composed of similar TFs transcribing families of related genes, sequencing experiments suggest instead that mixed clusters may be prevalent, as a panoply of different TFs binds promiscuously to the same chromatin region. The mechanisms underlying the formation of specialised or mixed factories remain elusive. With the aim of finding such mechanisms, here we develop a chromatin polymer model mimicking the chromatin binding-unbinding dynamics of different types of complexes of TFs. Surprisingly, both specialised (i.e. demixed) and mixed clusters spontaneously emerge, and which of the two types forms depends mainly on cluster size. The mechanism promoting mixing is the presence of non-specific interactions between chromatin and proteins, which become increasingly important as clusters become larger. This result, that we observe both in simple polymer models and more realistic ones for human chromosomes, reconciles the apparently contrasting experimental results obtained. Additionally, we show how the introduction of different types of TFs strongly affects the emergence of transcriptional networks, providing a pathway to investigate transcriptional changes following gene editing or naturally occurring mutations.</description>
      <author>gnegro2@ed.ac.uk (Antonio Suma)</author>
      <author>gnegro2@ed.ac.uk (Davide Marenduzzo)</author>
      <author>gnegro2@ed.ac.uk (Giada Forte)</author>
      <author>gnegro2@ed.ac.uk (Giuseppe Gonnella)</author>
      <author>gnegro2@ed.ac.uk (Giuseppe Negro)</author>
      <author>gnegro2@ed.ac.uk (Massimiliano Semeraro)</author>
      <author>gnegro2@ed.ac.uk (Peter Cook)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.103955</guid>
      <category>Chromosomes and Gene Expression</category>
      <category>Physics of Living Systems</category>
      <pubDate>Mon, 20 Jul 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-07-20T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>A coma pattern-based autofocusing method resolves bacterial cold shock response at single-cell level</title>
      <link>https://elifesciences.org/articles/110268</link>
      <description>Imaging-based single-cell physiological profiling holds great potential for uncovering fundamental bacterial cold shock response (CSR) mechanisms, but its application is impeded by severe focus drift during rapid temperature downshifts required for CSR induction. Here, we introduce LUNA (Locking Under Nanoscale Accuracy), an innovative autofocusing method that leverages the coma pattern of detection light to characterize focus drift. LUNA improves the focusing precision down to 3 nm and extends the focusing range to at least 40 times the objective depth of focus. These advancements enable us to investigate the complete dynamics of bacterial single-cell CSR, revealing continuous cellular growth and division. We resolve a three-phase adaptation process characterized by distinct growth deceleration dynamics, and show that bacterial cells maintain robust size regulation and coordinate uniform adaptation to cold shock through synchronized growth and elapsed cycles. Notably, a model based on scattering theory reconciles the paradox between the growth lag of batch culture and continuous single-cell growth. These findings fundamentally transform our understanding of bacterial CSR and highlight LUNA’s excellent potential for expanding state-of-the-art research in biology.</description>
      <author>shuqiang.huang@siat.ac.cn (Jinjuan Wang)</author>
      <author>shuqiang.huang@siat.ac.cn (Shuqiang Huang)</author>
      <author>shuqiang.huang@siat.ac.cn (Sihong Li)</author>
      <author>shuqiang.huang@siat.ac.cn (Xiaodong Cui)</author>
      <author>shuqiang.huang@siat.ac.cn (Xiongfei Fu)</author>
      <author>shuqiang.huang@siat.ac.cn (Yaxin Shen)</author>
      <author>shuqiang.huang@siat.ac.cn (Yue Yu)</author>
      <author>shuqiang.huang@siat.ac.cn (Zhixin Ma)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.110268</guid>
      <category>Computational and Systems Biology</category>
      <category>Physics of Living Systems</category>
      <pubDate>Mon, 06 Jul 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-07-06T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>The exquisite mechanics of a tsetse bite</title>
      <link>https://elifesciences.org/articles/112100</link>
      <description>Specialized anatomical structures in the mouth and feet of tsetse flies help them feed on blood from a variety of hosts.</description>
      <author>aacosta3@nd.edu (Álvaro Acosta-Serrano)</author>
      <author>aacosta3@nd.edu (Katelyn Fealy)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.112100</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Thu, 02 Jul 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-07-02T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Controlling the synchronization and symmetry breaking of coupled bacterial pili on active biofilm carpets</title>
      <link>https://elifesciences.org/articles/107609</link>
      <description>In the low Reynolds number regime, active biological systems utilize nonreciprocal cyclic activities to achieve motility, as seen in the spinning of bacterial flagella and the beating of cilia. Coupling among these active mechanical components leads to synchronization and emergence of metachronal waves. Here, we report that biofilms of &lt;i&gt;Pseudomonas nitroreducens&lt;/i&gt; form active carpet-like surfaces textured with diverse topological defects, generating Mexican-wave-like collective behavior in which bacteria periodically lift up. On these active surfaces, non-reciprocally coupled extension and retraction activities of bacterial pili drive these collective oscillations. Surprisingly, this collective behavior exhibits left-right asymmetry across the biofilm driving unidirectionally propagating waves. We discover that this directionality is primarily governed by an aging-related frequency gradient across the biofilm. Leveraging these insights, we further demonstrate the ability to control the collective dynamics of these waves, including symmetry breaking, transitions from spiral waves into target and propagating plane waves by manipulating the elastic properties of biofilms. Overall, our findings illuminate the fundamental role of nonreciprocally interacting active components in regulating synchronization, collective dynamics, and symmetry-breaking phenomena in biological systems.</description>
      <author>akocabas@ku.edu.tr (Alp Ünlü)</author>
      <author>akocabas@ku.edu.tr (Askin Kocabas)</author>
      <author>akocabas@ku.edu.tr (Baha Altın)</author>
      <author>akocabas@ku.edu.tr (Bora Karataş)</author>
      <author>akocabas@ku.edu.tr (Coşkun Kocabaş)</author>
      <author>akocabas@ku.edu.tr (Enes Talha Günay)</author>
      <author>akocabas@ku.edu.tr (İlker Yusuf Yaman)</author>
      <author>akocabas@ku.edu.tr (Mustafa Başaran)</author>
      <author>akocabas@ku.edu.tr (Neslihan Gedik)</author>
      <author>akocabas@ku.edu.tr (Şahin Kaya Özdemir)</author>
      <author>akocabas@ku.edu.tr (Yiğithan Gediz)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107609</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Thu, 25 Jun 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-06-25T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Building bundles by the numbers</title>
      <link>https://elifesciences.org/articles/111840</link>
      <description>The size and shape of cytoskeletal bundles, essential regulators of cell function, emerge from collective filament assembly rather than precise size-control mechanisms.</description>
      <author>andela.saric@ist.ac.at (Anđela Šarić)</author>
      <author>andela.saric@ist.ac.at (Christian Vanhille-Campos)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.111840</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 23 Jun 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-06-23T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Quantifying intracellular mechanosensitive response upon spatially defined mechano-chemical triggering</title>
      <link>https://elifesciences.org/articles/107220</link>
      <description>The mechanotransduction process relies on the interaction of mechanical and biochemical cues, transmitting cellular forces to intracellular organelles to activate biochemical pathways and elicit responses. This involves mechanoresponsive components like actin filaments, microtubules (MTs), and the lamin meshwork. Fluidic force microscopy (FluidFM), a force-controlled micropipette, allows for the manipulation of intact cells mechanically and chemically, providing a novel approach to study mechanotransmission in cells in situ. FluidFM combined with fluorescence lifetime imaging microscopy (FLIM) enables high-resolution mapping of intracellular tension dynamics. Here, we used cells with varying nuclear lamina compositions to explore the lamina’s role in initiating mechanoresponse to external cues. We found that A- and B-type lamins trigger nuclear mechanoresponse distinctly, with A-type lamins contributing to nuclear elasticity, whereas B-type lamins influence viscous response. Moreover, MTs underwent mechanical adaptation and assisted in releasing the tension in lamin A/C knockout (KO) cells, contrasting with healthy cells where MTs aid in preserving the tension locally rather than transferring it. This research provides insights into the dynamic mechanoresponse of cellular components and supports targeted therapies for mechanical stress-related diseases.</description>
      <author>elaheh.zare@alumni.ethz.ch (Elaheh Zare-Eelanjegh)</author>
      <author>elaheh.zare@alumni.ethz.ch (Ines Lüchtefeld)</author>
      <author>elaheh.zare@alumni.ethz.ch (Renard TM Lewis)</author>
      <author>elaheh.zare@alumni.ethz.ch (Tomaso Zambelli)</author>
      <author>elaheh.zare@alumni.ethz.ch (Ulrike Kutay)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107220</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Wed, 17 Jun 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-06-17T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Cognitive simplicity drives collective route improvements in homing pigeons</title>
      <link>https://elifesciences.org/articles/108054</link>
      <description>Cognitive abilities are central to how animals navigate complex environments. Beyond individual cognition, group living can also enhance navigation by pooling individually acquired information. One way this may be achieved is by following experienced leaders, which requires recognizing expertise within group members. Alternatively, accurate decisions could also emerge without expert opinions, through simpler mechanisms like the ‘wisdom of crowds’ principle that average out individual biases. Consequently, collective navigation strategies range from cognitively complex to simple, and yet, the prevalence or interplay of different collective strategies in nature remains unexplored. In this study, we asked: what is the navigation mechanism, requiring minimal cognitive demands, that is necessary and sufficient to quantitatively replicate the experimental results of a 2017 study on homing pigeons (&lt;i&gt;Columba livia&lt;/i&gt;), which showed that sequential chains of bird pairs flying home—similar to a game of telephone—led to shorter homing routes compared to control birds flying individually or in fixed pairs. Our results show that the experimental data aligns closely with the simplest strategy—route averaging. Surprisingly, the complex mechanism of selectively propagating the best flight through social learning offered no additional advantage. We further observed that mixed strategies, although not supported by the experimental data, in theory combined advantages from both averaging and active selection of better routes, resulting in even greater performance. Hence, our results highlight the potential for future research to investigate selective pressures shaping the evolution of cultural learning and trade-offs among different decision mechanisms theoretically available to social animals in nature.</description>
      <author>shoubhik.banerjee001@umb.edu (Albert B Kao)</author>
      <author>shoubhik.banerjee001@umb.edu (Fritz A Francisco)</author>
      <author>shoubhik.banerjee001@umb.edu (Shoubhik Chandan Banerjee)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.108054</guid>
      <category>Ecology</category>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 26 May 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-05-26T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Collective epithelial migration mediated by the unbinding of hexatic defects</title>
      <link>https://elifesciences.org/articles/105397</link>
      <description>Collective cell migration in epithelia relies on &lt;i&gt;cell intercalation&lt;/i&gt;: a local remodeling of the cellular network that allows neighboring cells to swap their positions. Unlike foams and passive cellular fluid, in epithelial intercalation, these rearrangements crucially depend on activity. During these processes, the local geometry of the network and the contractile forces generated therein conspire to produce a burst of remodeling events, which collectively give rise to a vortical flow at the mesoscopic length scale. In this article, we formulate a continuum theory of the mechanism driving this process, built upon recent advances toward understanding the hexatic (i.e., sixfold ordered) structure of epithelial layers. Using a combination of active hydrodynamics and cell-resolved numerical simulations, we demonstrate that cell intercalation takes place via the unbinding of topological defects, naturally initiated by fluctuations and whose late-times dynamics is governed by the interplay between passive attractive forces and active self-propulsion. Our approach sheds light on the structure of the cellular forces driving collective migration in epithelia and provides an explanation of the observed extensile activity of in vitro epithelial layers.</description>
      <author>giomi@lorentz.leidenuniv.nl (Dimitrios Krommydas)</author>
      <author>giomi@lorentz.leidenuniv.nl (Livio N Carenza)</author>
      <author>giomi@lorentz.leidenuniv.nl (Luca Giomi)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.105397</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 05 May 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-05-05T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Colony demographics shape nest construction in &lt;i&gt;Camponotus fellah&lt;/i&gt; ants</title>
      <link>https://elifesciences.org/articles/100706</link>
      <description>The ant nest serves as the skeleton of the ant superorganism. Similar to a skeleton, the nest expands as the colony grows and requires repair after catastrophic events. We experimentally compared nest excavation in colonies seeded from a single mated queen and allowed to grow for 6 months to excavation triggered by a catastrophic event in colonies with fixed demographics, where the age of each worker, including the queen, is known. The areas excavated by equal group sizes differed significantly between these conditions: heterogeneous populations in naturally growing colonies as well as cohorts of young ants dig larger areas than old ant cohorts. Moreover, we find that younger ants tend to dig slanted tunnels while older ants dig straight down. This is a novel form of age polyethism, where an ant’s age dictates not only her likelihood to engage in a task but also the way she performs the task. We further present a quantitative model that predicts that under normal growth, digging is predominantly performed by the younger ants, while after a catastrophe, all ants dig to restore lost nest volume. The fact that the nests of naturally growing colonies exhibit slanted tunnels strengthens this prediction. Finally, our results indicate how a colony’s demographic and physical history are sketched into the current structure of its nest.</description>
      <author>ofer.feinerman@weizmann.ac.il (Ehud Fonio)</author>
      <author>ofer.feinerman@weizmann.ac.il (Harikrishnan Rajendran)</author>
      <author>ofer.feinerman@weizmann.ac.il (Ofer Feinerman)</author>
      <author>ofer.feinerman@weizmann.ac.il (Roi Weinberger)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.100706</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Wed, 22 Apr 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-04-22T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Fragmentation and aggregation of cyanobacterial colonies</title>
      <link>https://elifesciences.org/articles/103503</link>
      <description>Fluid flow has a major effect on the aggregation and fragmentation of bacterial colonies. Yet, a generic framework to understand and predict how hydrodynamics affects colony size remains elusive. This study investigates how fluid flow affects the formation and maintenance of large colonial structures in cyanobacteria, using an experimental technique that precisely controls hydrodynamic conditions. We performed experiments on laboratory cultures and lake samples of the cyanobacterium &lt;i&gt;Microcystis&lt;/i&gt;, while their colony size distribution was measured simultaneously by direct microscopic imaging. We demonstrate that extracellular polymeric substances (EPS)-embedded cells formed by cell division exhibit significant mechanical resistance to shear forces. However, at elevated hydrodynamic stress levels (exceeding those typically generated by surface wind mixing), these colonies experience fragmentation through an erosion process. We also show that single cells can aggregate into small colonies due to fluid flow. However, the structural integrity of these flow-induced colonies is weaker than that of colonies formed by cell division. We provide a mathematical analysis to support the experiments and demonstrate that a population model with two categories of colonies describes the measured size distributions. Our results shed light on the specific conditions wherein flow-induced fragmentation and aggregation of cyanobacteria are decisive and indicate that colony formation under natural conditions is mainly driven by cell division, although flow-induced aggregation could play a role in dense bloom events. These findings can be used to improve prediction models and mitigation strategies for toxic cyanobacterial blooms and also offer potential applications in other areas, such as algal biotechnology or medical settings where the dynamics of biological aggregates play a significant role.</description>
      <author>y.z.sinzato@uva.nl (Jef Huisman)</author>
      <author>y.z.sinzato@uva.nl (Maziyar Jalaal)</author>
      <author>y.z.sinzato@uva.nl (Petra M Visser)</author>
      <author>y.z.sinzato@uva.nl (Robert Uittenbogaard)</author>
      <author>y.z.sinzato@uva.nl (Yuri Z Sinzato)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.103503</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Fri, 17 Apr 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-04-17T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Enhanced bacterial chemotaxis in confined microchannels occurs at lane widths matching circular swimming radius</title>
      <link>https://elifesciences.org/articles/102686</link>
      <description>Understanding bacterial behavior in confined environments is helpful for elucidating microbial ecology and developing strategies to manage bacterial infections. While extensive research has focused on bacterial motility on surfaces and in porous media, chemotaxis in confined spaces remains poorly understood. Here, we investigate the chemotaxis of &lt;i&gt;Escherichia coli&lt;/i&gt; within microfluidic lanes under a linear concentration gradient of L-aspartate. We demonstrate that &lt;i&gt;E. coli&lt;/i&gt; exhibits significantly enhanced chemotaxis in lanes with sidewalls compared to open surfaces. We attribute this phenomenon primarily to the intrinsic chiral clockwise circular motion of surface-swimming bacteria and the subsequent alignment effect upon collision with the sidewalls. By varying lane widths, we identify that an 8 μm width—approximating the radius of bacterial circular swimming on surfaces—maximizes chemotactic drift velocity. These results are supported by both experimental observations and stochastic simulations, establishing a clear proportional relationship between optimal lane width and the radius of bacterial circular swimming. Further geometric analysis provides an intuitive understanding of this phenomenon. Our results may offer insights into bacterial navigation in complex biological environments such as host tissues and biofilms, providing a preliminary step toward exploring microbial ecology in confined habitats and potential strategies for controlling bacterial infections.</description>
      <author>zhchi@ustc.edu.cn (Caijuan Yue)</author>
      <author>zhchi@ustc.edu.cn (Chi Zhang)</author>
      <author>zhchi@ustc.edu.cn (Junhua Yuan)</author>
      <author>zhchi@ustc.edu.cn (Rongjing Zhang)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.102686</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 14 Apr 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-04-14T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Revealing global stoichiometry conservation architecture in cells from Raman spectral patterns</title>
      <link>https://elifesciences.org/articles/101485</link>
      <description>Cells can adapt to various environments by changing their biomolecular profiles while maintaining physiological homeostasis. What organizational principles in cells enable the simultaneous realization of adaptability and homeostasis? To address this question, we measure Raman scattering light from &lt;i&gt;Escherichia coli&lt;/i&gt; cells under diverse conditions, whose spectral patterns convey their comprehensive molecular composition. We reveal that dimension-reduced Raman spectra can predict condition-dependent proteome profiles. Quantitative analysis of the Raman-proteome correspondence characterizes a low-dimensional hierarchical stoichiometry-conserving proteome structure. The network centrality of each gene in the stoichiometry conservation relations correlates with its essentiality and evolutionary conservation, and these correlations are preserved from bacteria to human cells. Furthermore, stoichiometry-conserving core components obey growth law and ensure homeostasis across conditions, whereas peripheral stoichiometry-conserving components enable adaptation to specific conditions. Mathematical analysis reveals that the stoichiometrically constrained architecture is reflected in major changes in Raman spectral patterns. These results uncover coordination of global stoichiometric balance in cells and demonstrate that vibrational spectroscopy can decipher such biological constraints beyond statistical or machine-learning inference of cellular states.</description>
      <author>kenichiro_kamei@cell.c.u-tokyo.ac.jp (Hidenori Nakaoka)</author>
      <author>kenichiro_kamei@cell.c.u-tokyo.ac.jp (Ken-ichiro F Kamei)</author>
      <author>kenichiro_kamei@cell.c.u-tokyo.ac.jp (Koseki J Kobayashi-Kirschvink)</author>
      <author>kenichiro_kamei@cell.c.u-tokyo.ac.jp (Miki Umetani)</author>
      <author>kenichiro_kamei@cell.c.u-tokyo.ac.jp (Takashi Nozoe)</author>
      <author>kenichiro_kamei@cell.c.u-tokyo.ac.jp (Yuichi Wakamoto)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.101485</guid>
      <category>Genetics and Genomics</category>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 14 Apr 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-04-14T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Detecting directed motion and confinement in single-particle trajectories using hidden variables</title>
      <link>https://elifesciences.org/articles/99347</link>
      <description>Single-particle tracking is a powerful tool for understanding protein dynamics and characterizing microenvironments. As the motion of unconstrained nanoscale particles is governed by Brownian diffusion, deviations from this behavior are biophysically insightful. However, the stochastic nature of particle movement and the presence of localization error pose a challenge for the robust classification of non-Brownian motion. Here, we present &lt;i&gt;aTrack&lt;/i&gt;, a versatile tool for classifying track behaviors and extracting key parameters for particles undergoing Brownian, confined, or directed motion. Our tool quickly and accurately estimates motion parameters from individual tracks. Further, our tool can analyze populations of tracks and determine the most likely number of motion states. We show the working range of our approach on simulated tracks and demonstrate its application for characterizing particle motion in &lt;i&gt;Saccharomyces cerevisiae&lt;/i&gt; and for biosensing applications in &lt;i&gt;Escherichia coli&lt;/i&gt;. aTrack is implemented as a stand-alone software, making it simple to analyze track data.</description>
      <author>simon.francois@protonmail.com (Caroline Boudoux)</author>
      <author>simon.francois@protonmail.com (Elisa Dultz)</author>
      <author>simon.francois@protonmail.com (François Simon)</author>
      <author>simon.francois@protonmail.com (Guillaume Ramadier)</author>
      <author>simon.francois@protonmail.com (Inès Fonquernie)</author>
      <author>simon.francois@protonmail.com (Janka Zsok)</author>
      <author>simon.francois@protonmail.com (Lucien E Weiss)</author>
      <author>simon.francois@protonmail.com (Michel Meunier)</author>
      <author>simon.francois@protonmail.com (Sergiy Patskovsky)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.99347</guid>
      <category>Physics of Living Systems</category>
      <category>Structural Biology and Molecular Biophysics</category>
      <pubDate>Tue, 07 Apr 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-04-07T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>A deep learning pipeline for mapping in situ network-level neurovascular coupling in multi-photon fluorescence microscopy</title>
      <link>https://elifesciences.org/articles/95525</link>
      <description>Functional hyperemia is a well-established hallmark of healthy brain function, whereby local brain blood flow adjusts in response to a change in the activity of the surrounding neurons. Although functional hyperemia has been extensively studied at the level of both tissue and individual vessels, vascular network-level coordination remains largely unknown. To bridge this gap, we developed a deep learning-based pipeline that uses two-photon fluorescence microscopy images of cerebral microcirculation to enable automated reconstruction and quantification of the geometric changes across the microvascular network, comprising hundreds of interconnected blood vessels, pre and post-activation of the neighboring neurons. The pipeline’s utility was demonstrated in the Thy1-ChR2 optogenetic mouse model, where we observed network-wide vessel radius changes to depend on the photostimulation intensity, with both dilations and constrictions occurring across the cortical depth, at an average of 16.1±14.3 μm (mean ± SD) away from the most proximal neuron for dilations; and at 21.9±14.6 μm away for constrictions. We observed a significant heterogeneity of the vascular radius changes within vessels, with radius adjustment varying by an average of 24 ± 28% of the resting diameter, likely reflecting the heterogeneity of the distribution of contractile cells on the vessel walls. A graph theory-based network analysis revealed that the assortativity of adjacent blood vessel responses rose by 152 ± 65% at 4.3 mW/mm&lt;sup&gt;2&lt;/sup&gt; of blue photostimulation &lt;i&gt;vs&lt;/i&gt;. the control, with a 4% median increase in the efficiency of the capillary networks during this level of blue photostimulation in relation to the baseline. Interrogating individual vessels is thus not sufficient to predict how the blood flow is modulated in the network. Our pipeline, enables tracking of the microvascular network geometry over time, relating caliber adjustments to vessel wall-associated cells’ state, and mapping network-level flow distribution impairments in experimental models of disease.</description>
      <author>maged.goubran@utoronto.ca (Adrienne Dorr)</author>
      <author>maged.goubran@utoronto.ca (Ahmadreza Attarpour)</author>
      <author>maged.goubran@utoronto.ca (Bojana Stefanovic)</author>
      <author>maged.goubran@utoronto.ca (James R Mester)</author>
      <author>maged.goubran@utoronto.ca (Joanne McLaurin)</author>
      <author>maged.goubran@utoronto.ca (Maged Goubran)</author>
      <author>maged.goubran@utoronto.ca (Margaret Koletar)</author>
      <author>maged.goubran@utoronto.ca (Mary E Hill)</author>
      <author>maged.goubran@utoronto.ca (Matthew W Rozak)</author>
      <author>maged.goubran@utoronto.ca (Shruti Patel)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.95525</guid>
      <category>Neuroscience</category>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 24 Mar 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-03-24T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>The cytoplasm of living cells can sustain transient and steady intracellular pressure gradients</title>
      <link>https://elifesciences.org/articles/105523</link>
      <description>Understanding the physical basis of cellular shape change in response to both internal and external mechanical stresses requires characterisation of cytoplasmic rheology. At subsecond time-scales and micron length-scales, cells behave as fluid-filled sponges in which shape changes necessitate intracellular fluid redistribution. However, whether these cytoplasmic poroelastic properties play an important role in cellular mechanical response over length- and time-scales relevant to cell physiology remains unclear. Here, we investigated whether and how a localised deformation of the cell surface gives rise to transient intracellular flows spanning several microns and lasting seconds. Next, we showed that pressure gradients induced in the cytoplasm can be sustained over several minutes. We found that stable pressure gradients can arise from the combination of cortical tension, cytoplasmic poroelasticity, and water flows across the membrane. Overall our data indicate that intracellular cytosolic flows and pressure gradients may play a much greater role than currently appreciated, acting over time- and length-scales relevant to mechanotransduction and cell migration, signifying that poroelastic properties need to be accounted for in models of the cell.</description>
      <author>m.malboubi@bham.ac.uk (Emad Moeendarbary)</author>
      <author>m.malboubi@bham.ac.uk (Guillaume Charras)</author>
      <author>m.malboubi@bham.ac.uk (Lulu IT Korsak)</author>
      <author>m.malboubi@bham.ac.uk (Majid Malboubi)</author>
      <author>m.malboubi@bham.ac.uk (Malti B Vaghela)</author>
      <author>m.malboubi@bham.ac.uk (Mohammad Hadi Esteki)</author>
      <author>m.malboubi@bham.ac.uk (Ryan J Petrie)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.105523</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Mon, 23 Mar 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-03-23T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Feeding rates in sessile versus motile ciliates are hydrodynamically equivalent</title>
      <link>https://elifesciences.org/articles/99003</link>
      <description>Motility endows microorganisms with the ability to swim to nutrient-rich environments, but many species are sessile. Existing hydrodynamic arguments in support of either strategy, to swim or to attach and generate feeding currents, are often built on a limited set of experimental or modeling assumptions. Here, to assess the hydrodynamics of these ‘swim’ or ‘stay’ strategies, we propose a comprehensive methodology that combines mechanistic modeling with a survey of published shape and flow data in ciliates. Model predictions and empirical observations show small variations in feeding rates in favor of either motile or sessile cells. Case-specific variations notwithstanding, our overarching analysis shows that flow physics imposes no constraint on the feeding rates that are achievable by the swimming versus sessile strategies – they can both be equally competitive in transporting nutrients and wastes to and from the cell surface within flow regimes typically experienced by ciliates. Our findings help resolve a long-standing dilemma of which strategy is hydrodynamically optimal and explain patterns occurring in natural communities that alternate between free swimming and temporary attachments. Importantly, our findings indicate that the evolutionary pressures that shaped these strategies acted in concert with, not against, flow physics.</description>
      <author>kanso@usc.edu (Eva Kanso)</author>
      <author>kanso@usc.edu (Jingyi Liu)</author>
      <author>kanso@usc.edu (John H Costello)</author>
      <author>kanso@usc.edu (Yi Man)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.99003</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Thu, 29 Jan 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-01-29T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Robust assessment of asymmetric division in colon cancer cells</title>
      <link>https://elifesciences.org/articles/104528</link>
      <description>Asymmetric partition of fate determinants during cell division is a hallmark of cell differentiation. Recent work suggested that such a mechanism is hijacked by cancer cells to increase both their phenotypic heterogeneity and plasticity and, in turn, their fitness. To quantify fluctuations in the partitioning of cellular elements, imaging-based approaches are used, whose accuracy is limited by the difficulty of detecting cell divisions. Our work addresses this gap, proposing a general method based on high-throughput flow cytometry measurements coupled with a theoretical framework. We applied our method to a panel of both normal and cancerous human colon cells, showing that different kinds of colon adenocarcinoma cells display very distinct extents of fluctuations in their cytoplasm partition, explained by an asymmetric division of their size. To test the accuracy of our population-level protocol, we directly measure the inherited fractions of cellular elements from extensive time lapses of live-cell laser scanning microscopy, finding excellent agreement across the cell types. Ultimately, our flow cytometry-based method promises to be accurate and easily applicable to a wide range of biological systems where the quantification of partition fluctuations would help account for the observed phenotypic heterogeneity and plasticity.</description>
      <author>mattia.miotto@roma1.infn.it (Chiara Giannattasio)</author>
      <author>mattia.miotto@roma1.infn.it (Domenico Caudo)</author>
      <author>mattia.miotto@roma1.infn.it (Fabio Giavazzi)</author>
      <author>mattia.miotto@roma1.infn.it (Giancarlo Ruocco)</author>
      <author>mattia.miotto@roma1.infn.it (Giorgio Gosti)</author>
      <author>mattia.miotto@roma1.infn.it (Giovanna Peruzzi)</author>
      <author>mattia.miotto@roma1.infn.it (Mattia Miotto)</author>
      <author>mattia.miotto@roma1.infn.it (Simone Scalise)</author>
      <author>mattia.miotto@roma1.infn.it (Valeria de Turris)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.104528</guid>
      <category>Cancer Biology</category>
      <category>Physics of Living Systems</category>
      <pubDate>Fri, 23 Jan 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-01-23T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Linking complex microbial interactions and dysbiosis through a disordered Lotka–Volterra model</title>
      <link>https://elifesciences.org/articles/105948</link>
      <description>The rapid advancement of environmental sequencing technologies, such as metagenomics, has significantly enhanced our ability to study microbial communities. The eubiotic composition of these communities is crucial for maintaining ecological functions and host health. Species diversity is only one facet of a healthy community’s organization; together with abundance distributions and interaction structures, it shapes reproducible macroecological states, that is, joint statistical fingerprints that summarize whole-community behavior. Despite recent developments, a theoretical framework connecting empirical data with ecosystem modeling is still in its infancy, particularly in the context of disordered systems. Here, we present a novel framework that couples statistical physics tools for disordered systems with metagenomic data, explicitly linking diversity, interactions, and stability to define and compare these macroecological states. By employing the generalized Lotka–Volterra model with random interactions, we reveal two different emergent patterns of species interaction networks and species abundance distributions for healthy and diseased microbiomes. On the one hand, healthy microbiomes have similar community structures across individuals, characterized by strong species interactions and abundance diversity consistent with neutral stochastic fluctuations. On the other hand, diseased microbiomes show greater variability driven by deterministic factors, thus resulting in less ecologically stable and more divergent communities. Our findings suggest the potential of disordered system theory to characterize microbiomes and to capture the role of ecological interactions on stability and functioning.</description>
      <author>ada.altieri@u-paris.fr (Ada Altieri)</author>
      <author>ada.altieri@u-paris.fr (Amos Maritan)</author>
      <author>ada.altieri@u-paris.fr (Andrea Rinaldo)</author>
      <author>ada.altieri@u-paris.fr (Edoardo Vincenzo Savarino)</author>
      <author>ada.altieri@u-paris.fr (Jacopo Pasqualini)</author>
      <author>ada.altieri@u-paris.fr (Samir Suweis)</author>
      <author>ada.altieri@u-paris.fr (Sonia Facchin)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.105948</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Mon, 12 Jan 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-01-12T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Probing the proteome</title>
      <link>https://elifesciences.org/articles/110102</link>
      <description>Raman spectroscopy can be used to predict cellular physiology and proteome composition in &lt;i&gt;E. coli&lt;/i&gt;.</description>
      <author>whl243@as.edu.tw (Chia-Liang Cheng)</author>
      <author>whl243@as.edu.tw (Wei-Hsiang Lin)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.110102</guid>
      <category>Genetics and Genomics</category>
      <category>Physics of Living Systems</category>
      <pubDate>Wed, 07 Jan 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-01-07T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Atypical collective oscillatory activity in cardiac tissue uncovered by optogenetics</title>
      <link>https://elifesciences.org/articles/107072</link>
      <description>Many biological processes emerge as frequency-dependent responses to trains of external stimuli. Heart rhythm disturbances, that is cardiac arrhythmias, are important examples as they are often triggered by specific patterns of preceding stimuli. In this study, we investigated how ectopic arrhythmias can be induced by external stimuli in cardiac tissue containing a localised area of depolarisation. Using optogenetic in vitro experiments and in silico modelling, we systematically explored the dynamics of these arrhythmias, which are characterised by local oscillatory activity, by gradually altering the degree of depolarisation in a predefined region. Our findings reveal a bi-stable system, in which transitions between oscillatory ectopic activity and a quiescent state can be precisely controlled, that is by adjusting the number and frequency of propagating waves through the depolarised area oscillations could be turned on or off. These frequency-dependent responses arise from collective mechanisms involving stable, non-self-oscillatory cells, contrasting with the typical role of self-oscillations in individual units within biophysical systems. To further generalise these findings, we demonstrated similar frequency selectivity and bi-stability in a simplified reaction–diffusion model. This suggests that complex ionic cell dynamics are not required to reproduce these effects; rather, simpler non-linear systems can replicate similar behaviour, potentially extending beyond the cardiac context.</description>
      <author>a.teplenin@lumc.nl (Alexander S Teplenin)</author>
      <author>a.teplenin@lumc.nl (Alexander V Panfilov)</author>
      <author>a.teplenin@lumc.nl (Antoine AF de Vries)</author>
      <author>a.teplenin@lumc.nl (Daniël A Pijnappels)</author>
      <author>a.teplenin@lumc.nl (Nina N Kudryashova)</author>
      <author>a.teplenin@lumc.nl (Rupamanjari Majumder)</author>
      <author>a.teplenin@lumc.nl (Tim De Coster)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107072</guid>
      <category>Computational and Systems Biology</category>
      <category>Physics of Living Systems</category>
      <pubDate>Wed, 07 Jan 2026 00:00:00 +0000</pubDate>
      <dc:date>2026-01-07T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>The evolution of interdisciplinarity and internationalization in scientific journals</title>
      <link>https://elifesciences.org/articles/107765</link>
      <description>There is a widely held perception that science is becoming more international—through multi-national collaborations—and interdisciplinary, drawing on knowledge from multiple domains. However, these hypothesized trends have not yet been quantitatively characterized. With the publication metadata from OpenAlex, we examine trends in two groups of journals: disciplinary journals in natural sciences, life sciences, social sciences, and multidisciplinary journals that publish articles in multiple fields. Supporting existing perceptions, we find an almost universal trend towards increasing internationalization of both sets of journals. Nevertheless, we find disparities: medicine journals are less international than journals in other disciplines and do not increase their levels of internationalization, whereas physics journals appear to be segregating between those that are international and those that are not. We also find that multidisciplinary journals have undergone significant shifts in their disciplinary focuses over the past century, whereas disciplinary journals appear to have largely maintained their degree of interdisciplinarity.</description>
      <author>amaral@northwestern.edu (Huaxia Zhou)</author>
      <author>amaral@northwestern.edu (Luis A Nunes Amaral)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.107765</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Wed, 31 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-31T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Postural adaptations may contribute to the unique locomotor energetics seen in hopping kangaroos</title>
      <link>https://elifesciences.org/articles/96437</link>
      <description>Hopping kangaroos exhibit remarkably little change in their rate of metabolic energy expenditure with locomotor speed compared to other running animals. This phenomenon may be related to greater elastic energy savings due to increasing tendon stress; however, the mechanisms which enable the rise in stress without additional muscle work remain poorly understood. In this study, we created a three-dimensional (3D) kangaroo musculoskeletal model, integrating 3D motion capture and force plate data, to analyse the kinematics and kinetics of hopping red and grey kangaroos. Using our model, we evaluated how body mass and speed influence (i) hindlimb posture, (ii) effective mechanical advantage (EMA), (iii) the associated tendon stress in the ankle extensors, and (iv) ankle work during hopping. We found that increasing ankle dorsiflexion and metatarsophalangeal plantarflexion likely played an important role in decreasing ankle EMA by altering both the muscle and external moment arms, which subsequently increased energy absorption and peak tendon stress at the ankle. Surprisingly, kangaroo hindlimb posture changes appeared to contribute to increased tendon stress, allowing more elastic energy storage at faster speeds. These posture-mediated increases in elastic energy storage and return could be a key factor enabling kangaroos to achieve energetic benefits at faster hopping speeds, but may limit the performance of large kangaroos due to the risk of tendon rupture.</description>
      <author>cclement@usc.edu.au (Alexis Wiktorowicz-Conroy)</author>
      <author>cclement@usc.edu.au (Christofer J Clemente)</author>
      <author>cclement@usc.edu.au (Craig P McGowan)</author>
      <author>cclement@usc.edu.au (Glen A Lichtwark)</author>
      <author>cclement@usc.edu.au (John R Hutchinson)</author>
      <author>cclement@usc.edu.au (Jonas Rubenson)</author>
      <author>cclement@usc.edu.au (Lauren Thornton)</author>
      <author>cclement@usc.edu.au (Taylor Dick)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.96437</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 16 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-16T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Exploiting fluctuations in gene expression to detect causal interactions between genes</title>
      <link>https://elifesciences.org/articles/92497</link>
      <description>Characterizing and manipulating cellular behavior requires a mechanistic understanding of the causal interactions between cellular components. We present an approach to detect causal interactions between genes without the need to perturb the physiological state of cells. This approach exploits naturally occurring cell-to-cell variability which is experimentally accessible from static population snapshots of genetically identical cells without the need to follow cells over time. Our main contribution is a simple mathematical relation that constrains the propagation of gene expression noise through biochemical reaction networks. This relation allows us to rigorously interpret fluctuation data even when only a small part of a complex gene regulatory process can be observed. We show how this relation can, in theory, be exploited to detect causal interactions by synthetically engineering a passive reporter of gene expression, akin to the established ‘dual reporter assay’. While the focus of our contribution is theoretical, we also present an experimental proof-of-principle to demonstrate the real-world applicability of our approach in certain circumstances. Our experimental data suggest that the method can detect causal interactions in specific synthetic gene regulatory circuits in &lt;i&gt;Escherichia coli,&lt;/i&gt; confirming our theoretical result in a narrow set of controlled experimental settings. Further work is needed to show that the approach is practical on a large scale, with naturally occurring gene regulatory networks, or in organisms other than &lt;i&gt;E. coli&lt;/i&gt;.</description>
      <author>andreas.hilfinger@utoronto.ca (Andreas Hilfinger)</author>
      <author>andreas.hilfinger@utoronto.ca (Euan Joly-Smith)</author>
      <author>andreas.hilfinger@utoronto.ca (Fotini Papazotos)</author>
      <author>andreas.hilfinger@utoronto.ca (Laurent Potvin-Trottier)</author>
      <author>andreas.hilfinger@utoronto.ca (Mir Mikdad Talpur)</author>
      <author>andreas.hilfinger@utoronto.ca (Paige Allard)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.92497</guid>
      <category>Computational and Systems Biology</category>
      <category>Physics of Living Systems</category>
      <pubDate>Tue, 16 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-16T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Advantageous and disadvantageous inequality aversion can be taught through learning of others’ preferences</title>
      <link>https://elifesciences.org/articles/102800</link>
      <description>While enforcing egalitarian social norms is critical for human society, punishing social norm violators often incurs a cost to the self. This cost looms even larger when one can benefit from an unequal distribution of resources, a phenomenon known as advantageous inequity—for example, receiving a higher salary than a colleague with the identical role. In the Ultimatum Game, a classic testbed for fairness norm enforcement, individuals rarely reject (or punish) such unequal proposed divisions of resources because doing so entails a sacrifice of one’s own benefit. Recent work has demonstrated that observing and implementing another’s punitive responses to unfairness can efficiently alter the punitive preferences of an observer. It remains an open question, however, whether such contagion is powerful enough to impart advantageous inequity aversion to individuals—that is, can observing another’s preferences to punish inequity result in increased enforcement of equality norms, even in the difficult case of Advantageous inequity? Using a variant of the Ultimatum Game in which participants are tasked with responding to fairness violations on behalf of another ‘Teacher’—whose aversion to advantageous (versus disadvantageous) inequity was systematically manipulated—we probe whether individuals subsequently increase their punishment unfairly after experiencing fairness violations on their own behalf. In two experiments, we found individuals can acquire aversion to advantageous inequity through observing (and implementing) the Teacher’s preferences. Computationally, these learning effects were best characterized by a model which learns the latent structure of the Teacher’s preferences, rather than a simple Reinforcement Learning account. In summary, our study is the first to demonstrate that people can swiftly and readily acquire another’s preferences for advantageous inequity, suggesting in turn that behavioral contagion may be one promising mechanism through which social norm enforcement—which people rarely implement in the case of advantageous inequality—can be enhanced.</description>
      <author>shen.zhang@mail.bnu.edu.cn (A Ross Otto)</author>
      <author>shen.zhang@mail.bnu.edu.cn (Oriel FeldmanHall)</author>
      <author>shen.zhang@mail.bnu.edu.cn (Sébastien Hétu)</author>
      <author>shen.zhang@mail.bnu.edu.cn (Shen Zhang)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.102800</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Thu, 11 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-11T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
    <item>
      <title>Theory of active self-organization of dense nematic structures in the actin cytoskeleton</title>
      <link>https://elifesciences.org/articles/93097</link>
      <description>The actin cytoskeleton is remarkably adaptable and multifunctional. It often organizes into nematic bundles such as contractile rings or stress fibers. However, how a uniform and isotropic actin gel self-organizes into dense nematic bundles is not fully understood. Here, using an active gel model accounting for nematic order and density variations, we identify an active patterning mechanism leading to localized dense nematic structures. Linear stability analysis and nonlinear finite element simulations establish the conditions for nematic bundle self-assembly and how active gel parameters control the architecture, orientation, connectivity, and dynamics of self-organized patterns. Finally, we substantiate with discrete network simulations the main requirements for nematic bundle formation according to our theory, namely increased active tension perpendicular to the nematic direction and generalized active forces conjugate to nematic order. Our work portrays actin gels as reconfigurable active materials with a spontaneous tendency to develop patterns of dense nematic bundles.</description>
      <author>alejandro.torressanchez@embl.es (Alejandro Torres-Sánchez)</author>
      <author>alejandro.torressanchez@embl.es (Guillermo Vilanova)</author>
      <author>alejandro.torressanchez@embl.es (Marco De Corato)</author>
      <author>alejandro.torressanchez@embl.es (Marco Pensalfini)</author>
      <author>alejandro.torressanchez@embl.es (Marino Arroyo)</author>
      <author>alejandro.torressanchez@embl.es (Waleed Mirza)</author>
      <guid isPermaLink="false">https://dx.doi.org/10.7554/eLife.93097</guid>
      <category>Physics of Living Systems</category>
      <pubDate>Mon, 08 Dec 2025 00:00:00 +0000</pubDate>
      <dc:date>2025-12-08T00:00:00Z</dc:date>
      <webfeeds:featuredImage url="https://elife-cdn.s3.amazonaws.com/observer/elife-logo-408x230.svg" height="230" width="408" type="image/svg"/>
    </item>
  </channel>
</rss>
