PLOS Biology: New Articles

A split nozzle and two-protein chain-like fibers define the tail architecture of Pseudomonas aeruginosa podophage A1002

2026-11-03T14:00:00Z

by Hao Pang, Yuan Chen, Zeng Peng, Hao Xiao, Wenyuan Chen, Xiaowu Li, Ping Chen, Jing Zheng, Hongrong Liu

Phage therapy offers unique advantages against antibiotic-resistant bacteria. However, high-resolution structural studies of phages targeting Pseudomonas aeruginosa—a top-seven global pathogen—particularly podophages, remain severely limited, directly impeding structure-based development of novel antimicrobials. In this study, we utilize cryo-EM to resolve the high-resolution intact structure of mature phage A1002, a podophage infecting carbapenem-resistant P. aeruginosa. Based on density maps combined with AlphaFold3 predictions, we identified 11 structural protein components from the head to the tail. Phage A1002 exhibits a distinctly elongated tail morphology distinct from other reported podophages. Notably, the A1002 nozzle employs a distinct assembly strategy, featuring the unique nozzle-rope protein and nozzle-base protein, which may have evolved through modular evolution and horizontal gene transfer. Furthermore, the nozzle-rope protein provides 11 adsorption sites for fiber dimers, and these dimers are assembled from two proteins, giving rise to two types of dimers: dimers 1–7 correspond to fiber I (gp40), and dimers 8–11 correspond to fiber II (gp41). The nozzle-rope protein and these dimers combine to form a chain-like fiber. The tail tube comprises a double-layered, elongated tube structure that functions to simultaneously increase tail length and provide docking sites for six chain-like fibers. These distinctive structural features provide the molecular basis for A1002’s broad-spectrum infection of drug-resistant P. aeruginosa and offer a novel molecular blueprint for rational design of structure-guided phage therapeutics.

An open-source eye-tracking system adaptable to diverse terrestrial vertebrates reveals state-dependent visual acquisition in lizards

2026-11-03T14:00:00Z

by Nimrod Leberstein, Tali Remenick, Milan Becker, Mark Shein-Idelson

Gaze shifts are fundamental to visual exploration and processing, yet empirical knowledge is largely confined to a small number of model species, limiting our understanding of general principles of visual acquisition across animals. Here, we introduce a versatile, low-cost, and open-source framework design for eye-tracking in small, freely moving animals. Leveraging photogrammetry, 3D modeling, and 3D-printing, we produce headmounts adaptable to diverse head-eye geometries, as we demonstrate for lizards, turtles, and mice. Detailed recordings in Pogona vitticeps, a laterally eyed ectotherm with a high-acuity retina, reveal a rich oculomotor repertoire with kinematics closely resembling the saccadic main sequence in primates. We found both movement-coupled large binocular saccades, which exhibited a strong axial bias as well as small, isotropic, and monocular saccades suggesting a capacity for visual exploration of local details. Visual acquisition strategies were strongly tied to behavioral states with periods of active sampling (3–5 Hz saccades) separated by periods of ocular stillness lasting many seconds and suggesting a visual acquisition strategy distinct from those commonly described in endothermic model species. Furthermore, active states were correlated with pupil constriction in contrast to mammals and similarly to birds. Our results demonstrate the utility of our experimental approach for understanding visual acquisition across terrestrial vertebrates. Such a multi-perspective view on natural visual acquisition across species will be essential for developing a generalized understanding of vision, its ecological functions, and its evolutionary trajectory.

The human hippocampus supports auditory coding and multisensory integration

2026-11-03T14:00:00Z

by Omri Raccah, Aryan Agarwal, Yannan Zhu, Nicholas B. Turk-Browne

The hippocampus receives convergent input from multiple sensory systems, yet in humans it has been studied almost exclusively through vision. Here we examine how the hippocampus contributes to sensory processing beyond the visual modality and to the multisensory integration of visual information with these other modalities. Participants were exposed to multiple repetitions of short naturalistic movie clips, each presented in four formats: auditory-only, visual-only, congruent audiovisual, and incongruent audiovisual (audio and video from different movies). Using high-resolution fMRI, we measured univariate activation and multivariate representations across the longitudinal axis and subfields of the human hippocampus. Whereas univariate analyses detected only visual responses across hippocampal subregions, with no activation for auditory stimuli and no benefit of congruent stimuli, multivariate analyses revealed robust representations of both auditory and visual scenes. The posterior hippocampus showed enhanced pattern similarity for congruent stimuli relative to unisensory stimuli, especially in the left hemisphere, demonstrating multisensory facilitation. The anterior hippocampus showed crossmodal decoding between auditory and visual versions of the same clip, driven by the right hemisphere, suggesting a more abstract representation. Finally, whole-brain searchlight analyses revealed parallel effects in cortical regions known to support multisensory integration. These findings advance understanding of auditory and multisensory coding in the human hippocampus, revealing specialization and lateralization along its longitudinal axis.

A deep genetic structure phylogenomically frames the closest algal relatives of land plants

2026-11-03T14:00:00Z

by Maaike J. Bierenbroodspot, Cäcilia F. Kunz, Elisa S. Goldbecker, Maike Lorenz, Iker Irisarri, Thomas Pröschold, Tatyana Darienko, Jan de Vries

Discerning the nature of the last common ancestor of land plants (embryophytes) and algae allows to retrace the adaptations that ushered in the conquest of land by plants. For this, the closest streptophyte algal relatives of embryophytes hold key information. Albeit initially coming as a surprise due to their plain body plans, all major phylogenomic efforts have concluded that the Zygnematophyceae are the algal sisters to land plants. The Zygnematophyceae are the streptophyte algal class with the greatest species richness and while we now have ample genome information on a few select members of zygnematophytes, our understanding of the genomic divergence as well as genetic potential for key traits is limited by a lack of phylodiverse data that accounts for this diversity and integrates it into a phylogenomic framework. We here sequenced 43 new transcriptome datasets for the Zygnematophyceae and built a phylogenomic tree based on a total of 104 zygnematophyceaen transcriptomes and 2243 loci. We recover a deep genetic structure for the Zygnematophyceae: Despite the deep split between Spirogyrales and their unicellular sister group Desmidiales, most Spirogyrales emerged after pronounced genetic divergence, accommodating the attainment of multicellularity and divergent traits such as unique cell and plastid division. Overall, our data capture signatures of massive ancient radiations that could only be revealed thanks to a phylodiverse sampling. Recognizing the deep genetic divergences and a vast evolutionary history of the Zygnematophyceae are key to illuminate the nature of the algal progenitors of land plants.

Infant presence and mother-infant conflict predict fetal loss in wild mandrills

2026-11-03T14:00:00Z

by Nikolaos Smit, Berta Roura-Torres, Axelle Delaunay, Alice Baniel, Elise Huchard, Marie J. E. Charpentier

Female fitness depends on reproductive pace and offspring survival, both of which are determined by the ability to balance resource allocation between current and future reproduction. Using 11 years of data on 356 pregnancies (52 of which resulted in fetal loss) from 117 wild female mandrills, we show that females who conceive while still caring for a young infant experience a greater probability of fetal loss as well as increased mother-infant behavioral conflict in the form of maternal rejection. In addition, females whose infants throw more tantrums show a greater probability of fetal loss, consistent with observations from other species where living offspring can interfere in parental reproduction. Finally, females who lose a fetus show greater subsequent reproductive success (produce more surviving infants and show shorter inter-birth intervals) than females who give birth but their infants die soon after birth. These findings suggest that fetal loss may represent an adaptive physiological response to the energetic constraints imposed by overlapping gestation and maternal care, potentially limiting the fitness costs associated with short inter-birth intervals and concurrent investment in multiple dependent offspring.

LEM-3/ANKLE1 nuclease prevents the formation of abnormal syncytium to safeguard neuronal differentiation

2026-11-02T14:00:00Z

by Siyu Deng, Chaogu Zheng

In animal development, cells exit the cell cycle after a final round of cell division to differentiate into specialized cell types. However, the impact of failed cytokinesis on the fate specification of postmitotic cells, especially neurons, remains poorly understood. We analyzed the Caenorhabditis elegans mutants lacking the midbody-tethered endonuclease LEM-3/ANKLE1, which resolves chromatin bridges during cytokinesis. Using genetic analysis, fluorescence microscopy, and RNA visualization, we found that unresolved DNA bridges lead to the formation of stable intercellular bridges, creating binucleate syncytia between touch receptor neurons and sister cells, which allows thorough cytoplasmic mixing despite independent nuclear transcription. In some cases, the cytoplasmic linkage between sister cells also led to the suppression of neuronal fates and prevention of apoptotic fates. Thus, LEM-3 prevents syncytium formation to ensure proper cellular differentiation.

Resistance mutation supply modulates the benefit of CRISPR immunity against virulent phages in Pseudomonas aeruginosa

2026-11-02T14:00:00Z

by Rosanna C. T. Wright, Simon C. Lovell, Anna Richmond, Christian Harrison, Eleri Ashworth, Aras Kadioglu, Joanne L. Fothergill, Ville-Petri Friman, Edze R. Westra, Michael A. Brockhurst

Only a fraction of bacterial genomes encode CRISPR-Cas systems, but the selective causes of this variation are unexplained. How naturally virulent bacteriophages (phages) select for CRISPR immunity has rarely been tested experimentally. Here, we show against a panel of genetically and functionally diverse virulent phages that CRISPR immunity was not universally beneficial to Pseudomonas aeruginosa, and its fitness effect varied strongly between phages in predictable ways. In addition to mechanisms known to alter the effectiveness of CRISPR immunity, such as encoding a matching spacer or a protective nuclear shell, we show that the fitness effect of CRISPR immunity negatively associated with the probability of evolving receptor-based resistance to the phage via spontaneous mutation. The supply of resistance mutations differed strongly between very closely related lipopolysaccharide-binding phages and was associated with variation at the C-terminus of the tail fibre protein altering residues involved in hydrogen bonding and the predicted binding site. Our results show that CRISPR immunity is more beneficial against virulent phages that are harder to evolve resistance to via receptor mutations, suggesting that virulent phage community composition and diversity will be important drivers of the prevalence of CRISPR immunity.

CFL1-dependency of discrete cell behaviours driving mouse spinal zippering

2026-11-02T14:00:00Z

by Abigail R. Marshall, Andrea Krstevski, Henry Crosswell, Rahul Shah, Eirini Maniou, Nicholas D. E. Greene, Andrew J. Copp, Gabriel L. Galea

Epithelial fusion is critical for formation of many embryonic tissues. The developing mammalian spinal cord fuses by zippering, through cell behaviours dependent on F-actin turnover. We propose a caudal-to-rostral sequence of surface ectoderm cell behaviours which drive zippering progression in mice, and test the requirement for the F-actin severing protein CFL1 in this process. Key zipper-advancing behaviours are: (i) constriction of supracellular actomyosin cables; (ii) extension of filopodial/lamellipodial protrusions at periodic intervals; (iii) constriction of leading-edge cell borders bringing together protrusions which establish ‘pioneering’ contacts across the midline; (iv) cell-cell and v. cell-ECM adhesion remodelling; (vi) zipper advancement through cell partner exchange. In wild-type embryos, CFL1 is enriched at the leading edge of surface ectoderm cells adjacent to the zippering point and localised within some protrusions. Conditional Cfl1 deletion in the surface ectoderm produces denser F-actin stress fibres, makes filopodial protrusions excessively stable, diminishes their exploratory movements which may establish nascent contacts, and impairs junctional constriction of cells at the point of fusion. Zippering speed is reduced ~30% in conditional Cfl1-deleted embryos and ~30% develop spina bifida. We therefore propose that impaired filopodial dynamicity and junctional constriction limits the sequence of behaviours driving spinal zippering, predisposing to spina bifida.

Fungal suppression by bacterial metabolite-activated human intestinal γδT-cells is disrupted in Crohn’s disease

2026-11-02T14:00:00Z

by Liya Mathew, Sean L. Carlson, Michael Savage, Claire Pardieu, Megan B. O’Brien, Ellie Crawley, Paul Harrow, Ann-Kristin Kaune, Edward Devlin, Emily L. Priest, Marilena Crescente, Kimberly Martinod, James Boot, SoFong Cam Ngan, Marco Gasparetto, Klaartje Kok, James O. Lindsay, Jonathan P. Richardson, Julian R. Naglik, Andrew J. Stagg, Matthias Eberl, Siu Kwan Sze, Carol A. Munro, Neil E. McCarthy

Gut symbionts condition mucosal immunity to resist infection by enteropathogens, but the specific microbes and mechanisms involved differ significantly between host species. In higher primates, bacterial metabolite HMB-PP is sensed by a specialized population of Vγ9Vδ2+T-cells, which we now report can potently suppress growth of endogenous fungi in human intestinal organ cultures. In healthy intestine, HMB-PP-stimulated Vδ2+ T-cells restricted outgrowth of keystone fungus Candida albicans via a mechanism that required IL-22. In Crohn’s disease (CD), Vδ2+ T-cells were poorly responsive to HMB-PP and permitted outgrowth of C. albicans strains that formed toxin-producing filaments, triggered neutrophil extracellular traps, and induced macrophage IL-1β release ex vivo. Genomic and proteomic analysis of the Candida isolates suggested increased tissue adhesion of CD-derived strains, which rapidly invaded the gut barrier in an ‘intestine-on-a-chip’ model. These data reveal that bacterial activation of Vδ2+ T-cells suppresses fungal pathobionts in human gut via an IL-22-dependent mechanism that is dysregulated in CD.

Emotion knowledge is structured in a grid-like coordinate system in the human ventromedial prefrontal cortex

2026-11-02T14:00:00Z

by Yumeng Ma, Philip A. Kragel

Human emotional experiences vary widely in everyday life, yet they are systematically organized within a continuous affective space defined by valence and arousal. Although this circumplex organization has shaped decades of research, its neural implementation remains unclear. Here, we asked whether abstract emotion concepts are encoded using grid-like coordinate principles in the human brain. During fMRI, participants tracked trajectories through affective space conveyed through morphs of facial expressions and sequences of phrases. We found that ventromedial prefrontal cortex (vmPFC) encoded affective space with robust hexadirectional modulation characteristic of grid-like coding. This coordinate representation generalized across stimulus modalities, indicating abstraction beyond perceptual features. The grid-like signal reflected a metric organization of emotion concepts independent of overt behavior, whereas distance-related signals in vmPFC predicted trial-by-trial affective judgements. Together, these findings suggest that emotion knowledge is structured by a grid-like coordinate system in the human brain that can support predictive inference and flexible decision-making.

How early microbial encounters shape adult behavior

2026-10-30T14:00:00Z

by Kyu-Chan Cho, Won-Jae Lee

Microbes are increasingly recognized as modulators of host behavior, but the underlying mechanisms are poorly understood. A new PLOS Biology study reveals a microbiome-to-gut-to-neuron pathway linking developmental microbial exposure to later food avoidance. Microbes are increasingly recognized as modulators of host behavior, but the underlying mechanisms are poorly understood. This Primer discusses a new PLOS Biology study that reveals a microbiome-to-gut-to-neuron pathway linking developmental microbial exposure to later food avoidance.

Rethinking neurodegeneration: Placing disease in its physiological context

2026-10-30T14:00:00Z

by Joanna Clarke, Sarah Jäkel

Research into neurodegeneration is often confined to a single disease, cell type or mechanism. A new collection of articles explores neurodegeneration within its physiological context, looking beyond diseased neurons to the surrounding tissue microenvironment. Research into neurodegeneration is often confined to a single disease, cell type or mechanism. This Editorial highlights a new collection of articles that explore neurodegeneration within its physiological context, looking beyond diseased neurons to the surrounding tissue microenvironment.

Transient feedforward communication between somatosensory and premotor cortex supports goal-directed behavior

2026-10-29T14:00:00Z

by Yadollah Ranjbar-Slamloo, Tsukasa Kamigaki

Goal-directed behavior requires sensory information to be transformed into motor commands, yet the precise temporal structure of communication between sensory and motor cortices during this process remains poorly understood. By simultaneously recording spiking activity from primary somatosensory cortex (S1) and secondary motor cortex (M2) in mice performing a tactile delayed go/no-go task, we identified a brief, stimulus-triggered communication window that predicted behavioral success. Time-shifted canonical correlation analysis revealed a sharp, feedforward surge in S1 → M2 coupling peaking at a short latency, as expected for a potentially direct transmission pathway. This transient interaction conveyed stimulus-selective information such that the S1 → M2 communication subspace aligned with stimulus-coding axes in both regions. In contrast, M2 → S1 feedback interactions were weaker and delayed. Brief optogenetic suppression of S1 reduced both M2 stimulus selectivity and behavioral discriminability, consistent with a functional role of the transient S1 → M2 coupling. These findings demonstrate that sensorimotor transformation is supported not by sustained linear coupling along the stimulus- or choice- axis, but by a short-lived and highly selective feedforward communication channel that rapidly transmits reliable sensory representations into motor-planning circuits.

Full-length genomes evolve in parallel in a long-term evolution experiment with phage φX174

2026-10-29T14:00:00Z

by Eva Bons, Hélène Chabas, Hannelore MacDonald, Alejandro Escalera Ledermann, Sira Ösze, Jenny Dunstan, Nicolas Ochsner, Daniel C. Angst, Sebastian Bonhoeffer, Roland R. Regoes

The study of evolution in organisms with high mutation rates requires detailed data on the genomic composition of the population. Here we report on an innovative use of high-throughput sequencing technology combined with rapid experimental evolution that allowed us to follow the genetic diversification of four independent bacteriophage populations for 412 generations in extraordinary detail. One of our goals was to assess phylodynamic methods that use genetic information to infer key parameters of the population history. Because phylodynamic methods assume neutral evolution, we did not actively impose any selection pressures in our evolution experiment (in addition to those inherent in the bacterial cell environment). Tracing over 80′000 bacteriophage genomes, representing 884 distinct genotypes, we find that the patterns of viral diversification result in largely non-congruent genotype distributions, but also document multiple instances of parallel evolution. Unlike previous observations of parallelism in viral evolution, we do not just see the parallel evolution of mutations at single sites, but on the level of full-length genomes. Computer simulations that recapitulate our experiments in great detail show that this degree of parallelism is inconsistent with neutral evolution. We further show that the observed extent of parallel evolution biases phylodynamic analysis of migration rates, and wrongly estimates significant migration between the independent evolution lines. Our approach is applicable to many other viruses and paves the way to advanced population genetic investigations that aim to shed light on phenomena that relate to genetic linkage across the genome.

Viral disease outcomes are indistinguishable between experimentally infected bats and rodents

2026-10-29T14:00:00Z

by Maxwell J. Farrell, Samantha K. Tucker, Nardus Mollentze, Daniel G. Streicker

A common explanation for bats being a conspicuous source of zoonotic viruses is their purported ability to coexist with viruses without suffering overt disease. Widespread acceptance of the idea that bats have unusual antiviral traits has catalyzed the discovery of unique features of bat immune systems which may have translational value as broad-spectrum antivirals, particularly if they evolved as a byproduct of bats’ unique life history rather than through conventional co-evolutionary processes. Surprisingly, whether bats compared to other host groups suffer less disease from co-evolved viruses or from viruses generally has not been formally assessed. Here, synthesizing 86 years of experimental infections, involving 54 viruses, 85 host species, and over 5,600 animals, we document disease in bats following inoculation by taxonomically diverse viruses, including ones that are relatively benign in humans. The occurrence of overt disease, the likelihood of mortality, and the severity of disease in bats were indistinguishable from those experienced by rodents, another group associated with many zoonotic viruses. These patterns were consistent when considering only bat-associated viruses inoculated into bats and rodent-associated viruses inoculated into rodents and among inoculations which lacked shared co-evolutionary history. Instead, disease outcomes following infection were shaped by experimental design, viral host range, and evolutionary context. Unexceptional disease in bats from novel or co-evolved infections suggests that order-level host life history traits such as flight have inconsistent consequences for antiviral immunity and highlights the need to evaluate the functional properties of putatively unique features of bat immunity in vivo. While these results do not exclude the possibility of developing broader-acting or more potent antivirals from bat immune systems or diminish the potential value of mechanistic insights into bat immunity, they suggest that bat immune systems were shaped by conventional co-evolutionary processes rather than through unique circumstances that endow exceptional antiviral defenses.

Alzheimer’s disease research must connect vascular molecular phenotypes with physiology

2026-10-28T14:00:00Z

by Thomas S. Lewis, Jessica Wagner, Jonas J. Neher

Molecular profiling studies have mapped vascular alterations in Alzheimer’s disease, but have not proven a role for them in pathology. Longitudinal studies are needed to link molecular and structural changes to vascular mechanics, hemodynamics, and tissue perfusion. Molecular profiling studies have mapped vascular alterations in Alzheimer’s disease, but have not proven a role for them in pathology. This Perspective argues for longitudinal studies to link molecular and structural changes to vascular mechanics, hemodynamics and tissue perfusion.

Correction: Free long-chain fatty acids trigger early postembryonic development in starved Caenorhabditis elegans by suppressing mTORC1

2026-10-27T14:00:00Z

by Meiyu Ruan, Fan Xu, Na Li, Jing Yu, Fukang Teng, Jiawei Tang, Cheng Huang, Huanhu Zhu

Conserved spike epitopes persist in generalist bat sarbecoviruses

2026-10-27T14:00:00Z

by Matthew B. Frieman

Bat sarbecoviruses differ in the range of mammalian ACE2 receptors they can use, complicating predictions of spillover risk. Two new studies in PLOS Biology link receptor breadth with antigenic relatedness and reveal conserved spike epitopes targetable by antibodies. Bat sarbecoviruses differ in the range of mammalian ACE2 receptors they can use, complicating predictions of spillover risk. This Primer comments on two new studies in PLOS Biology that link receptor breadth with antigenic relatedness and reveal conserved spike epitopes targetable by antibodies.

fruitless is essential for male Aedes aegypti mosquito attraction to female flight sounds

2026-10-27T14:00:00Z

by YuMin M. Loh, Alberto J. Thornton, WenWei Loh, Tai-Ting Lee, Wan-Tze Chen, Yifeng Y. J. Xu, Jia Xin Yap, Yuichiro Tsuchiya, Daniel F. Eberl, Matthew P. Su, Azusa Kamikouchi

Male mosquitoes locate females through strong and innate attraction to female flight sounds, the basis of mating in the world’s deadliest animal. In contrast, females do not show any sound attraction behaviors. Despite being documented for almost a century, the molecular underpinnings of these behavioral dimorphisms remain unknown. Here, we found that by disrupting the male-specific isoform of fruitless (referred to as fruM) in Aedes aegypti, fruM mutant males show complete abolition of sound attraction behaviors, resulting in failure of mutant males to locate females for mating. We identified strong fruitless expression in control male ears, with the loss of FruM severely disrupting mutant male ability to amplify female flight sounds. fruM mutant male ears also propagate frequency-specific, sound-evoked electrical signals at about one-sixth the magnitude of control males, significantly reducing the amount of auditory information relayed to the brain. fruitless thus plays a significant role in determining proper male peripheral hearing function underlying mating. Transcriptomic analyses of mosquito ears identified essential hearing genes under the transcriptional influence of FruM via direct or indirect actions, thus shaping male-specific hearing cellular machineries that support male attraction to female flight sounds. Our work demonstrates that FruM commands male-specific hearing behaviors involved in mating by directly controlling the earliest stages of auditory organ performance, sound amplification and acoustic signal detection. Our findings show that FruM is essential for male-specific reproductive behaviors in mosquitoes.

Structural basis for inhibition of the lipid flippase MurJ by phage lysis protein Sgl^PP7 suggests convergent evolution with other Sgl peptides

2026-10-27T14:00:00Z

by Kaito Hosoda, Hidetaka Kohga, Sixian Wu, Hiroyuki Tanaka, Hideki Shigematsu, Ryoji Miyazaki, Min Fey Chek, Tomoya Tsukazaki

Some bacteriophages encode lysis proteins that inhibit essential bacterial processes, and elucidating their mechanisms is valuable for developing antibacterial strategies against drug-resistant pathogens. We determined the cryo-EM structure of the complex between the essential Escherichia coli lipid II flippase MurJ and the phage lysis protein Sgl^PP7. Structural, mutational, and molecular dynamics (MD) simulation analyses revealed that Sgl^PP7 binds along the intramembrane cleft of MurJ and inserts its C-terminal tail into the internal cavity, stabilizing MurJ in an outward-facing conformation. Structural comparison with Lys^M (Sgl^M) and Sgl^CJ3 showed that these sequence-divergent Sgl proteins stabilize MurJ in the outward-facing conformation through distinct binding modes, consistent with the possibility of convergent evolution toward MurJ inhibition.

Pollinator abundance shapes sexual selection in an angiosperm

2026-10-27T14:00:00Z

by Estelle Barbot, Mathilde Dufaÿ, Tim Janicke, Benoit Lapeyre, Denis Orcel, François Rousset, Jeanne Tonnabel

Sexual selection is a central force in evolutionary biology that has been shown to shape phenotypes and population dynamics in animals. While this selective force is increasingly recognized in flowering plants, theory predicts that anisogamy generates sex differences in the fitness benefits of acquiring additional mates—a pattern well supported in animals but with limited tests in plants. Plant studies rely solely on genetic parentage analyses to estimate mate numbers, thereby conflating performance in accessing mates with success in gamete fertilization. Pollinators add an ecological layer, as their behavior and abundance can influence competition for access to mates and their gametes. Here, we disentangle consecutive episodes of sexual selection in the hermaphroditic plant Brassica rapa by combining direct observations of Bombus terrestris movements with genetic paternity analyses in experimental populations, thus providing independent estimates of the observational number of mates acquired and realized fertilization success. Our approach identifies pollen competition for ovules as the primary arena for sexual selection in B. rapa. Competition for access to mates constitutes a secondary force and was found to be stronger in the male compared to the female sex function, as predicted by classic theory. Experimentally reduced pollinator abundance modulated the balance between pre- and post-pollination sexual selection, increasing the opportunity for selection on mate acquisition. Ignoring pollinator movements led to biased estimates of pre-pollination sexual selection. Our findings demonstrate that sexual selection in plants unfolds across multiple, sequential episodes shaped by ecological context.

Tolerance measured at one developmental stage mispredicts climate resilience in an animal with a complex life cycle

2026-10-26T14:00:00Z

by Hao Song, Tingyu Shi, Meijie Yang, Xiaoyan Liu, Zhuoqing Li, Pu Shi, Yu Wu, Bassem Allam, Andrew Jeffs, Bradley Skelton, Tao Zhang

Forecasts of whether marine species can evolve fast enough to survive climate change rely largely on single-stage tolerance assays, tacitly assuming that tolerance measured at one developmental stage reflects adaptive capacity across the organism’s life cycle. We test this assumption in a common marine bivalve (Mercenaria mercenaria) and find that it fails in sign, not degree: larval and post-metamorphic tolerance to end-century ocean acidification are strongly negatively correlated (r = −0.53, 95% CI [−0.69, −0.33]) across family-level, pedigree-conditioned and animal model estimates, with pervasive rank reversals among the top performers of each stage. A multivariate analysis of the among-family covariance matrix G shows why: under acidification, 57% of the among-family variance collapses onto a single dominant axis that loads positively on every larval trait and negatively on every post-metamorphic trait, whereas under ambient conditions the same families show no cross-stage covariance at all. Acidification therefore does not merely depress performance—it reorganizes the genetic architecture into a cross-stage conflict. Under ramping RCP 8.5 forcing this conflict geometry dictates the direction—not merely the magnitude—of adaptation: only balanced multi-stage selection preserves family diversity, whereas single-stage selection systematically erodes the opposite axis. In complex life cycles, resilience is a geometric property of ontogeny that forecasts cannot compress into a single-stage without inverting the sign of the answer.

Therapeutic delivery systems need to focus on cellular precision to target neurodegeneration

2026-10-26T14:00:00Z

by Lavanya Gupta, Sinem Agilkaya, Kim Susann Keller, Ebru Ercan-Herbst

The central problem when delivering drugs to the brain is no longer crossing the blood–brain barrier, but delivering therapeutics to the right cells, in the right regions to target neurodegeneration, within a dynamically changing neurovascular unit. Crossing the blood–brain barrier is no longer a problem for delivering therapeutics to the brain. This Perspective argues that the main challenge is now how to deliver therapeutics to the right cells, in the right regions to target neurodegeneration, within a dynamically changing neurovascular unit.

High-resolution paleobiome reconstructions highlight ecological and historical dynamics underpinning global terrestrial vertebrate diversity

2026-10-23T14:00:00Z

by Alexander Skeels, Julian Rogger, Marcel Cardillo, Alexander Farnsworth, Daniel J. Lunt, Dirk Nikolaus Karger

Past climate change has repeatedly reshaped Earth’s biomes, yet how their expansion and contraction influence biodiversity patterns through time remains unclear. Competing hypotheses propose that either historical biome area has a strong influence on diversity, or that biodiversity responds rapidly to environmental change, such that present-day biome area and energy are sufficient to explain diversity patterns. Progress in testing these ideas has been limited by sparse and inconsistent proxy data and the coarse resolution of existing paleoclimate models. Here, we reconstructed global biome histories for the Cenozoic (66–0 Ma) by downscaling five different paleoclimate simulations. Estimates of change in biome area through time were generally consistent among alternative climate models and with the empirical proxy record. Accounting for variation among models, we found that present-day area and energy were consistently better predictors of vertebrate diversity than historical measures. These findings suggest biodiversity tracks the ecological limits set by shifting biomes, leaving sparse legacy of past dynamics. Our results highlight the importance of integrating multiple paleoclimate reconstructions when assessing the historical drivers of biodiversity.

Dynamism under the hood: Coevolutionary maintenance of variation in hosts and parasites

2026-10-23T14:00:00Z

by Andrea L. Graham, David A. Chang van Oordt

Why do hosts and parasites vary so much? A new study in PLOS Biology reveals that infection outcomes strongly depend upon interacting effects of host and parasite genotypes, offering an evolutionary explanation for profound and persistent variability. Why do hosts and parasites vary so much? This Primer explores a new study in PLOS Biology revealing that infection outcomes strongly depend upon interacting effects of host and parasite genotypes, offering an evolutionary explanation for profound and persistent variability.

Host–virus interactions dominate fitness and conceal additive genetic variation

2026-10-22T14:00:00Z

by Aleksei Belyi, Yiyang Du, Alastair J. Wilson, Ben Longdon, Francis M. Jiggins

Host–parasite coevolution is expected to generate strong selection for resistance and infectivity that has the potential to erode genetic variation. Despite this, natural populations often retain extensive genetic variation in these traits. Genotype-by-genotype interactions on fitness can generate negative frequency-dependent selection, which helps maintain this variation by preventing any host or pathogen genotype from retaining a permanent advantage. Because these interactions place genetic variance in the interaction term rather than in additive differences among hosts or pathogens, that variance is masked from directional selection and can remain ‘cryptic’. Here we combine coevolutionary modelling with large‑scale experimental infection assays to quantify how host-pathogen interactions structure fitness variance in a vertically transmitted virus system, Drosophila melanogaster and sigma virus. Simulations show that coevolution typically erodes additive genetic variance in host and pathogen fitness, concentrating variance in host-virus interaction terms. Consistent with these predictions, experiments spanning 90 host-virus genotype combinations reveal that transmission, viral load, and virulence are overwhelmingly governed by host-virus genetic interactions rather than host or virus main effects. As a result, neither host resistance alleles nor viral genotypes confer consistently higher fitness across genetic backgrounds. Interactions tend to be sex‑specific, further limiting heritable fitness variation. Our results demonstrate that coevolution can substantially mask heritable genetic variation from directional selection by rendering fitness context-dependent. This extensive cryptic genetic variation may be revealed either when ecological or evolutionary conditions shift, or when the process of coevolution itself alters the direction of selection. This demonstrates the need to account for genotype-specific interactions when forecasting evolutionary responses.

A cortical semantic map integrates fractions and integers in the human brain

2026-10-22T14:00:00Z

by Daniela Valério, Samuel Debray, Alireza Karami, Maxime Cauté, Nicolás Gravel, Stanislas Dehaene

How does the human brain represent the meaning of abstract symbols? Some theories postulate the existence of semantic spaces where concepts occupy positions that reflect their conceptual relationships. In the number domain, psychological evidence suggests that integers are represented along a mental number line which, with education, integrates higher-level number concepts such as fractions. To test this hypothesis, we recorded whole-brain 7T fMRI responses to integer and fraction symbols during an active magnitude comparison task designed to engage magnitude processing. Consistent with predictions, we found both behavioral and neural numerical distance effects. Activation vectors in intraparietal, inferior temporal, prefrontal, hippocampal, and parahippocampal cortices formed a two-dimensional semantic space organized by numerical magnitude and domain (fractions versus integers). Gaussian fits revealed a topographic map of numerical preferences in the anterior inferior parietal cortex, common to both domains. Our results suggest that, when educated adults engage in an explicit magnitude comparison task, their brain can construct an ordered representation that integrates fractions and integers, with a topographic organization in the anterior IPS/IPL.

Non-adaptive evolutionary forces predominantly shape nucleotide composition near human transcription start sites

2026-10-21T14:00:00Z

by Yi Qiu, Emilie Hebraud, Fanny Pouyet, Alexander F. Palazzo

In the human genome, mutation rates vary along genes, yet how their fine-scale structure contributes to gene evolution has remained largely unexplored. Here, we map inherited mutations at single-nucleotide resolution and uncover a striking hypermutation peak at transcription start sites (TSSs) of human protein-coding genes. This pattern is observed both in population polymorphisms and in de novo mutations from parent-offspring trios, and is dependent on transcriptional activity in testes. We also find similar hypermutation peaks at TSSs used to produce long noncoding RNAs and at intergenic RNA Polymerase II pause sites. In addition, we identify distinct mutational signatures at exon-intron boundaries and in introns. By comparing the current nucleotide content to predicted equilibrium levels, inferred from mutation and fixation rates, and by analyzing derived ancestral frequency spectrums, we detect signals that are compatible with a low level of ongoing background GC-biased gene conversion (gBGC) throughout the region and ancestral elevated gBGC activity that is centered right downstream from the TSS. Using a forward-in-time simulation algorithm, we show that the current nucleotide composition surrounding the TSS of protein-coding genes is best explained by local mutation biases coupled to ongoing and ancestral patterns of gene conversions. Our simulations allow us to infer several features of these gBGC events. Overall, these findings indicate that the nucleotide composition around TSSs is largely shaped by non-adaptive forces, particularly mutation bias and gBGC.

A macrophage-targeted TIMD4 Peptide-Nanoparticle attenuates colitis symptoms and monocyte recruitment in a mouse model

2026-10-21T14:00:00Z

by Huimin Liu, Yuzhen Wang, Ruiqing Yu, Kexin Liu, Dezhi Zheng, Bo Wang, Yuan Chang, Bing Liu, Xuetian Yue, Zhuanchang Wu, Chunyang Li, Xiaohong Liang, Chunhong Ma, Guohua Liu, Jianhua Li, Leiqi Xu, Lifen Gao

Macrophages play a pivotal role in the pathogenesis of inflammatory bowel disease (IBD). T-cell immunoglobulin and mucin domain-containing molecule 4 (TIMD4) is involved in the regulation of tissue-resident macrophages. TIMD4 expression is elevated in colonic tissues from patients with ulcerative colitis (UC) and mice with dextran sulfate sodium (DSS)-induced colitis, but its role in IBD pathogenesis remains unclear. In this study, we found that Timd4 deficiency aggravated DSS-induced colitis, accompanied by increased infiltration of monocytes into the colonic tissues. Treatment with a CCR2 antagonist attenuated colonic inflammation and reduced monocyte infiltration into colonic tissues in Timd4 KO mice. Mechanistically, in vitro studies revealed that TIMD4 stabilized the LKB1-STRAD-MO25 complex via its intracellular domain, thereby activating the AMPK pathway and suppressing NF-κB-dependent chemokine production in macrophages. Based on these findings, we designed a TIMD4-derived peptide and developed a macrophage-targeted nanoparticle system (T4_(365–378)‑NPs). Treatment with T4_(365–378)-NPs reduced P65 phosphorylation and attenuated DSS-induced colitis in mice. Treatment with either T4_(365–378)-NPs or the CCR2 antagonist attenuated DSS-induced colitis, and no statistically significant differences in the assessed outcomes were detected between the two groups. Administration of T4_(365–378)-NPs before DSS exposure also attenuated subsequent colitis. Furthermore, combining the T4_(365–378)‑NPs with anti-α4β7 or anti-TNF-α antibodies produced greater improvements than either monotherapy in the DSS-induced colitis model. These findings support further preclinical evaluation of TIMD4-derived peptide delivery as a potential therapeutic approach for intestinal inflammation.

Oxidative signaling thresholds shape vulnerability in the central and peripheral nervous systems

2026-10-19T14:00:00Z

by Shuji Wakatsuki, Toshiyuki Araki

Neurodegeneration is frequently associated with oxidative stress, yet the mechanisms that convert reactive oxygen species (ROS) into irreversible degenerative signals remain incompletely understood. Neurons in the central and peripheral nervous systems often differ in their responses to injury, but these differences cannot be reduced to a simple contrast between weak and strong antioxidant capacity. This Essay proposes that neuronal vulnerability is shaped by multilayered signaling thresholds comprising ROS production, antioxidant and thiol buffering, redox-sensitive signal detection, molecular gating, and commitment to degeneration, survival, or repair. This framework may help explain selective neuronal vulnerability in neurodegenerative diseases and identify intervention points downstream of global ROS suppression.

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