Biology subjects

Ye, H.

Publications and source records attributed to Ye, H..

At least 19 recordsLinked to original sources

bioRxiv2026

Endosperm secretion remodels the maternal seed coat

In flowering plants and mammals, maternal tissues must accommodate the growth of the offspring they enclose. The maternal seed coat expands around the developing embryo and endosperm. Endosperm pressure and hormonal signals coordinate seed-coat development1,2, but whether the endosperm directly promotes maternal cell elongation remains unclear. Here we show that the coenocytic Arabidopsis endosperm directly supplies cell-wall-loosening proteins to maternal seed-coat walls. The seed-size-regulating HAIKU-WRKY10 pathway activates an endosperm secretory programme enriched in cell-wall-associated proteins. These proteins spread through a shared extracellular domain across multiple inner seed-coat layers, revealing an extensive functional maternal-filial interface through which the endosperm reaches maternal cells it does not directly contact. Among these proteins, three expansins are necessary and sufficient for maternal cell elongation and seed growth. The endosperm therefore promotes its own growth by enabling expansion of the maternal tissues that enclose it. Paternal DNA methylation and maternal Polycomb activity jointly regulate this programme, with Polycomb also required for timely shutdown of expansin expression. These findings link parental epigenetic states to maternal tissue expansion through proteins supplied by the offspring. This cross-generational control of growth parallels epigenetically regulated signaling from mammalian extraembryonic tissues3, suggesting a shared strategy for adapting the maternal environment to offspring development.

plant biology↗

bioRxiv2026

Reinforcement learning with evolutionary priors unlocks multi-site enzyme optimization from sparse experimental feedback

Industrial enzymes underpin sustainable manufacturing, yet natural proteins rarely combine the activity, robustness and application compatibility required for practical use. Engineering such properties requires identifying beneficial combinations of interacting mutations within vast sequence spaces that are too large to search exhaustively and too sparsely sampled to model reliably. Here we introduce AlphaVariant, a reinforcement-learning (RL) framework that couples a generative evolutionary prior with iteratively updated low-N fitness models to enable feedback-driven search of large combinatorial protein sequence spaces. Across six experimentally measured protein fitness landscapes, AlphaVariant ranked first on the three large, non-enumerable multi-site landscapes. In two successive rounds of savinase activity optimization, AlphaVariant-designed libraries yielded 75.4% and 83.8% activity-improved variants among experimentally characterized candidates even as the accessible mutation space expanded from 25 to 67 positions. The search identified beneficial mutation combinations involving up to 17 structurally dispersed sites and produced a variant with 7.1-fold higher activity than wild type after only two design-test cycles. We then extended AlphaVariant to jointly optimize activity, thermostability and a patent-informed constraint for intellectual-property freedom. This multi-objective search yielded variants that outperformed the commercial protease Uno 100 L in both biochemical assays and application-relevant detergent washing tests. These results demonstrate that generative RL can efficiently navigate vast protein fitness landscapes, progressively incorporate multiple engineering objectives and convert sparse experimental feedback into enzyme variants with industrially relevant performance, effectively resolving the limits of biocatalyst engineering.

bioinformatics↗

bioRxiv2026

scPRIME-seq uncovers synchronized multimodal molecular collapse facilitated by pre-neoplastic epigenetic burden in prostate cancer

Tumorigenesis involves alterations across the genome, epigenome and transcriptome, yet how these layers interact to drive malignant transformation remains unclear, largely due to the lack of scalable multimodal single-cell approaches. Here, we developed scPRIME-seq, a high-throughput platform for simultaneous single-cell profiling of transcriptome, genome and DNA methylome, and applied it to 436,908 cells from 29 prostate cancers and 15 benign tissues. This multimodal atlas resolved dynamic changes across 30 cell types and a unified tumorigenic trajectory. Integrated analysis revealed a cell-state transition tipping point, where the onset of aneuploidy is temporally coupled with global methylomic alterations and transcriptomic rewiring. Early focal epigenetic alterations, including TMEM106A promoter hypermethylation and the emergence of hypomethylated domains, were present in founder aneuploid clones and benign tissues, indicating a pre-neoplastic origin of epigenetic burden. These pre-neoplastic alterations coincide with transcriptomic changes that affect epithelial interactions with stromal and immune compartments, promoting a putative tumor-permissive microenvironment. scPRIME-seq provides a high-throughput multimodal framework for identifying conserved, cell-intrinsic molecular programs underlying tumorigenesis.

cancer biology↗

bioRxiv2026

m6A-Driven Intratumoral Cholesterol Biosynthesis Fuels Castration-Resistant Prostate Cancer Progression

Both nuclear pore complexes (NPCs) and RNA N6-methyladenosine (m6A) machinery are indispensable for proper cellular function. Although their collaborative roles in the nuclear export of messenger RNAs (mRNAs) have been reported, it remains ambiguous whether and how this collaboration may contribute to cancer progression. Here we identify a functional cooperation between NPCs and m6A signaling that promotes the development of castration-resistant prostate cancer (CRPC). We showed that nuclear export of m6A-modified mRNAs, mediated by the interaction between RNA methyltransferase METTL3 and the nucleoporin NUP93, is functionally coupled to cholesterol biosynthesis. Given that cholesterol-fueled intratumoral androgen production is one of the mechanisms driving CRPC, we demonstrated that overexpression of the wild-type METTL3 or NUP93, but neither the enzymatically dead METTL3 nor the mutant NUP93 that loses METTL3-interacting capability, elevates intracellular levels of androgens, activates AR signaling under castrate condition, and promotes androgen-independent growth of prostate cancer cells both in vitro and in vivo. Importantly, pharmacological inhibition of METTL3 or targeted demethylation on mRNAs encoding key cholesterol biosynthesis enzymes effectively suppressed CRPC malignancy. Together, these findings uncover a therapeutically targetable m6A-METTL3-NUP93 axis that links nuclear mRNA export and metabolic reprogramming to fuel CRPC progression, providing a conceptually new strategy for the treatment of this lethal disease.

cancer biology↗

bioRxiv2026

Loss of DNA Demethylase Enhances Arsenic Resistance Via Reducing of PIN2 Antisense Long Noncoding RNA

DNA methylation dynamics regulate diverse plant stress responses, but the mechanisms governing arsenic (As) tolerance through epigenetic pathways remain largely unknown. Here we report that Arabidopsis mutants lacking the DNA demethylase, REPRESSOR OF SILENCING (ROS1), show substantially enhanced As resistance. Integrating transcriptome and methylome data, we found that PIN-FORMED 2 (PIN2), encoding an auxin efflux carrier that also transports As out of cells, represents a key ROS1 target. In ros1, we observed increased methylation in the last exon of PIN2, a region functioning as the promoter for an antisense long non-coding RNA (lncRNA). Hypermethylation of the promoter suppresses the antisense lncRNA, which follows reduction of sense PIN2 transcription. As a result, PIN2 expression increases in ros1 mutants during As exposure, enhancing As tolerance. Analysis of ros1 pin2 double mutants confirmed that PIN2 acts downstream of ROS1 in As tolerance. Our study demonstrates an epigenetic pathway in which ROS1 regulates As tolerance by controlling PIN2 expression through antisense lncRNA-mediated transcriptional interference, offering new epigenetic strategies using plants in heavy metal contaminated environments.

plant biology↗

bioRxiv2026

Sleep spindles stabilize human thalamocortical networks, inhibiting pathological disruptions

The thalamus coordinates sleep-dependent brain function including memory consolidation, sensory gating, and network stability through spindle oscillations. Thalamocortical circuits are also affected in many neurological and neuropsychiatric disorders. Yet how human thalamocortical circuits respond to pathological disruptions remain poorly understood. Here, we leveraged interictal epileptiform discharges (IEDs) as spontaneous perturbations to probe spindle-generating circuits and thalamocortical dynamics in vivo. Using multi-night intracranial recordings spanning multiple thalamic nuclei and cortical regions in 55 individuals with epilepsy, we investigated interactions between sleep spindles and epileptic activity across timescales from milliseconds to days. Sleep spindles were associated with IED suppression, whereas IEDs increased subsequent spindle probability, revealing bidirectional interactions between physiological and pathological activity. Nights with lower IEDs corresponded to increased spindle occurrence, longer duration, and faster frequency, reflecting a more stable thalamocortical state. These findings propose sleep spindles as potential regulators of thalamocortical networks that actively respond to and regulate pathological activity.

neuroscience↗

bioRxiv2026

Soft-Robotic Magnetic Microfluidic Catheter for Delivery of Aqueous-Based Dual-Component Embolic Formulations

Transcatheter embolization requires materials that can be steered through tortuous vessels, solidify rapidly in situ, remain clearly visible under fluoroscopy, and, ideally, carry therapeutic cargo without harming tissue. To meet these requirements, we present a fully water-based, two-component PEI-PEG hydrogel delivered through a soft-robotic, microfluidic catheter that keeps the precursors separate until they meet in a millimetre-scale mixing chamber at the tip. Fast amide cross-linking converts the liquid pair into a self-supporting gel within seconds, eliminating organic solvents and preventing catheter blockage. By adjusting precursor ratio and flow regime, the gel's stiffness and viscosity can be tuned over orders of magnitude, with the same chemistry allowing to occlude both high-flow arteries and fragile micro-vessels. The platform was validated in three escalating models. First, in ex-vivo perfused human placenta, the hydrogel filled targeted branches without reflux or fragmentation, demonstrating controlled delivery in clinically relevant vasculature. Next, in three porcine embolizations, splenic, hepatic and ascending pharyngeal arteries, the material achieved stable, selective occlusion with no migration, vasospasm or recanalization, showing seamless compatibility with standard interventional workflows. Finally, in rats bearing orthotopic liver tumours, drug-loaded hydrogel delivered through the hepatic artery concentrated doxorubicin inside tumours while sparing healthy tissue, confirming its potential for precision chemoembolization. These results position the PEI-PEG hydrogel and microfluidic catheter as a unified, image-guided platform that couples robust mechanical occlusion with site-specific drug delivery, offering a biocompatible alternative to current liquid embolics and expanding the therapeutic reach of minimally invasive embolization procedures.

bioengineering↗

bioRxiv2026

A patient-centric therapeutic paradigm uncouples prostate cancer suppression from systemic metabolic collapse

The clinical benefits of cancer therapies are often compromised by the tolerable adverse effects that impair systemic organismal health and may evolve into latent life threats. Here, we identified profound abiraterone-induced but androgen-independent metabolic perturbations in prostate cancer patients and developed Lifehug-9892 to balance tumor therapy with systemic metabolic homeostasis. By integrating population cohorts with high-resolution metabolomics, we demonstrate that abiraterone induces profound systemic lipidomic dysregulation, characterized by the massive, pathological accumulation of desmosterol. Abiraterone inhibits but stabilizes DHCR24, leading to a metabolic trap in patients showing elevated levels of both desmosterol and cholesterol. Desmosterol accumulation is highly lipotoxic, potently triggering endothelial cell senescence and necrosis, macrophage foam cell formation, murine atherosclerosis, and hepatic senescence. To mechanistically uncouple and therapeutically rescue this systemic metabolic collapse, Lifehug-9892 was rationally designed to selectively retain on-target CYP17A1 inhibition while completely sparing DHCR24 function. Lifehug-9892 maintains potent tumor-suppressive activity while fully preserving the desmosterol-cholesterol metabolic axis and preventing systemic cardiovascular and hepatic damage. Our study uncovers a critical mechanistic link between drug-induced metabolic dysregulation and organismal health in cancer patients, providing a biochemical framework for developing patient-centric targeted therapies that preserve host homeostasis.

cancer biology↗

bioRxiv2026

Dynamic Nanoparticle Assembly-Based Biomedical Microrobots

Precise drug delivery within anatomically complex tissues demands systems capable of both active navigation and deep tissue access, properties that have remained difficult to reconcile in existing nanocarriers and microrobots. Here we introduce Dynabots, a dynamic microrobotic assembly constructed from multifunctional nanoparticles covalently linked by thermally cleavable molecular connectors. This nanoparticle-rich architecture enables the integration of magnetic, imaging, and therapeutic components while preserving a high content of functional material. Collective assembly imparts enhanced magnetic responsiveness and maneuverability, enabling controlled navigation through tortuous biological environments. Upon exposure to mild thermal stimuli, the assemblies undergo programmed disassembly, releasing individual nanoparticles that can diffuse through tissue for localized therapeutic action. We establish the programmable transitions, biocompatibility, and therapeutic efficacy of this process across in vitro and in vivo models, including real-time fluoroscopic guidance within anatomically realistic phantoms and live rodent and porcine systems. By integrating magnetic control, reconfigurable architecture, and stimulus-triggered disassembly, Dynabots unite navigational precision with tissue permeability, providing a versatile platform for adaptive and deep-tissue drug delivery.

bioengineering↗

bioRxiv2026

A GPX4 phosphorylation switch by FGFR1 guards against ferroptosis

Ferroptosis is driven by lipid peroxidation, yet the mechanisms by which cells rapidly adjust their sensitivity to ferroptosis in response to extracellular cues remain elusive. We identify a direct phosphorylation switch controlling the activity of glutathione peroxidase 4 (GPX4), the core ferroptosis regulator. The receptor tyrosine kinase FGFR1 directly binds and phosphorylates GPX4 at Tyr180/Tyr196 in a kinase-dependent manner, requiring its Tyr730 as a docking site. This phosphorylation enhances GPX4s catalytic activity and suppresses ferroptosis. In cardiac ischemia/reperfusion injury, the FGFR1-GPX4 axis is suppressed, and a selective FGFR1 agonist (FGF-1{Delta}NT) reactivates it to protect against ferroptosis-mediated damage. Critically, a phosphorylation-deficient GPX4 knock-in mouse exhibits hypersensitivity to injury and non-responsive to this agonist, proving that GPX4 phosphorylation is essential. Our findings reveal a rapid mechanism for regulating ferroptosis via GPX4 tyrosine phosphorylation, directly linking receptor tyrosine kinase signaling to ferroptosis, and offering new strategies for treating ischemic-and other ferroptosis-associated diseases.

Cell Biology↗

bioRxiv2026

Repetition Selectively Reconfigures Offset-Defined Temporal Integration in Auditory Cortex

Auditory perception requires integrating sound over time, but whether cortical integration windows are fixed or adaptively shaped by recent sensory history remains unclear. Because auditory offset responses are shaped by the temporal structure preceding sound termination, they provide a readout of offset-defined temporal integration. Here, we recorded single-unit activity in awake rat auditory cortex while presenting 512-ms click trains with inter-click intervals of 1, 2, 4, 8 or 16 ms. Each stimulus was repeated ten times, allowing repetition number to index increasing adaptation. Across 271 offset-responsive neurons, repetition strongly compressed the maximal ICI capable of evoking a significant offset response and produced a smaller population-level shift in preferred ICI. These preferred-ICI changes were heterogeneous across neurons, with bidirectional shifts at the single-neuron level. In contrast, the effective temporal window measured with irregular-regular click trains remained stable at the population level, despite neuron-level variability. AAF and A1 further showed distinct repetition-dependent tuning profiles. These findings suggest that adaptation selectively reconfigures ICI-based offset tuning while preserving a population-level local regularity window, revealing flexible and stable components of cortical temporal integration.

neuroscience↗

bioRxiv2026

Chromosomal rearrangements 1 and sequence similarity drivepreferential allosyndetic introgression from a wild relative into wheat

Recombination in polyploid genomes is generally constrained to homologous or homoeologous chromosomes; however, how chromosomal rearrangements influence recombination between chromosomes remains unclear. Here, we demonstrate that large-scale chromosomal rearrangements in the wild relatives of wheat are associated with recombination involving non-homoeologous chromosomes or arms during alien gene introgression under conditions that permit homoeologous recombination mediated by ph1b. Using a wheat chromosome 6A monosomic-induced 6AS*6CL Robertsonian translocation combined with ph1b-mediated recombination, we generated 17 independent recombinants carrying a new stem rust resistance gene, Sr69, from Aegilops caudata chromosome arm 6CL. Unexpectedly, 94.1% (16 of 17) of recombinants resulted from exchanges with wheat group-7 chromosomes rather than with the homoeologous group-6 chromosome. Comparative sequence- and marker-based analyses identified a 67-Mb rearranged interval on Ae. caudata 6CL that corresponds to telomeric regions of the long arms of wheat group-7 chromosomes. Sequence similarity within this interval was quantitatively associated with recombination frequency, with higher similarity corresponding to more frequent translocations. Physical and optical mapping showed that recombination within the rearranged interval generated compensating 7A/6C, 7B/6C, and 7D/6C translocations, whereas recombination outside this region produced non-compensating 6A/6C exchanges. An independent case involving the powdery mildew resistance gene Pm7C showed a similar correspondence between a rearranged 7CL region and preferential introgression into wheat 7DS. Together, these results indicate that ph1b-mediated recombination involving structurally altered chromosomes is driven by local chromosomal structure and sequence similarity rather than strict homoeologous group identity. This provides a mechanistic basis for harnessing untapped beneficial genes from structurally rearranged alien genomes. Significance StatementAlien gene introgression is a powerful strategy for wheat improvement, typically relying on ph1b-mediated recombination between homoeologous chromosomes. The genomic basis and outcomes of introgression from structurally rearranged alien chromosomes remain unclear. Here, we show that ph1b-induced recombination can efficiently target wheat-allosyntenic blocks in rearranged alien genomes, preferentially transferring genes from structurally altered alien segments into their syntenic regions on wheat chromosomes of different homoeologous groups. Crossover formation is governed by extended sequence similarity within corresponding intervals rather than strict collinearity across entire homoeologous chromosomes. As many wild species exhibit extensive genome rearrangement, these findings and methodologies expand access to underexploited genetic diversity embedded within highly rearranged wild genomes for wheat improvement.

genetics↗

bioRxiv2026

Next-Generation Soybean Haplotype Map as A Genomic Resource for Enhanced Trait Discovery and Functional Analysis

We present a global soybean haplotype map generated from whole-genome sequencing of 1,278 Glycine max and Glycine soja accessions, comprising 11.37 million SNPs and 2.05 million short insertions and deletions. This map (GmHapMap-II) captures unprecedented worldwide genetic diversity, reflecting the broad extent of the global soybean gene pool. Population structure analyses revealed six geographically distinct subpopulations that affected the linkage and shaped the recombination. The haplotype variation map was used to identify novel genomic regions associated with crude protein content on chromosome 15 that were not detected by a lower SNP density array. LD-based haplotype analysis revealed a superior haplotype for crude protein content. The constructed haplotype map enabled detailed characterization of haplotype diversity and copy number polymorphism at the SCN-associated rhg-1 and Rhg-4 loci, revealing both novel haplotype structures and germplasm lines with elevated CNV relative to previously characterized genotypes. We employed the HapMap matrix for a multi-class variations ML-based genomic prediction approach to predict phenotypes for SCN and catalogued the gene-centric haplotypes in a user-friendly database. The analysis revealed the extent of deleterious alleles present in the soybean germplasm and how breeders have deployed beneficial alleles and purged deleterious ones. The haplotype map will serve as a major genomic resource for trait-based mapping, enhancing efforts in the genomics-enabled development of improved cultivars.

genomics↗

bioRxiv2026

Existence of Causation without Correlation in Transcriptional Networks

It is commonly assumed that lack of correlation is evidence for lack of causal relationship. Here, however we show that in transcriptional networks, causal linkages can exist in the absence of correlation. We find that a substantial proportion of transcribed genes in yeast and in mouse, show evidence of state-dependent (nonlinear) and temporally coordinated dynamics in their expression patterns (65-77%). Using a test that accommodates this fact, we uncover strong causal relationships that are invisible to correlation-based analyses for both yeast and mouse models. Specifically, for yeast we detect uncorrelated causal relationships for the transcriptional regulators WHI5 and YHP1, and can verify these relationships experimentally. These genes reside at important checkpoints in the cell cycle where multiple signals are integrated at single nodes, giving rise to causal relationships, that despite being uncorrelated, can be accurately detected (71-78%) using a nonlinear causality test.

systems biology↗

bioRxiv2026

A Bear-Specific Coding Exon in TMEM41B Is Associated with Cold Adaptation

AbstractBears exhibit an unusual form of hibernation in which core body temperature remains relatively high despite profound suppression of whole-body metabolism. How such a warm yet hypometabolic state is achieved remains poorly understood. Here, through integrative analysis of 238 RNA-seq datasets spanning seven species, we identify transmembrane protein 41B (TMEM41B) as an evolutionarily conserved factor associated with thermogenic capacity. Loss of Tmem41b in mice and Drosophila results in severe cold intolerance, whereas its overexpression enhances thermogenic performance, supporting a conserved role in heat production. Comparative genomic analyses reveal a bear-specific 51-amino acid N-terminal extension in TMEM41B, arising from a 5' untranslated region mutation that converts a premature stop codon into coding sequence. Interactome profiling indicates that this bear-specific isoform differs from the canonical TMEM41B in its protein interaction landscape, including reduced association with components of mitochondria-associated endoplasmic reticulum membranes such as voltage-dependent anion-selective channel protein 1 (VDAC1). Consistent with this altered interaction profile, the extended isoform is associated with reduced mitochondrial oxidative activity. Functional analyses further suggest that the 51- amino acid extension modulates multiple cellular programs, including suppression of oxidative phosphorylation and myogenic differentiation alongside activation of osteogenic pathways, collectively biasing cells toward a hypometabolic state. Notably, expression of the polar bear TMEM41B isoform in mice induces a torpor-like phenotype under fasting conditions. Together, these findings identify TMEM41B as a conserved regulator of thermogenic capacity and suggest that evolutionary modification of its N terminus may contribute to metabolic suppression and energy conservation during bear hibernation.

evolutionary biology↗

bioRxiv2025

Temporal boundary gating of auditory sensitivity

Perception unfolds over time, but whether continuous sounds are sampled with uniform sensitivity is unknown. We combine human psychophysics, EEG and rodent neurophysiology to show that local auditory change detection is strongly gated by stimulus boundaries. In humans, brief perturbations inserted at different temporal positions within 0.5-1-s tones revealed an inverted U-shaped sensitivity profile: detection was attenuated near sound onset and offset and maximal mid-epoch, with EEG change responses showing a closely matching dependence on change timing. Electrocorticography in awake rats exhibited homologous temporal weighting, and analogous profiles for amplitude changes and visual motion demonstrated cross-feature and cross-modal generality. To uncover circuit mechanisms, we recorded single units along the inferior colliculus-medial geniculate body-auditory cortex pathway together with laminar local field potentials in A1. Onset-locked suppression of change responses emerged in midbrain and was progressively amplified in thalamus and cortex, whereas the full start-end profile was expressed in granular-layer alpha-gamma power. A simple biophysically grounded model in which onset responses saturate and cortical populations integrate over finite temporal windows recapitulates this pattern, explaining how stimulus boundaries disrupt prospective and retrospective integration and thereby degrade change detection near the beginning and end of sounds.

neuroscience↗

bioRxiv2025

Genome assembly and population genomic analysis of Aegilops caudata uncover a rich source for disease and insect pest resistance for wheat improvement

Aegilops caudata L. is a rich source of resistance genes to major wheat pathogens and pests, yet its complex genome structure and lack of a reference sequence have hindered genetic analysis, gene discovery, and introgression. Here, we report a high-quality genome sequence assembly of Ae. caudata accession S740-69, integrated with optical mapping to precisely delineate introgressed segments from structurally altered genomic regions in wheat-Ae. caudata translocation lines carrying a novel stem rust resistance gene. Resequencing and phenotyping of 95 diverse accessions, coupled with k-mer-based association mapping, enabled population-level identification of several novel loci for resistance to wheat pests and diseases, such as greenbug and stem rust. Virus-induced gene silencing confirmed Aecau6C01G127270 (SrAect1) as the first functionally characterized stem rust resistance gene from Ae. caudata. This new genomic framework provides a foundation for systematic mining of resistance genes in this species and their efficient introgression into wheat.

genomics↗

bioRxiv2025

Echoes as Signal, Not Noise: Reverberation Sharpens Sensitivity to Temporal Structure

Sensitivity to temporal structure is fundamental to hearing, yet how natural reverberation shapes this sensitivity is unclear. Here we identify echo-facilitated temporal sensitivity (EFTS), a principle whereby the auditory system exploits echoes to selectively enhance responses to rapid temporal changes. Using transitional click trains with subtle inter-click-interval (ICI) shifts, we first show that increasing echo strength systematically enlarges the sound-level step at ICI transitions in both recorded and simulated stimuli, sharpening the physical boundary between segments of distinct temporal structure. In humans, psychophysical detection of ICI changes improves monotonically with echo level in both simulated and real free-field environments, while a late EEG change response scales with echo strength as onset responses remain comparatively stable. In awake rats, electrocorticography over auditory cortex reveals parallel echo-dependent enhancement of transition-evoked activity. Single units exhibit echo-level-dependent amplification of change-related firing and improved neurometric discriminability. Laminar local field potential and current source density analyses further show that echo-dependent divergence emerges first in granular and infragranular layers before propagating to supragranular cortex, consistent with thalamocortical drive followed by intracortical amplification. Together, these findings establish EFTS as a cross-species mechanism that reframes echoes as structured signals the brain uses to sharpen temporal integration in everyday listening.

neuroscience↗