SEARCH · Search bioRxiv

Results for “systems biology”

Search indexed bioRxiv preprints in genomics, neuroscience, cell biology and bioinformatics. Read source abstracts and check manuscript versions; preprints are not peer reviewed.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

242 records · Page 3Linked to original sources

bioRxiv2026

Living electronic transistors with tunable conductivity

Electroactive bacteria, like Shewanella oneidensis, can couple the oxidation of organic electron donors to the reduction of external conductive surfaces, such as minerals and electrodes, by utilizing multiheme cytochromes to carry charge from within the cell to external surfaces. Additionally, multiheme cytochromes facilitate gateable, long-distance (micrometer-scale) redox conduction along the outer membrane and across multiple cells bridging electrodes. While electroactive microbes are being used to develop bioelectrochemical devices, there have been limited efforts to use synthetic biology to exert additional control over microbes serving as device components. Thus, this work implements an optogenetic biofilm patterning gene circuit and a small molecule sensor in S. oneidensis to simultaneously control cell deposition and cytochrome expression. This allows for photolithographic patterning of biofilms possessing tunable electrical properties controlled with small molecules. This system demonstrates tunable electrochemical activity, redox conduction, intrinsic biofilm conductivity, and negative differential transconductance as a function of cytochrome expression. Additionally, temperature-dependent measurements of this tunable biofilm conduction reveal changes in activation energy as a function of cytochrome expression. Through this combination of synthetic biology and electrochemistry, simultaneous control over biofilm geometry and conductivity sheds light on fundamental microbial electron transport processes, and it enables the construction of living electronic devices.

synthetic biology↗

bioRxiv2026

Scalable proxiloids enable human-relevant assessment of kidney proximal tubule toxicity

Drug-induced injury to the human proximal tubule (PT) is a leading cause of acute kidney injury and drug attrition, yet remains difficult to predict preclinically. PT toxicity arises from the coupling of transporter-mediated xenobiotic accumulation and high oxidative metabolic demand. Current models lack key aspects of PT physiology or are difficult to scale for toxicity testing. New Approach Methodologies (NAMs) address this challenge through human-relevant in vitro systems. Here we introduce proxiloids, a scalable suspension-based human induced pluripotent stem cell differentiation strategy. Within 14 days, proxiloids form lumenized, polarized tubular organoids enriched for PT identity, with functional transport and oxidative metabolic competence. Proxiloids are compatible with genetically encoded reporters and standard multiwell assays, enabling detection of defined stress responses. They recapitulate aminoglycoside nephrotoxicity with greater sensitivity than matched two-dimensional cultures and detect adefovir-induced mitochondrial toxicity not predicted in rodents. Together, proxiloids provide a scalable, human-relevant NAM for PT nephrotoxicity assessment.

cell biology↗

bioRxiv2026

Modelling human haematopoietic stem cell commitment ex vivo identifies IL-33 as a regulator of megakaryopoiesis

Commitment events to specific blood lineages arise from single hematopoietic stem cells (HSCs) and are influenced by stress, inflammation and disease. However, the understanding of how such events are regulated in human haematopoiesis is limited by the lack of tractable in vitro models. In this study, we introduce a novel Early Progenitor Differentiation (EPD) assay to study the initial lineage commitment of human 49+ HSCs, in a system faithfully recapitulating cell states observed in vivo. Combining single cell -omics approaches and single cell functional assays, we show that IL-33 acts directly on human 49f+ HSCs activating the MAPK pathway to enhance their commitment towards Megakaryocytic-Erythroid-Mast cell Progenitors and subsequently megakaryopoiesis. This occurs without affecting HSC self-renewal via accelerated establishment of chromatin programmes associated with Erythroid and Megakaryocyte and mast cells lineages. Our findings demonstrate the utility of the EPD model to identify molecular regulators of human HSC differentiation and uncover a new role of IL-33 in haematopoiesis.

cell biology↗

bioRxiv2026

FibrilNet maps conserved and tissue-specific molecular environments across systemic amyloidoses

Systemic amyloidoses are initiated by distinct amyloidogenic precursor proteins but frequently contain recurrent extracellular, complement, lipid-transport and matrix-remodelling components. Whether these recurrent proteins form a conserved systems-level environment across amyloid diseases, and how strongly that environment depends on precursor and tissue context, remains unresolved. We developed FibrilNet, a network framework that integrates experimentally defined amyloid proteomes with a human protein protein interaction graph and Gene Ontology derived semantic information. FibrilNet compares topology-only random walk with restart (RWR) with ontology aware semantic RWR in frozen leave-one-out module reconstruction and precursor-seeded prioritization tasks. The human graph contains 17,997 proteins and 925,977 physical interactions, with a 9-dimensional semantic representation of interaction context. In expanded cardiac transthyretin amyloidosis (ATTR), semantic-RWR increased mean reciprocal rank (MRR) from 0.00167 to 0.05015 and Recall@100 from 0.0199 to 0.3377, improving 132 of 151 held-out targets. Significant semantic gains were also observed in renal serum amyloid A amyloidosis (AA) and leukocyte chemotactic factor 2 amyloidosis (ALECT2). Across compact ATTR, light-chain amyloidosis (AL), AA and ALECT2 modules, APCS, VTN and TIMP3 formed a direct four-disease recurrent core, while APOE occurred in three of four modules. A tissue-aware ATTR analysis showed limited overlap between cardiac and neurologic modules (19 shared proteins; Jaccard 0.0569). In the hTTR-A97S peripheral-nerve model, semantic-RWR significantly improved reconstruction of the 202-protein mapped neurologic module, with the strongest evidence concentrated in the downregulated proteomic program. TTR-seeded propagation improved with semantic information but remained weak in absolute terms, separating precursor identity from the distributed downstream molecular environment. These results support a multilayer model in which a restricted conserved amyloid environment coexists with precursor-, tissue- and disease-specific organization

bioinformatics↗

bioRxiv2026

Morphologic intratumoral heterogeneity from routine whole-slide histopathology is prognostic for survival in primary central nervous system lymphoma: development in the LOC Network and international external validation

Background: Clinical scores incompletely capture outcomes in primary central nervous system lymphoma (PCNSL). We quantified morphologic heterogeneity in pretreatment hematoxylin and eosin (H\&E) whole slides. Patients and methods: Three independent cohorts of immunocompetent, HIV- and EBV-negative patients treated recently were analyzed: LOC 2023 (122 slides), phase III BLOCAGE-01 (245 slides; NCT02313389), and external Barcelona (BCN; 41 slides). UNI embeddings, prototype learning, spatial metrics, and elastic-net Cox regression defined ITH-C. Results: Models achieved bootstrap-corrected concordance of 0.797--0.834. Age-, sex-, and KPS-adjusted ITH-C HRs were 1.29 (95\% CI 1.01--1.64), 1.27 (1.07--1.51), and 2.13 (1.35--3.37), respectively. Adding ITH-C increased MSKCC C-index from 0.671 to 0.717, 0.560 to 0.593, and 0.588 to 0.706. Spatial transcriptomics linked ITH-C to immune programs. Conclusions: Routine H\&E encodes prognostic spatial heterogeneity in PCNSL. ITH-C complements clinical scores, supporting prospective risk stratification.

bioinformatics↗

bioRxiv2026

Salicylic acid-triggered apoplastic proteolysis releases cryptic phytocytokines with distinct immunogenic functions

Plants rely on an innate immune system to defend against pathogens through various molecular responses. In addition to classical damage- and pathogen-associated molecular patterns (DAMPs and PAMPs), plants produce endogenous signaling peptides termed phytocytokines that amplify and regulate immune responses following stress. Although most characterized phytocytokines originate from dedicated precursor proteins, the contribution of multifunctional proteins to phytocytokine generation remains poorly understood. Here, we show that salicylic acid (SA) rapidly remodels the maize apoplastic peptidome through an early, transient proteolytic program driven by apoplastic serine hydrolases. Time course peptidomics identified fourteen candidate phytocytokines, including two cryptic peptides, PC13 and PC14, released from the stress-associated zinc-finger protein ZmSAP7 and the migration inhibitory factor-like protein ZmMDL1, respectively. Both peptides activated immune-associated gene expression but triggered distinct transcriptional responses and exerted opposing effects on Ustilago maydis infection, with PC13 enhancing resistance and PC14 promoting susceptibility. Biochemical analysis demonstrated that PMSF-sensitive apoplastic serine proteases directly process ZmMDL1 to release PC14. Together, our findings uncover a SA-responsive proteolytic pathway that generates functionally distinct phytocytokines from multifunctional proteins, expanding the repertoire of immune signaling peptides and revealing an additional layer of regulation in plant defense.

plant biology↗

bioRxiv2026

Clonal memory in human embryonic stem cells biases fate potential during endoderm differentiation

Cell fate decisions during development are shaped not only by extrinsic signals but also by heritable intrinsic states passed on across cell division. The extent to which this phenomenon, termed clonal memory, can explain the persistent heterogeneity observed from directed differentiation of human embryonic stem cells is unclear. Here, we combine lineage tracing with single-cell transcriptomics and chromatin accessibility profiling to track clonal behaviour across human embryonic stem cell differentiation towards definitive endoderm. Using a lentiviral barcoding system coupled with a split-well sampling strategy, we find that clonally related cells exhibit reproducible, probabilistic fate outcomes that cannot be explained by signalling environment alone. Fate-biased clones are transcriptionally indistinguishable at the pluripotent stage yet display distinct chromatin accessibility landscapes at lineage-specific cis-regulatory elements. Pre-existing accessibility at these lineage-specific regulatory regions distinguish clones that undergo successful endoderm differentiation from those that generate off-target mesoderm derivatives. Together, these findings provide an explanation for how off-target populations arise during directed differentiation, identifying heritable chromatin states within pluripotent cultures as a source of variability relevant to stem cell-derived in vitro models and cell therapies.

developmental biology↗

bioRxiv2026

Neogenin-1 marks myeloid-primed fetal hematopoietic stem cells that undergo progressive lineage-restriction with age

During aging, hematopoietic stem cells (HSCs) increasingly shift from balanced to myeloid-biased differentiation, resulting in reduced lymphoid output and impaired adaptive immunity. The question of whether this lineage bias is established in a subset of HSCs during early development or primarily emerges with aging warrants further investigation. Here, we investigate whether myeloid-biased HSCs (my-HSCs) are established at the fetal liver stage by specifically examining Neogenin-1 (NEO1), a previously defined marker of my-HSCs. We identify two distinct populations of Hoxb5+ HSCs in the fetal liver: NEO1+ and NEO1-, with NEO1+ HSCs exhibiting transcriptional and functional characteristics consistent with my-HSCs. With age, my-HSC-associated transcriptional programs become increasingly reinforced across the Hoxb5+ pHSC compartment, with NEO1+ cells showing early enrichment of this program and both NEO1+ and NEO1- cells acquiring broader myeloid-biased features in aging. These findings suggest that lineage programming can begin early in development and is further shaped by age-related changes, potentially contributing to the functional decline observed in the aging hematopoietic system.

developmental biology↗

bioRxiv2026

Beyond benchmark accuracy: machine-learning turnover-number predictors require system-level validation

Enzyme turnover numbers (kcat) are essential for kinetic models and enzyme-constrained genome-scale metabolic models (ecGEMs), but measured values are sparse and therefore increasingly estimated using machine learning (ML). Although these predictors are commonly evaluated by global regression metrics, their practical utility depends on how errors propagate through downstream models. We benchmarked six current kcat predictors on a curated BRENDA-derived dataset and five of them on EnzyExtract. To assess the influence of training-set proximity, we compared each benchmark dataset with the available training data for each predictor. We then used the predicted kcat values to parameterize ecGEMs of Saccharomyces cerevisiae and evaluated growth predictions across 19 conditions. We find that benchmark accuracy is moderate even on the BRENDA-derived dataset and drops sharply on EnzyExtract, where all predictors achieve R2 values of 0.20 or lower. This decline is accompanied by substantially lower overlap between the benchmark and training datasets, with exact sequence matches ranging from 24% to 78% for BRENDA, compared with 9% to 26% for EnzyExtract. However, that overlap alone does not explain differences in generalization across predictors. Moreover, downstream performance is also not explained by benchmark ranking. Across 19 conditions, none of the tool-specific ecGEMs consistently reproduces the experimentally observed variation in growth. In glucose minimal medium, the weakest benchmark performer yields the most accurate growth prediction in the downstream ecGEMs, whereas higher-ranked predictors produce larger deviations in growth. We trace this mismatch to localized errors at high-leverage positions in yeast's metabolic network, where underpredicted mitochondrial ADP/ATP carrier turnover numbers restrict adenine nucleotide exchange and impose an apparent limitation on cytosolic ATP supply. Relaxing this constraint shifts predicted growth toward the experimental reference. Thus, ML-derived kcat values can affect not only quantitative growth predictions but also the phenotype a mechanistic model appears to identify. These results argue for application-driven validation of biological parameter predictors in the downstream systems they are intended to support.

bioinformatics↗

bioRxiv2026

A Microneurosurgical Survival Platform for Elucidating Mechanisms of Brain Tumor Recurrence and Metastasis

Brain tumor recurrence remains the leading cause of mortality in neuro-oncology, and there is a lack of preclinical models replicating the clinical cycle of surgical resection and relapse. To bridge this gap, we developed a novel microneurosurgical survival platform in mice using the NICO Myriad system. We orthotopically implanted pediatric medulloblastoma cells into the mouse cerebral cortex or cerebellum, followed by longitudinal microneurosurgical resection. Bioluminescence imaging and gross fluorescence verified successful resection, local and distal recurrence and metastasis. Comparative bulk RNA sequencing revealed extensive stage-specific transcriptomic divergence alongside conserved core gene sets (2,702 genes in the cerebral cortex and 3,240 genes in the cerebellum) across primary, locally recurrent, and distally recurrent stages. Pathway analysis shows activation of cellular growth, second messenger signaling, and cellular stress adaptation pathways. Targeted qPCR validation demonstrated that post-surgical relapse is driven by a distinct molecular program: recurrent tumors downregulate primary developmental drivers (PTCH1, MYCBP2), canonical suppressors (FOS, PTEN), and chromatin regulators (HDAC2), while selectively upregulating post-transcriptional machinery (RBM8A), endosomal trafficking regulators (RAB5C), acetyltransferases (NAA15), and the m6A RNA demethylase ALKBH5. These findings reveal that medulloblastoma shifts from a primary oncogenic state toward post-transcriptional and transcriptomic survival mechanisms following surgery. Identifying persistent candidates within this conserved core framework provides a roadmap for next-generation precision immunotherapies.

cancer biology↗

bioRxiv2026

Structural basis for catalytic and inhibitory divergence between archaeal and bacterial ammonia monooxygenases

Ammonia oxidation initiates nitrification and is closely linked to microbial N2O production. Ammonia monooxygenase (AMO) catalyzes the first and rate-limiting step of nitrification and is widespread across evolutionarily distinct ammonia-oxidizing archaea (AOA) and bacteria (AOB). The ocean is the largest biome for AOA and AOB, which have distinct ecological niches and markedly different sensitivities to nitrification inhibitors. However, the lack of archaeal AMO structures and inhibitor-bound AMO complexes has hindered mechanistic understanding of the architectural, catalytic, and inhibitory divergence between these two enzyme systems. Here, we report high-resolution cryo-electron microscopy (cryo-EM) structures of marine archaeal AMO captured in active and inactivated states within its native membrane environment, together with inhibitor-bound structures of estuarine bacterial AMO. Archaeal AMO forms an unexpected cup-shaped homotrimer composed of eight subunits per protomer and exhibits substantial architectural divergence from bacterial AMO. Integrated structural, biochemical, kinetic, and computational analyses reveal distinct periplasmic architectures, copper-center organization, and hydrophobic channels between archaeal and bacterial AMOs for ammonium acquisition, catalysis and inhibitor response. These findings provide a structural and mechanistic framework for understanding how archaeal and bacterial AMOs have diverged to distinct ammonia-oxidizing strategies and inhibitor susceptibilities across environmentally important ammonia oxidizers.

molecular biology↗

bioRxiv2026

Half-match recombination drives bridge RNA-guided excision and off-target insertion

IS110-family bridge recombinases are a recently identified class of compact, RNA-guided editors in which a bridge RNA (bRNA) directs the recombination of a donor DNA into a target site. In the current model, the bRNA engages fully complementary donor and target sequences within a single synaptic complex to drive double-stranded recombination, implying that the transposon is cut from its donor site rather than copied, yet neither the strandedness of the excised intermediate nor the requirement for full complementarity has been tested directly. Here we reconstituted IS621 recombination in a cell-free transcription-translation system, building representative arrangements of the excision and insertion reactions and characterizing the outcomes. We find that IS621 predominantly excises a single strand, releasing a single-stranded circle and leaving the donor site intact, consistent with copy-and-paste transposition. By introducing mismatches into the bRNA target sequences, we further find that excision proceeds independently of target-site complementarity, relying strictly on donor-arm recognition; we term this "half-match" recombination, because a substrate matching only half of the bRNA is sufficient. We also find half-match activity during insertion, both in vitro and in a published genome-editing experiment, where it accounts for approximately half of non-target insertion reads. Half-match recombination provides both a mechanistic explanation for off-target insertion and a framework for the rational design of high-fidelity bridge recombinases.

molecular biology↗

bioRxiv2026

Cross-Kingdom Control: Yeast Prion Protein Modulates Host Physiology in Drosophila

Prions, once mainly studied for their pathogenic roles, are now gaining recognition as adaptive elements in microbial physiology. Over one-third of wild yeast isolates harbor prion proteins, yet their impact on host-microbe interactions remains poorly characterized. Given the ecological dominance of yeasts in the Drosophila mycobiome, we leveraged the Drosophila melanogaster-Saccharomyces cerevisiae system to investigate how the mycobiome-derived prion, [MRPL10+], modulates host physiology. We show that flies exposed to [MRPL10+] yeast exhibit significantly enhanced cold tolerance and increased locomotor activity. This effect persists with heat-killed yeast and diluted culture, suggesting a stable, potent bioactive factor. Using the genetically diverse Drosophila Global Diversity Lines (GDL), we identified natural variation in responsiveness to [MRPL10+] yeast. Genome-wide association and functional RNAi screening revealed a gut-brain signaling axis involving genes critical for digestion, intercellular communication, transcription regulation, and neural transmission. Notably, serotonin and octopamine pathways were essential for [MRPL10+]-induced changes in cold tolerance and locomotion, implicating neuromodulatory circuits in prion-mediated microbial signaling. Our findings establish a mechanistic link between a fungal prion and host metabolic and neural adaptation. This work provides the first genetic dissection of a prion-mediated host-microbe interaction, laying the groundwork for investigating beneficial prions in complex microbial communities and highlighting a new dimension of the mycobiomes influence on animal physiology.

evolutionary biology↗

bioRxiv2026

Operando Failure Diagnosis and Performance Dynamics in Microbial Fuel Cells Treating Mine Waste

Bench-scale microbial fuel cells (MFCs) treating mining wastewater frequently exhibit operational variability and uncharacterized degradation that obscure true biocatalytic performance. To decouple genuine biological treatment effects from mechanical failures, this paper presents an integrated diagnostic framework validated on two bench-scale systems treating heavy-metal-rich gold mine tailings. The first system evaluates Micractinium inermum algal bio-augmentation (System 1), while the second compares Psychrobacter alimentarius- and Trichococcus patagoniensis-dominated anodic consortia (System 2). To overcome single-reactor constraints, the framework integrates paired time-series statistical modeling, an adaptive percentile-floor change-point detector, equivalent-circuit modeling, and baseline-corrected spectroscopy (XRD/FTIR). Applying the framework to these systems uncovers previously masked dynamics: statistical analysis demonstrates that algal biocatalysis provides no voltage advantage under stable operation (+0.17%) but increases output by 27.54% under diurnal perturbation, while periodicity analysis links these diurnal shifts to the chamber photoperiod. Furthermore, heavy-metal remediation (up to 97.7%) is governed by system-level physicochemical mechanisms rather than algal-specific processes. The change-point detector successfully isolates distinct failure modes, distinguishing a recoverable excursion from terminal structural collapse. Finally, equivalent-circuit modeling reveals that the superior power density of Trichococcus consortia is driven by combined improvements in internal resistance and open-circuit voltage. Ultimately, pairing statistical controls with automated fault detection resolves operational ambiguity, offering a scalable baseline for health monitoring in bio-electrochemical wastewater treatment.

bioengineering↗

bioRxiv2026

The circadian system is affected by Alzheimers disease independently from amyloid beta deposits

Circadian disruption, notably sleep disturbances, serves as an early indicator of Alzheimers disease (AD), preceding cognitive symptoms like memory loss. The suprachiasmatic nucleus (SCN) governs biological rhythms and receives direct retinal input via melanopsin-expressing retinal ganglion cells (mRGCs) to synchronize with environmental light cycles. The anatomical and functional basis for circadian disruption in AD remains unclear. Here, we explored the multi-level relationships between gene expression, the SCN connectome, and regulations of sleep and circadian rhythms in the APP/PS1 mouse model. The sleep architecture of APP/PS1 mice displayed significantly reduced rapid eye movement sleep (REM), associated with a reduced daily core body temperature amplitude and locomotor hyperactivity. Lastly, APP/PS1 mice showed an impaired response to acute light pulse stimulation and present hyperactivity of mRGCs at a young age and hypoactivity of these cells at older ages. These physiological functions are known to be, at least in part, regulated by the SCN, the main target of mRGCs. We noted several modifications in SCN connectomics using serial blockface electron microscopy (SBEM), including a reduction of the dendro-dendritic chemical synapse (DDCS) network that receives a large part of the retinal input and is thought to be crucial for synchronicity between SCN neurons. In addition, we observed multiple signs of dystrophy, including modifications of the shape of dendrites and cell soma, accumulation of aggregated lysosomes, and swelling of axons. At the same time, we investigated the changes in gene expression using spatial transcriptomics. The SCN presents changes in the expression of genes associated with synapse formation, cell adhesion, and neurite growth. These results suggest that, despite the absence of amyloid plaques in the ventral hypothalamus, the SCN of APP/PS1 mice still undergo profound gene expression changes, impacting connectomics and physiological functions. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=157 SRC="FIGDIR/small/744599v1_ufig1.gif" ALT="Figure 1"> View larger version (39K): org.highwire.dtl.DTLVardef@ceedb0org.highwire.dtl.DTLVardef@156cfaaorg.highwire.dtl.DTLVardef@5bc262org.highwire.dtl.DTLVardef@36df4d_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2026

Unbiased and scalable reduction of diverse bacterial genomes

The genome is a complex, integrated system where the functions and regulatory interactions of its many components remain poorly understood. Genome minimization aims to reduce genomic complexity by removing non-essential elements to reveal the fundamental building blocks of cellular life. However, current minimization strategies are often slow and species-specific due to a reliance on prior information, and limited to producing single, isolated strains, which obscures the diverse ways a genome can adapt to large-scale DNA removal. Here we show the development and application of Stochastic Lineage-based Iterative Minimization (SLIM) a modular, high-throughput platform for unbiased genome reduction across phylogenetically diverse bacteria. We apply SLIM to generate a library of genome-reduced Escherichia coli lineages. We then interrogate the lineages, identifying both universal and lineage-specific transcriptional and translational reprogramming in response to deletions. We demonstrate that these expression dynamics drive environment-dependent fitness, allowing us to pinpoint a single gene deletion in one genome-reduced lineage as the driver of a measurable environmental growth defect. Beyond E. coli, we successfully deploy SLIM in phylogenetically distinct bacterial taxa to rapidly reduce the genomes of Shigella flexneri and Pseudomonas putida, distinct genus and order respectively from E. coli, without species-specific optimization. Our results establish a scalable, generalizable framework for navigating the vast landscape of minimized genomes, providing a powerful new tool for functional discovery and the rational design of synthetic genomic chassis.

synthetic biology↗

bioRxiv2026

DNA Damage and Repair Mechanisms in Duckweed (Spirodela polyrhiza) Under Ultraviolet-B (UV-B) Light Stress

Exposure to Ultraviolet-B (UV-B) light can adversely affect plant growth and cellular integrity by inducing oxidative stress and DNA damage. In this study, we investigated UV-B-induced DNA damage and repair responses in the aquatic monocotyledonous plant species Spirodela polyrhiza (duckweed). We exposed 13-day-old duckweed plantlets to broadband UV-B light for 1-10 min, followed by recovery periods of up to 24 h under normal growth conditions. We observed progressive chlorosis, wilting, and diminished plant vigor with longer durations of UV-B light exposure. Agarose gel electrophoresis demonstrated compromised genomic DNA integrity immediately after UV-B light treatment, with partial restoration of DNA quality during recovery. Immuno-slot blot assays established the accumulation of two major UV light-induced photoproducts, cyclobutane pyrimidine dimers (CPDs) and 6-4 pyrimidine-pyrimidone photoproducts [(6-4)PPs], in a dose-dependent manner following UV-B light exposure. Notably, the abundance of these DNA lesions declined substantially after recovery, indicating activation of endogenous DNA repair mechanisms. Staining with 3,3-diaminobenzidine revealed elevated accumulation of hydrogen peroxide immediately following UV-B exposure, suggesting enhanced oxidative stress. Collectively, these findings demonstrate that S. polyrhiza possesses efficient mechanisms for sensing, repairing, and mitigating DNA damage induced by oxidative stress resulting from UV-B light exposure. This study highlights the potential of duckweed as an effective model system for investigating DNA damage and repair pathways under UV-B light stress in plants.

plant biology↗

bioRxiv2026

Shared neurogenesis onset is sufficient to explain bilateral matching in the vertebrate retina

Bilateral symmetry is a hallmark of many paired organs and often essential for optimal functionality. The vertebrate eyes are a prominent example of this, as the matched development of the two retinas is required for accurate visual processing. While macroscopic aspects of symmetry emergence across systems have been investigated, how bilateral matching is maintained once cells start to differentiate remains less understood. Here we address this question using the zebrafish retina as a model to follow neurogenic programs in vivo at single-cell resolution. We perform quantitative 3D live imaging of both retinas simultaneously and directly compare neurogenesis onset and propagation within and across embryos. We find that neurogenic waves initiate at the retinal poles and progress towards the mid-retina in a conserved spatiotemporal pattern. Within embryos, the two eyes exhibit highly similar neurogenesis dynamics when it comes to timing of neurogenesis onset, cell number increase, and spatial wave progression. Across embryos, however, variability is larger. While these observations hint at active inter-retinal coordination, a stochastic model predicts that a shared onset of neurogenesis can be sufficient to explain bilateral matching. Targeted genetic perturbation experiments support this prediction. We find that altering wave propagation affects patterning but not bilateral similarity. Disrupting neurogenesis onset timing, however, reduces bilateral symmetry between eyes. Thus, the combination of experiment and theory identifies synchronized neurogenesis onset as a key determinant of bilateral symmetry, revealing a minimal principle for how reproducible development of paired organs can emerge from stochastic processes.

developmental biology↗