Biology subjects

Qiu, S.

Publications and source records attributed to Qiu, S..

At least 19 recordsLinked to original sources

bioRxiv2026

NeuroPilot: Longitudinal intravital neural imaging across scales and modalities through an agentic platform

Longitudinal intravital imaging is essential for understanding how neural populations evolve across behavioral states, yet converting large-scale recordings into biological insight remains a fundamental challenge because neural signals are degraded by noise, non-rigid motion, and heterogeneous recording conditions. Here we introduce NeuroPilot, an agentic framework that transforms neural imaging analysis into a closed-loop, context-aware process, integrating a multimodal large language model with callable computational imaging modules to adaptively coordinate workflows from raw recordings to population-level readouts. Across heterogeneous imaging and experimental regimes, NeuroPilot restores motion-degraded recordings and supports consistent neural signal recovery, detection, and tracking in challenging deep-brain, freely moving, and longitudinal settings. These enable neuronal population tracking across spinal stimulation paradigms, deep-brain imaging, and continuous 24-hour mPFC recordings aligned with spontaneous sleep-wake behavior. By converting heterogeneous intravital recordings into stable population activity maps, NeuroPilot supports behavioral decoding and reveals structured neural dynamics across behavioral states and transitions. NeuroPilot establishes a scalable agentic paradigm for neural imaging analysis, expanding experimental access to the measurement, visualization, and interpretation of neural population activity.

neuroscience↗

bioRxiv2026

Charting sex divergence in the human brain across the lifespan

Biological sex fundamentally shapes human brain organization, but sex-specific normative neuroanatomical trajectories across the lifespan remain largely uncharted. Here, we constructed independent, sex-specific lifespan brain charts using structural neuroimaging data from 59,915 healthy individuals (29,760 males and 30,155 females) ranging in age from 266 postconception days to 100 years. By examining 296 structural phenotypes across global, cortical, and subcortical measures, these models revealed widespread sex differences in maturational timing, with males reaching peak milestones later than females. These trajectories demonstrate that sex differences evolve dynamically, with phenotype-specific windows of emergence and maximal separation. Compared with conventional sex-pooled references, sex-specific models achieved superior predictive accuracy and reduced misestimation of individual deviations in healthy populations. Across five neuropsychiatric conditions, sex-specific models improved the detection of extreme deviations and revealed both shared and sex-dependent patterns of disorder-related neuroanatomical abnormalities. These sex-specific charts establish tailored normative references for assessing brain development, ageing, and disease.

neuroscience↗

bioRxiv2026

FLASH X-rays preserve neutrophil chromatin to boost antitumor immunity

Ultrahigh dose-rate FLASH radiotherapy spares normal tissue while preserving antitumor activity, positioning it as a promising technology in radiation oncology, but its immunomodulatory mechanisms remain elusive. Here, using a bilateral subcutaneous tumor model in mice, we show that 8-Gy FLASH X-rays, versus an equal dose of conventional dose-rate (CONV) X-rays, elicit a robust abscopal antitumor effect with anti-PD-1 therapy. Single-cell transcriptome and T cell receptor (TCR) profiling reveal that FLASH X-rays plus anti-PD-1 enhance antitumor immune infiltration and TCR clonal expansion in both irradiated and abscopal tumor lesions. Mechanistically, the ultrashort temporal continuity of FLASH dose delivery conserves chromatin compaction in neutrophils during exposure and inhibits neutrophil extracellular trap (NET) formation, thereby dismantling NET-mediated CD8+ T-cell exclusion within primary tumors. Conversely, CONV or split-dose FLASH X-rays induce marked chromatin modifications prior to dose completion, leading to chromatin hyper-relaxation which promotes NETosis and consequently abrogates systemic antitumor immunity. Notably, this detrimental effect can be reversed by pharmacologically suppressing PARylation-mediated chromatin modification and decondensation in neutrophils. These findings identify radiation-induced aberrant chromatin relaxation in neutrophils as a critical determinant of radioimmunotherapy outcomes, providing a rationale for redefining the FLASH effect and advancing its clinical translation.

cancer biology↗

bioRxiv2026

Temporal organization of shared brain states characterizes heterogeneity in major depressive disorder

Major depressive disorder (MDD) is biologically heterogeneous, but how this variability is expressed in the temporal organization of brain activity remains unclear. Using resting-state functional MRI from 2,225 participants, we applied hidden Markov modeling to identify recurrent brain states and quantify their temporal organization. Five states formed a shared repertoire across individuals with MDD and healthy controls, while MDD-related alterations were distributed across states, functional systems, and temporal properties. Within MDD, unsupervised clustering of state occupancy, persistence, and switching delineated two prototype neurodynamic architectures characterized by preferential deployment of ACS/VSS or MAS/DMS states within a preserved state repertoire and broadly similar transition backbone. The architectures showed different within-group brain-symptom associations and symptom-network patterns. Connectome transcriptome analyses organized architecture-state imaging patterns into three transcriptomic state families shared across architectures, and contrasting group-level deployment patterns were recovered in an independent MDD cohort. These findings suggest that MDD heterogeneity is expressed not only through spatially distributed neural alterations, but also through differences in how a common repertoire of recurrent brain states is organized over time.

bioinformatics↗

bioRxiv2026

Melanoma evolution in the lymph node shapes systemic outcomes

Lymph node (LN) metastasis predicts poor patient outcomes, but the mechanistic drivers that shape metastatic fitness, immune evasion, and clinical impact remain elusive. While preclinical models indicate that active tumor adaptation is necessary for LN metastasis, observations of clonal heterogeneity in human tumors has supported a stochastic model of passive and continuous seeding. Reconciling LN metastasis as a passive or active process is essential to understanding if LN metastasis is simply a marker of disease progression or a clinically informative therapeutic target. Here, we report evidence that LNs are active niches that facilitate ongoing melanoma evolution to progressively subvert immune surveillance and enable progression. To construct a spatial trajectory of LN metastasis, we examined paired primary melanomas and metastatic sentinel LNs through integrated genomic, phenotypic, and immunologic analyses. In contrast to a model of continuous seeding, we observe that early dissemination from the primary tumor is followed by extensive intra-nodal diversification, indicating that metastatic outgrowth requires ongoing adaptation within the LN. As clones evolve in the LN, they re-differentiate towards a melanocytic state and reprogram the microenvironment for immune exclusion. In further evolved clones, loss of inflammatory interferon signaling and induction of p53 and mitochondrial stress are associated with decreased overall survival. Collectively, these results implicate the LN as a critical battleground for melanoma progression, where tumor evolution drives adaptation and immune escape to biologically link regional metastasis to patient survival.

cancer biology↗

bioRxiv2026

Normative modelling of cortical networks identifies subtypes of type 2 diabetes associated with distinct clinical and transcriptomic profiles

Type 2 diabetes (T2D) is characterized by substantial clinical heterogeneity, yet its neurobiological substrates remain unclear. Here, we leverage normative modelling of cortical morphometric networks to quantify individual-level brain deviations using structural MRI data from 3,723 participants (1,941 T2D patients and 1,782 healthy controls) across three independent cohorts. Data-driven clustering reveals two robust T2D biotypes characterized by widespread positive (biotype 1) and negative (biotype 2) brain deviations. Despite comparable overall metabolic burdens, these biotypes feature distinct brain-metabolic coupling patterns: biotype 1 is primarily associated with lipid metabolism, whereas biotype 2 reflects a multifactorial metabolic burden spanning glycaemic control, adiposity, lipid, vascular risks, and disease duration. These divergent brain vulnerability profiles have distinct cognitive consequences; notably, biotype 2 shows poorer performance in complex cognitive tasks, aligning with negatively deviated connectivity gradients along the sensorimotor-to-association axis. Spatial transcriptomic analyses further link biotype 2 deviations to gene expression patterns enriched in insulin signalling, mitochondrial functions, tight junctions, and neurodegenerative disease pathways, alongside specific involvement of inhibitory neurons and oligodendrocyte lineage cells. Our findings provide a neurobiological understanding of T2D heterogeneity and establish a data-driven framework for characterizing personalized brain vulnerability, with implications for advancing precision diabetes medicine.

neuroscience↗

bioRxiv2026

A framework for quality assurance in human intracranial electrophysiology

Intracranial electroencephalography (iEEG) provides an unprecedented opportunity to directly record neural activity and causally perturb the human brain through electrical stimulation. Yet, the increasingly collaborative nature and complexity of modern iEEG studies pose substantial challenges for experimental control, data quality, and standardization. Unlike most experimental modalities, human iEEG data are acquired within dynamic clinical environments, where patient condition, recording quality, hardware configuration, and experimental protocols may vary across recording sessions and collaborating sites. The resulting heterogeneity creates opportunities for technical and procedural failures that often remain undetected until downstream analyses, when corrective action is no longer possible. Here, we present a framework for standardized session-level quality assurance in human iEEG research and provide an open-source implementation compatible with Brain Imaging Data Structure (BIDS)-organized datasets. The framework defines four complementary domains of quality assessment crucial for human iEEG studies: protocol fidelity, behavioral integrity, stimulation validation, and signal quality. These domains integrate electrophysiological recordings, behavioral event logs, and stimulation metadata to verify data completeness, confirm participant engagement, validate stimulation delivery, and identify potentially compromised recording channels. Automated quality metrics and standardized diagnostic visualizations are generated following each testing session, enabling rapid identification of technical and procedural failures while corrective action is still possible. By providing a standardized approach to session-level quality assurance, the framework improves data integrity, enhances reproducibility, facilitates analyst training, and supports harmonized data collection across laboratories and clinical sites.

neuroscience↗

bioRxiv2026

Neuropil aggrecan, not perineuronal nets, closes the critical period for visual plasticity

Perineuronal nets (PNNs) are widely reported to close developmental critical periods and restrict experience-dependent plasticity. Here we tested this model by selectively eliminating gene expression for aggrecan (Acan), an essential component of PNNs. In visual cortex, PNNs predominantly ensheath parvalbumin-positive (PV+) interneurons. Deletion of Acan in inhibitory neurons eliminated PNNs but did not prevent closure of the critical period. By comparison, deletion of Acan in all neurons, or only in excitatory forebrain neurons, sustained critical-period plasticity in adult mice. Visual plasticity in adults was associated with reduced cortical excitatory synaptic inputs onto layer 2/3 PV+ interneurons and increased expression of some immediate early genes in visual cortex but normal response strength and tuning properties of layer 2/3 excitatory neurons. These findings rectify long-standing models that misattribute closure of the critical period to PNNs and identify that aggrecan expressed by excitatory neurons resident in the surrounding neuropil limits visual plasticity.

neuroscience↗

bioRxiv2026

Noncanonical Circular RNAs and Potential Functions

Circular RNAs (circRNAs) are ubiquitous in eukaryotes; dysregulated circRNA expression is linked to diseases, including lung cancer. In contrast to canonical circRNAs arising from exon-intron boundaries, noncanonical circRNAs originating within exonic, intronic, and intergenic regions have typically been dismissed as transcriptional noise or technical artifacts. To explore circRNA diversity and appreciate their functions, we developed an algorithm to identify both canonical and noncanonical circRNAs without relying on genome annotation, enabling the identification of circRNAs of all types and in newly sequenced or poorly annotated species. Results from lung cancer cells revealed that noncanonical circRNAs constituted over two-thirds of the circRNA population and were expressed more abundantly than canonical circRNAs, and genes with fewer and shorter exons were hotspots for noncanonical circRNA and circRNA isoform production. Further analyses showed that many noncanonical circRNAs were indeed endogenous circRNAs transcribed within cells rather than experimental artifacts, were potentially translated into proteins or peptides, and were conserved across species. Moreover, we validated 65 noncanonical circRNAs in NCI-H23 cells using multiple bioassays and demonstrated that both exonic and intergenic noncanonical circRNAs influenced cell viability. CircRNA profiles in tumor and tumor-adjacent tissues of lung cancer patients revealed tissue-specific expression and differentially expressed canonical and noncanonical circRNAs from cognate genes involved in cancer-related pathways, indicating their potential clinical relevance. This study confirmed the authenticity of noncanonical circRNAs and provided the first experimental evidence that noncanonical circRNAs influence cancer cell phenotypes. These findings broaden our understanding of circRNA biology, highlighting their widespread genomic distribution, diverse functions, and potential clinical relevance.

molecular biology↗

bioRxiv2026

Lineage-Specific Neofunctionalization of Polyacetylene-Directing UGT76 Glycosyltransferases in Campanulaceae

Polyacetylene glycosides exhibit notable pharmacological activities, yet the glycosyltransferases acting on their polyacetylene scaffolds remain unknown. Here we report a telomere-to-telomere genome assembly of Codonopsis pilosula and, guided by spatial metabolomics, characterize three UDP-glycosyltransferases: CpUGT76BG1 and CpUGT76BG2 catalyze the direct glycosylation of lobetyol to lobetyolin, while CpUGT94BY2 performs subsequent sugar-sugar coupling to produce lobetyolinin, with each activity confirmed by in planta overexpression. Structural modeling reveals that CpUGT76BG1 and CpUGT76BG2 employ a deep hydrophobic tunnel to fully encase the linear polyacetylene chain, a binding architecture distinct from the shallow pockets used by canonical plant UGTs for planar aromatic substrates. Ancestral sequence reconstruction across eleven nodes partitions the UGT76 lineage into three functionally distinct evolutionary stages, tracing the trajectory from an ancestral shallow pocket to this specialized deep architecture. These findings establish the key glycosylation steps of polyacetylene glycoside biosynthesis, define a tunnel-based paradigm for non-planar substrate recognition, and reveal how tandem duplication-driven active site remodeling generates metabolic novelty.

evolutionary biology↗

bioRxiv2026

Machine Learning Gap-Fills Missing Transporter Kinetics in Biosystems Across Scales

Understanding transporter kinetics is essential for deciphering metabolite exchanges in biosystems, particularly for cells subject to substrate gradients. Nevertheless, the prediction of transporter kinetic parameters, maximum rate per gram protein (Vmax) and Michaelis-Menten constant (Km), has not yet been tackled. Here, we developed the first compound-protein interaction machine learning model of transporter Vmax and Km, MMTKPred, which achieved R2=0.553, RMSE=1.155 mmol/hr/g Protein and R2=0.330, RMSE=0.935 mM for log10-scaled Vmax and Km prediction, respectively. Moreover, we demonstrated MMTKPreds predictive power across biosystem scales, from capturing transporter kinetics modulated by point mutations and substrate changes at the molecular level, to enabling substrate-sensitive metabolic modelling of non-model yeasts at the cellular level, and rationalizing inter-species substrate competition in co-cultures. Collectively, MMTKPred effectively models metabolite transport spanning from molecular to multi- species scales, thereby offering a computational tool for rational microbial cell factory optimization. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/735998v2_ufig1.gif" ALT="Figure 1"> View larger version (62K): org.highwire.dtl.DTLVardef@18e7bb6org.highwire.dtl.DTLVardef@15bec93org.highwire.dtl.DTLVardef@8ce92org.highwire.dtl.DTLVardef@31fb44_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIMMTKPred, first transporter kinetics CPI model, reaches [~]1 log10 RMSE for Vmax and Km. C_LIO_LIMMTKPred captures the effects of point mutations and substrate changes on transporters. C_LIO_LIPredicted kinetics enables substrate sensitivity in metabolic flux modelling. C_LIO_LIPredicted kinetics explains inter-species substrate competition outcomes. C_LI

systems biology↗

bioRxiv2026

Cognitive function depends upon Satb2 gene dosage in cortical projection neurons

SATB2-associated syndrome (SAS) is a severe neurodevelopmental disorder caused by de novo heterozygous SATB2 mutations, yet how haploinsufficiency disrupts brain development remains poorly understood. While homozygous Satb2 loss causes profound embryonic cell-fate defects, we demonstrate using a heterozygous mouse model that SAS phenotypes emerge primarily during postnatal circuit maturation. Integrating chromatin profiling, transcriptomics, electrophysiology, and behavior, we show that SATB2 acts as a dose-sensitive chromatin regulator that binds conserved enhancer-promoter landscapes to orchestrate networks linked to human intelligence. Although excitatory neuron subtype specification is preserved, Satb2 heterozygotes adopt an intermediate epigenetic state that drives cell-type-specific dysregulation of genes enriched for intellectual disability risk variants. Consequently, mutant neurons exhibit simplified dendritic arborization, reduced intrinsic excitability, and weakened layer 2/3-to-layer 5 intracortical connectivity. These circuit deficits culminate in the disorganization of the somatosensory barrel cortex and severe impairments in whisker-dependent texture discrimination. Finally, by restricting Satb2 heterozygosity to the cortex, we decouple these cortical sensory deficits from subcortical vocalization phenotypes. Together, our work links SATB2 dosage to chromatin architecture and postnatal circuit maturation, revealing a critical, post-mitotic therapeutic window for intervention in SAS.

neuroscience↗

bioRxiv2026

Closed-loop neurofeedback reshapes preparatory brain states to bias subsequent pain processing

Pain perception is strongly influenced by neural states preceding stimulus onset, yet whether such preparatory states can be causally reshaped remains unclear. Using a double-blind design, we tested whether closed-loop neurofeedback can reconfigure preparatory brain dynamics to influence subsequent pain processing. Real, but not sham, feedback enabled learning-dependent enhancement of pre-stimulus oscillations in primary somatosensory cortex and their trans-hemispheric propagation. Training also selectively reduced transitions between EEG microstates associated with salience and attentional control, indicating reorganization of preparatory brain states. These neural changes were accompanied by attenuated pain-evoked cortical responses and reduced pain perception. Sequential mediation analyses further revealed that somatosensory enhancement predicted microstate reorganization, which in turn suppressed pain-evoked responses. Together, these findings demonstrate that closed-loop neurofeedback can causally reshape preparatory brain states to bias subsequent sensory processing.

neuroscience↗

bioRxiv2026

Multiscale transcriptomic organization of the human brain with DigitalBrain

The human brain varies across anatomical regions, cell types, development, aging and disease states, yet existing single-cell transcriptomic resources remain fragmented and difficult to integrate into a unified biological model. Here we present DigitalBrain, a human brain-specific atlas and foundation-model framework for organizing diverse and fragmented human brain transcriptomic data across scales. We first built DigitalBrain-Atlas, a harmonized whole-brain single-cell resource comprising 16.35 million transcriptomes from 2,143 donors across 165 brain regions, spanning the human lifespan and multiple neurological and clinical conditions. We then developed DigitalBrain-M1, a Transformer-based model that jointly encodes gene identity and expression magnitude to learn a shared embedding space for cells and genes. Across held-out datasets, DigitalBrain supported robust single-cell integration, clustering and cell-type annotation while preserving major biological structure and reducing technical fragmentation. Beyond these benchmarks, the learned embeddings revealed emergent large-scale hierarchical organization of the human brain, linking anatomically distinct regions into higher-order patterns consistent with known functional systems. Applied to human hippocampal aging, DigitalBrain identified cell-type-specific aging sensitive gene sets, highlighted dentate gyrus granule cells as a particularly age-sensitive population, and discovered selective reorganization of gene programs related to synaptic transmission, postsynaptic structure, membrane excitability and axon guidance during aging. Cross-dataset convergence was strongest at the level of functional modules and recurrent aging sensitive genes. Together, these results demonstrate that DigitalBrain is a brain-specific framework for mapping human brain organization across scales, and as an early step towards a complete virtual organ for the human brain.

bioinformatics↗

bioRxiv2026

Intranasal immunization with live-attenuated RSV-vectored SARS-CoV-2 vaccines elicits antigen-specific systemic and mucosal immunity and protects against viral challenge and natural infection

The emergence of new SARS-CoV-2 variants and breakthrough infections underscores the need for next-generation vaccines capable of protecting from natural infection and/or preventing virus transmission to others. Intranasal vaccination offers a promising approach by eliciting local immune responses in the nasal mucosa, the primary site of infection and reservoir for transmissible virus. We evaluated two live-attenuated, respiratory syncytial virus vectored vaccines in which the RSV F and G surface glycoproteins were replaced with a chimeric SARS-CoV-2 Spike protein from either the ancestral USA/WA-1/2020 strain (MV-014-212) or the Delta variant (MV-014-212-delta). A single intranasal dose of either vaccine elicited systemic and mucosal immunity in K18-hACE2 mice, including serum neutralizing antibodies, Spike-specific memory B cells and plasmablasts, and Spike-specific CD8 lung-resident memory T cells. Although MV-014-212-delta vaccination provided the best protection against Delta variant virus challenge, both vaccines decreased viral loads in nasal discharge, lung and brain, and reduced weight loss and mortality. In naturally acquired infection studies, vaccinated hamsters exposed to infected cagemates exhibited minimal weight loss, limited viral replication within the nasal mucosa, and attenuated lung pathology. Therefore, intranasal RSV-vectored vaccines can elicit broad protective respiratory immunity, suggesting that this platform could be leveraged for other respiratory pathogens.

immunology↗

bioRxiv2026

Circular RNA identification using a genomic language model and a small number of authenticated examples

Genomic language models (gLMs) hold great promise for deciphering biological sequences, yet their effectiveness is hindered by the limited number of experimentally verified examples available for model training, a ubiquitous bottleneck for supervised machine learning. To overcome this challenge, we developed circFormer, the first gLM-driven approach for circular RNA (circRNA) identification. circFormer integrates curriculum learning with gLM fine-tuning: a Nucleotide Transformer model is first trained on a small set of validated circRNAs, the resulting model is used as a teacher to score [~]2.3 million noisy candidates, and the model is then fine-tuned with the noisy candidates along with their scores to improve prediction. Operating either as a standalone predictor or as a filter for existing pipelines, circFormer consistently outperformed traditional machine-learning approaches in accuracy and robustness. Among 50 circFormer-selected candidates that were overlooked by most existing tools, experimental validation using RNase R digestion and RT-qPCR confirmed 94.1% (32/34) of the evaluable candidates as genuine circRNAs. To enhance interpretability, we introduced a model-agnostic, dual-level explainable AI strategy that reveals mechanistic signatures of circRNA formation. circFormer provides a scalable, interpretable, and generalizable framework for converting noisy high-throughput data into reliable functional annotations, highlighting a practical path forward for gLM-based genomics in data-scarce settings.

bioinformatics↗

bioRxiv2026

Developmental Elimination of Electrical Synapses by UNC-51/UNC-76-Mediated Vesicular Transport

Neural circuit maturation requires precise elimination of transient synaptic connections, but how electrical synapses are eliminated remains unknown. Using C. elegans PLM mechanosensory neurons, we found that gap junctions form transiently during early development and are subsequently eliminated as the circuit matures. These transient electrical synapses drive high-frequency calcium oscillations, and optogenetic ablation of early gap junctions abolishes calcium dynamics and disrupts chemical synapse formation, demonstrating their critical developmental function. Through forward genetic screening, we identified the conserved kinase UNC-51/ULK as essential for elimination. UNC-51 phosphorylates the kinesin adaptor UNC-76/FEZ to initiate RAB-10-dependent retrograde trafficking, progressively depleting innexin proteins from the synaptic site. Disrupting this pathway prevents elimination, causing persistent electrical synapses and neuronal hyperactivity. These findings establish a conserved framework for developmental elimination of functionally essential transient electrical connectivity.

cell biology↗

bioRxiv2026

Mitochondria Organize Gap Junctions to Enable Neural Circuit Scaling

Neural circuits must maintain function during dramatic growth-driven expansion. While chemical synapses can be independently reorganized in pre- and postsynaptic neurons, gap junctions physically couple partner cells, requiring coordinated spatial redistribution--a process whose mechanisms remain unknown. Using the C. elegans mechanosensory circuit, we show that gap junctions undergo stereotyped developmental reorganization, transitioning from clustered to dispersed configurations as partner neurites elongate. Forward genetic screening identified RIC-7, a mitochondrial adaptor protein, as essential for this redistribution. Loss of RIC-7 prevents gap junction dispersal, trapping partner neurites at clustered sites and severely impairing electrical transmission. Mechanistically, RIC-7 directs mitochondrial positioning to gap junctions, where mitochondria recruit the microtubule-organizing component PTRN-1 to locally enhance microtubule dynamics. Disrupting mitochondrial transport (miro-1;mtx-2 mutants) or PTRN-1 function phenocopies ric-7 defects, while metabolic dysfunction does not, establishing a non-metabolic role for mitochondria in organizing synaptic architecture. Remarkably, RIC-7 expression in one neuron alone suffices to restore gap junction and partner neurite distribution across both coupled cells. Structural modeling suggests mechanical adhesion between docked hemichannels enables this coordinated reorganization. These findings establish mitochondria as mobile organizers of synaptic spatial architecture, demonstrate that proper junction distribution is essential for electrical transmission efficacy, and reveal how cell-autonomous mechanisms can achieve bilateral structural coordination during circuit growth.

neuroscience↗