Biology subjects

Du, Z.

Publications and source records attributed to Du, Z..

At least 19 recordsLinked to original sources

bioRxiv2026

NIK stabilization reprograms the pancreas toward chronic pancreatitis and pancreatic lipomatosis

Pancreatic lipomatosis, characterized by progressive adipose replacement of the exocrine pancreas, is a known consequence of chronic pancreatitis. Despite its clinical relevance, the mechanisms driving lipomatosis remain poorly understood. Here, we used a pancreas-specific NF-{kappa}B-inducing kinase (NIK) stabilization mouse model to investigate how sustained non-canonical NF-{kappa}B signaling contributes to chronic pancreatitis and pancreatic lipomatosis. NIK stabilization initiated a rapid and fully penetrant pancreatic remodeling program, leading to acinar cell death already by the end of the first week of age. Deep learning on high-definition spatial transcriptomics revealed a progressive loss of acinar identity resulting in acinar-to-ductal metaplasia (ADM) formation and identified GPA33 as a novel surface marker of ADMs. Over time, ADM lesions underwent apoptosis, leading to progressive loss of pancreatic parenchyma, organ atrophy, and extensive adipose replacement. Mechanistically, Relb deletion fully rescued the NIK-induced pancreatic phenotype, demonstrating that chronic pancreatitis and lipomatosis require RelB-dependent non-canonical NF-{kappa}B signaling in this model. Together, these findings define a RelB-dependent pathway linking sustained NIK stabilization to chronic pancreatitis and pancreatic lipomatosis. Our study provides a model for studying the development of pancreatic lipomatosis and for exploring potential therapeutic approaches.

cancer biology↗

bioRxiv2026

Unraveling APA dynamics during quiescence transitions reveals Pabp modulation of sod2 expression via APA to regulate cellular quiescence

Quiescence is a reversible proliferation arrest enabling cells to adapt to environmental changes, yet the post-transcriptional mechanisms governing its transitions remain poorly understood. Here, we map genome-wide alternative polyadenylation (APA) dynamics across 15 time points of quiescence transitions in fission yeast using 3'-end RNA sequencing. We reveal that APA undergoes extensive remodeling: driving global 3'UTR lengthening during early quiescence entry, 3' UTR shortening upon quiescence establishment, and progressive reversal to proliferative-state lengths during quiescence exit. Integrating 3' UTR dynamics with differential expression analysis, we identify candidate genes potentially regulated through APA-mediated 3' UTR mechanisms. We demonstrate that sod2, encoding mitochondrial superoxide dismutase, autoregulates its mRNA and protein levels via APA-dependent 3' UTR changes. Disrupting proximal APA site of sod2 in a mitophagy-deficient (atg43{Delta}) background exacerbates quiescence maintenance defects and mitochondrial dysfunction. We further identify Pabp as an upstream regulator of sod2 APA. This study establishes the temporal APA remodeling during quiescence transitions and reveals a Pabp-APA-sod2 regulatory axis governing post-transcriptional control of cellular quiescence.

cell biology↗

bioRxiv2026

Precision cooling assists electrical stimulation: Breaking selectivity barriers in nerve control

Peripheral neuromodulation can relieve pain through sensory activation or conduction block. However, electrical stimulation of mixed nerves couples these intended effects to unwanted neural activity. Here we demonstrate local cooling can separate targeted from off-target neural activity. In the rat sciatic nerve, precooling reduced the onset response to kilohertz-frequency stimulation by about 90% and maintained block in the target pathway during rewarming. During low-frequency stimulation, spatially graded cooling suppressed A{delta} enriched activity and blocked nontarget propagation. This produced a directional, A{beta} biased afferent output. A cooling-electrical neural digital twin predicted both responses and linked them to field-edge transition dynamics and spatially separated control of recruitment and conduction. These findings provide a mechanistically grounded route beyond the targeting limits of electrical stimulation alone.

bioengineering↗

bioRxiv2026

A biologically supported global RNA architecture of cucumber mosaic virus satellite RNA

Satellite RNAs (satRNAs) are parasitic subviral agents whose biological activities are mediated largely by specific sequence determinants and structured RNA elements. Establishing biologically supported global RNA structures is therefore essential for understanding how RNA architecture underlies satRNA functions. Cucumber mosaic virus (CMV) satRNA is one of the best-characterized models for investigating satRNA structure-function relationships; however, a biologically supported global RNA architecture of CMV satRNA has yet to be established. Here, we applied AlphaFold3 modeling to predict the global structure of CMV satRNA T1 (sat-T1). Initial full-length structure modeling generated multiple long-distance interactions that lacked biological support. We therefore used fragment-based modeling, combined with chemical probing, evolutionary covariation, and compensatory mutagenesis, to derive a biologically supported global secondary structure. To determine whether structurally distant regions could interact in the context of the full-length RNA, we engineered a structure-guided T1-ZD mutant that preserved the supported secondary structure while reducing alternative base-pairing possibilities. Full-length AlphaFold3 modeling of T1-ZD largely recapitulated the proposed architecture, while one predicted model revealed a long-distance interaction that was subsequently supported by compensatory mutagenesis analysis. These findings suggest that the 3' terminus of sat-T1 may undergo conformational switching between alternative structural states. Together, our work establishes a biologically supported global RNA architecture for CMV sat-T1 and provides a structural framework for investigating the molecular basis of satRNA function.

microbiology↗

bioRxiv2026

A Context-Conditional Audit of Trial-Pairing-Dependent Neural Gain in Motor-Cortex Decoding

ObjectiveNeural-only decoding performance does not identify how much prediction neural history adds beyond task structure or recent output. We tested how this increment changes when context and temporal information boundaries are made explicit. ApproachWe defined context-conditional neural gain as held-out error reduction from adding context-residualized neural history to a context model. Fully nested, whole-trial cross-fitting excluded predicted trials from nuisance preprocessing, fitting, and selection. Trial replacement tested reliance on correct neural-behavioral pairing. Matched-seed calibration and linear and nonlinear sensitivities accompanied two Neural Latents Benchmark datasets, nine paired LINK dates (18 development sessions), and 20 prespecified untouched LINK sessions from the same macaque. Main resultsIn LINK, fixed neural-only R2 near 0.31 coexisted with gains of 0.3012/0.3125 beyond phase, 0.0193/0.0209 beyond geometry by phase, and 0.0077/0.0098 beyond that context plus measured-output history for center-out/random-target tasks. Fully nested analysis retained positive means for two neural feature definitions; replacement made all four negative. Geometry-conditional spiking-band-power gain reduced context-model mean squared error by 4.92%. In the untouched sample, geometry-conditional gain was positive in 20/20 sessions (mean 0.02158), contracted to 0.00755 with measured-output history, and exceeded replacement in 20/20. MC_Maze showed gain 0.00051 beyond a strong template, whereas MC_RTT retained 0.06846 beyond lag-matched cursor history. Three prespecified nonlinear-neural random-feature maps preserved this contrast while changing magnitudes. SignificanceUnder the tested specifications, neural gain depended on context, information availability, and model family, and the residual correction depended on correct trial pairing. Neural-decoding reports should therefore state the outcome, context, temporal boundary, model class, grouped validation, and pairing control. The audit is predictive and model-relative, not causal.

neuroscience↗

bioRxiv2026

Climate warming reduces the speed and predictability of polygenic adaptation to salinity decline

Climate change exposes populations to multiple stressors simultaneously, yet our understanding of how the addition of one stressor alters adaptation to another remains poor. As a result of climate change, high-latitude coastal habitats are experiencing rapid salinity decline, resulting in serious impacts on food webs and ocean circulation. Here, we examine how temperature increase impacts adaptation to salinity decline, in terms of the speed, genomic response, and repeatability of adaptation. We performed replicated Evolve-and-Resequence experiments over 20 to 25 generations in the model copepod Eurytemora carolleeae (Atlantic clade of the E. affinis species complex). Under salinity decline alone, replicate selection lines exhibited a polygenic response involving 66 selected haplotype blocks, with increasing parallelism among the replicate lines through Generation 20. Fitness (egg number) declined sharply over the first four generations but underwent full Evolutionary Rescue, recovering to ancestral levels by Generation 10. In contrast, imposing temperature increase on the salinity decline lines resulted in significantly lower parallelism among the selection lines, along with delayed and incomplete Evolutionary Rescue. Only 14% of selected SNPs were shared between the two selection regimes, and Gene Ontology analyses revealed largely distinct functional categories of genes under selection. These results show that adding warming to salinity decline can alter the genomic trajectory of salinity adaptation, slowing and impeding Evolutionary Rescue, and reducing the repeatability of polygenic responses. Our findings have direct implications for predicting evolutionary responses to realistic, multi-stressor climate change in high-latitude coastal ecosystems experiencing simultaneous ocean freshening and warming.

evolutionary biology↗

bioRxiv2026

CSGDA: A Cell State-Guided Graph Domain Adaptation Network for Single-Cell Drug Response Prediction

Intratumoral heterogeneity drives cancer recurrence and metastasis, yet single-cell drug response prediction faces severe "cross-domain" challenges, such as applying in vitro models to in vivo tissues or inferring metastatic resistance from primary tumors. These scenarios trigger distribution shifts arising from heterogeneous sequencing platforms, distinct tissue microenvironments, and metastatic evolution--problems rarely addressed by existing methods. We introduce CSGDA, a cell state-guided graph domain adaptation framework designed to predict drug responses across these biological heterogeneities. CSGDA incorporates biological priors to map gene expression into functional cell states, guiding a structure learning module to construct robust cell topology. To conquer distribution shifts, the model employs graph domain adaptation combined with a novel overlap penalty mechanism. Extensive benchmarks on five scRNA-seq datasets demonstrate that CSGDA outperforms state-of-the-art methods, achieving an average gain of [~]6% in ACC and AUPR. Beyond prediction accuracy, we employed integrated gradients to effectively pinpoint key genes involved in drug resistance within a challenging cross-metastasis cisplatin dataset. These findings underscore CSGDAs superior performance in single-cell drug response prediction and its potential in resolving single-cell heterogeneity, paving the way for precision medicine.

bioinformatics↗

bioRxiv2026

The MIRO1-BAX Complex Dictates Life and Death at the Mitochondrial Gate

BAX macropores in the outer mitochondrial membrane (OMM) are canonical mediators of apoptosis, but whether the same pore structure can drive distinct cell death pathways remains unclear. Here, we identify the OMM protein MIRO1 as a context-specific modulator of BAX activity. Mechanistically, MIRO1 binds BAX via MIRO1s N-terminal domain to promote macropore formation and the release of mitochondrial DNA (mtDNA) into the cytoplasm, triggering the STING-pIRF3 signaling axis. In glioma cells, this pathway sustains GPX4 expression via pIRF3-mediated transcriptional activation and confers ferroptosis resistance while bypassing inflammation. By contrast, in Parkinsonian neurons, the MIRO1-BAX complex promotes mitochondrial-stress-induced apoptosis. Using structure-guided drug discovery, we developed first-in-class small molecules that allosterically disrupt the MIRO1-BAX complex by engaging MIRO1s distal GTPase pocket. These compounds sensitize glioma cells to ferroptosis and protect neurons from apoptosis. Our findings reveal a disease-specific mitochondrial switch for life-death decisions and illuminate the molecular logic by which cells exploit and interpret OMM permeabilization.

Cell Biology↗

bioRxiv2026

Hippocampal Glucuronyl C5-epimerase promotes stress resilience by directly engaging PI3K through a non-enzymatic mechanism

Major depressive disorder (MDD) seriously affects human physical and mental health and causes global socioeconomic burdens. Stress-induced depressive etiology is linked to dendritic atrophy in the hippocampus, however, the underlying mechanism was poorly understood. Here, we identify that glucuronyl C5-epimerase (Glce), a heparan sulfae-modifying enzyme, as a critical regulator of hippocampal dendritic integrity and stress resilience. Genetic ablation of Glce in the hippocampal excitatory neurons is sufficient to induce dendritic atrophy and depressive-like behaviors, whereas its restoration rescues these deficits. Notably, Glce levels are reduced in the plasma of depressed individuals. We further find that Glce functions independently of its enzymatic activity, instead binding directly to and activating PI3K (p85/p110), thereby triggering an Akt/CREB/BDNF signaling cascade. Together, our findings uncover a non-canonical role for Glce and establish that Glce-PI3K-BDNF axis is essential for maintaining hippocampal structure and behavioral resilience, thereby highlighting a critical role of Glce in the pathophysiology of depression.

neuroscience↗

bioRxiv2026

OmniAge: a compendium of aging omic biomarkers links mitotic clocks to clonal hematopoiesis and causality

Interest in aging omic biomarkers has grown due to their ability to quantify biological age. Most of these biomarkers have been derived in blood and fall into many diverse categories, yet relatively little is known about their correlative patterns, especially between biomarkers from different categories. Here we present the OmniAge R and Python package, a collection of 413 aging omic biomarkers representing 12 different categories, including traditional epigenetic clocks, epigenetic mitotic clocks, DNA methylation-based proxies for clonal hematopoiesis and inflammaging, causal clocks, cell-type specific epigenetic clocks and single-cell transcriptomic clocks. By studying their inter-class correlations across large blood datasets, we reveal associations of mitotic age with clonal hematopoiesis subtypes and causal clocks, which are predictive of cancer risk. Using proxies of serum protein levels, we further dissect associations with mitotic clocks, clonal hematopoiesis and causal clocks into distinct biological processes mapping to key aging pathways. Applying OmniAge to multi-modal data of sorted immune cell-types reveals that age-acceleration derived from transcriptomic and epigenetic clocks correlate, but that this is driven by underlying cell-type heterogeneity. In summary, the OmniAge package is an exploratory tool for evaluating large numbers of aging omic biomarkers, and to aid discovery and generate new hypotheses.

bioinformatics↗

bioRxiv2026

Probiotic Lactiplantibacillus plantarum VB165 improves metabolic disorders in Insulin-Resistant Mice

This study investigated the effects of Lactiplantibacillus plantarum VB165, a probiotic strain with intrinsic -glucosidase inhibitor (AGI) activity, on metabolic disorders in high-fat diet (HFD)-induced insulin-resistant (IR) mice. Male C57BL/6 mice were divided into four groups: normal control diet (NCD), NCD supplemented with VB165, HFD, and HFD supplemented with VB165. After 16 weeks, VB165 supplementation significantly attenuated HFD-induced weight gain and reduced epididymal and inguinal white adipose tissue indices. VB165 also improved glucose intolerance and insulin resistance (IR), as demonstrated by oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT), and lowered fasting blood glucose, fasting insulin, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) levels. Additionally, it ameliorated dyslipidemia by reducing serum total cholesterol, triglycerides, and low-density lipoprotein cholesterol (LDL-C), while alleviating hepatic steatosis and adipocyte hypertrophy. Mechanistically, VB165 enhanced intestinal barrier function by upregulating tight junction proteins (ZO-1 and Occludin), reduced systemic inflammation by lowering LPS, IL-6, and IL-1{beta}. Gut microbiota analysis revealed that VB165 modulated community composition, suppressing HFD-enriched genera (e.g., Ileibacterium and Coriobacteriaceae_UCG_002) and promoting beneficial taxa (e.g., Faecalibaculum and Oscillibacter). These findings demonstrate that L. plantarum VB165 improves HFD-induced metabolic disorders via multi-target mechanisms, highlighting its potential as a probiotic intervention for IR and related metabolic diseases.

microbiology↗

bioRxiv2026

Impacts of genome architecture on the repeatability of polygenic adaptation

A central but poorly resolved question regards how genome architecture shapes the selection response and repeatability of polygenic adaptation. We addressed this question using Evolve-and-Resequence experiments under rapid salinity decline in two sibling species (clades) of the invasive copepod Eurytemora affinis complex that differ strikingly in chromosome number (15 versus 4). The 4-chromosome genome arose from chromosomal fusions of the ancestral 15-chromosome genome, bringing together coadapted alleles at fusion sites. Across 10-20 generations of selection, both clades adapted to low salinity but followed divergent evolutionary trajectories. The selection lines of the 15-chromosome clade exhibited highly parallel genomic responses, whereas the 4-chromosome clade lines showed delayed and less repeatable responses. Forward genetic simulations revealed that strong synergistic epistasis among beneficial alleles best explained elevated parallelism in the 15-chromosome clade. Additional simulations varying chromosome number and epistasis revealed that strong positive epistasis, combined with high chromosome numbers, enhances parallelism by enabling recombination to assemble coadapted allelic combinations. In contrast, the high starting frequency of beneficial alleles in the 4-chromosome clade lines indicated selection on standing variation, likely acting on alternative linked haplotypes. These findings demonstrate that genome architecture and gene-gene interactions jointly determine the dynamics and predictability of polygenic adaptation.

evolutionary biology↗

bioRxiv2026

A Clinically Silent Resistance Phenotype That Promotes Acinetobacter baumannii Survival During Colistin Therapy

Acinetobacter baumannii is a major cause of multidrug-resistant nosocomial infections, particularly ventilator-associated pneumonia, for which therapeutic options are increasingly limited. Colistin, a polymyxin antibiotic, is a drug of last resort for A. baumannii, boasting high susceptibility rates. Yet, despite relatively low rates of breakpoint-defined colistin resistance, clinical outcomes are highly variable, and the bacterial strategies that enable survival during colistin therapy remain poorly understood. Here, we integrate supervised machine-learning-guided genomic prioritization with functional, physiological, and in vivo analyses to interrogate the genetic basis of colistin response in A. baumannii. Machine-learning analysis of clinical isolates identified candidate loci associated with colistin survival, many of which did not alter minimum inhibitory concentration (MIC) when disrupted. Instead, growth-dynamic assays uncovered a subset of mutants capable of maintaining fitness upon inhibitory colistin exposure despite classification as susceptible via standardized antibiotic susceptibility testing. We define this phenotype as clinically silent resistance (CSR), a genetically encoded, MIC-independent survival state. Using a murine pneumonia model, we further demonstrate that CSR mutants thrive during colistin therapy in vivo. Together, these findings reveal a hidden layer of colistin survival that is not captured by standard susceptibility testing and highlight fundamental limitations of breakpoint-centric paradigms for predicting treatment outcomes in A. baumannii.

microbiology↗

bioRxiv2026

Ancient persistence and newfound diversity of CR1-group retrotransposons across chordates

Retrotransposons are mobile, repetitive DNA sequences that are ubiquitous across eukaryotes and widely recognised as key drivers of both gene and genome evolution. The CR1 group of retrotransposons is thought to have been present in the most recent common ancestor of chordates [~]560 mya, and is the dominant retrotransposon in the majority of chordate species. The advent of long-read sequencing technologies has enabled the assembly of high-quality genomes from representatives of almost all major chordate orders, enabling comparative analysis with deeply divergent species. To better understand the composition of CR1-group elements (CGEs) in chordates, we systematically characterised full-length, recently active transposable elements across representative species from every available extant order of chordate. Our analysis uncovered previously unknown phylogenetic relationships of CGEs within and between species and has pushed back the origin of certain CR1-group subclades by tens of millions of years. Additionally, entirely novel elements with no close relatives in existing databases were uncovered within several of the species analysed. We also detected numerous putative horizontal transfer events, many of which had not been previously documented. Overall, this investigation has provided the first chordate-wide analysis of an element that is historically understudied yet plays a pivotal role in genome biology and evolution.

evolutionary biology↗

bioRxiv2025

Optogenetic Proximity Labeling Maps Spatially Resolved Mitochondrial Surface Proteomes and a Locally Regulated Ribosome Pool

Outer mitochondrial membranes (OMM) function as dynamic hubs for inter-organelle communication, integrating bidirectional signals, and coordinating organelle behavior in a context-dependent manner. However, tools for mapping mitochondrial surface proteomes with high spatial and temporal resolution remain limited. Here, we introduce an optogenetic proximity labeling strategy using LOV-Turbo, a light-activated biotin ligase, to profile mitochondrial surface proteomes with improved precision, temporal control, and reduced background. By fusing LOV-Turbo to a panel of variants of an OMM-anchored protein, Miro1, we generate spatially distinct baits that resolve modular architectures and regulatory states of the OMM proteomes across diverse conditions, a database we name MitoSurf. Building on this proteomic map, we present RiboLOOM, a platform that defines LOV-Turbo labeled ribosomes and their bound mRNAs at the mitochondrial surface. MitoSurf and RiboLOOM uncover a spatially distinct ribosome pool at the OMM that is maintained by Miro1, enabling local mRNA engagement and translation of mitochondria-related proteins. These findings establish Miro1 as a key organizer of mitochondrial protein biogenesis through spatial confinement of surface-associated ribosomes. Our platform reveals an uncharted layer of mitochondrial surface biology and provides a generalizable strategy to dissect dynamic RNA-protein-organelle interfaces in living cells.

cell biology↗

bioRxiv2025

A near-complete lamprey genome illuminates ancestral vertebrate innovations

The origin of vertebrates is characterized by a suite of phenotypic innovations, yet the underlying genetic mechanisms remain poorly understood. As a living representative of jawless vertebrates, the lamprey serves as a pivotal model for investigating the genomic basis of early vertebrate evolutioin. Here, we report a near telomere-to-telomere (T2T) genome assembly of the reissner lamprey (Lethenteron reissneri), generated from sperm DNA that is not subject to programmed genome rearrangement. The 1.25 Gb assembly resolves over 97% of chromosome sequences into single contigs, enabling reconstruction of previously inaccessible genomic regions. Centromeres display highly diversified, lamprey-specific repeat units and structural architectures, whereas telomeres contain both conserved and lineage-specific satellite repeats. Deep transcriptomic profiling across representative organs and developmental stages substantially improved genome annotation. Comparative genomic analyses revealed a major expansion of 1,562 gene families at the base of the vertebrate lineage, and they are significantly enriched for functions related to neural development, skeletal formation, and cardiac function, echoing the known phenotypic innovations in vertebrates. Notably, the CDH2 gene family underwent vertebrate-specific copy number expansion and acquired conserved cis-regulatory elements (CREs), highlighting its potential role in shaping the early vertebrate circulatory system. Histological analyses and functional knockout experiments demonstrated that one CDH2 paralog (CDH2_H) is essential for lamprey heart development and chamber formation, playing a critical role in the emergence of the closed circulatory system in early vertebrates. This high-quality lamprey genome provides a foundational resource for dissecting the genetic basis of key innovations that shaped vertebrate evolution.

genomics↗

bioRxiv2025

Nuclear factor kappa B subunits and IkappaB family are modulated in the ovine endometrium during early pregnancy

Pregnancy modulates the endometrial immune responses to establish maternal immune tolerance, and nuclear factor kappa B (NF-{kappa}B) subunits and I{kappa}B family are involved in the maternal innate and adaptive immune responses. It, nevertheless, is unclear if early pregnancy regulates the expression of NF-{kappa}B subunits and inhibitor of NF-{kappa}B (I{kappa}B) family in the ovine endometrium. In this study, ovine endometria were sampled at day 16 of the estrous cycle (N16), and at days 13, 16, and 25 of pregnancy (P13, P16, and P25), and mRNA and protein expression of NF-{kappa}B subunits and I{kappa}B family was analyzed by RT-qPCR, western blot, and immunohistochemistry. The results revealed that the expression of all NF-{kappa}B subunits was decreased at P25 compared with N16 both in mRNA and protein expression, but the expression of B cell leukemia-3, I{kappa}B, I{kappa}B kinase {gamma}, and I{kappa}B{delta} was increased at P25 compared with N16 both in mRNA and protein expression. I{kappa}B{beta}, however, was downregulated during early pregnancy, and the expression of I{kappa}B{varepsilon} and I{kappa}B{zeta} was decreased at P13 and P16 compared with N16 and P25 both in mRNA and protein expression. In summary, early pregnancy changed the expression of NF-{kappa}B subunits and I{kappa}B family in the ovine endometrium both in mRNA and protein expression, which may be essential for maternal immune tolerance and embryo implantation.

immunology↗

bioRxiv2025

Negative-Valence Neurons in the Larval Zebrafish Pallium

An organisms survival depends on the rapid classification of sensory events as either harmful or beneficial. In mammals, this computation is partially performed by neurons in the amygdala that respond to signals with negative or positive valence. The larval zebrafish pallium is thought to contain homologs of the mammalian amygdala, isocortex, and hippocampus; however, the signals encoded by pallial neurons remain largely uncharacterized. Using two-photon light-sheet microscopy to image 7-9-day-old zebrafish that express pan-neuronal GCaMP6s, we recorded calcium dynamics throughout the brain while presenting a panel of strongly aversive stimuli including infrared heat, electric shock, and a whole-field looming shadow, together with milder threats including vibration, loud sound, light transitions, and a partial looming stimulus. A compact cluster of neurons in the rostrolateral dorsal pallium (Rl) responded vigorously to strongly noxious and fully looming stimuli, but not to the milder cues. In contrast, neurons in the ventromedial pallium and habenula responded to all stimuli tested. Rl neurons are characterized by high Tiam2a expression, suggesting they can be genetically accessed. Thus, our results identify a locus of negative valence neurons in the teleost pallium.

neuroscience↗