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Biology subjects

Jiang, J.

Publications and source records attributed to Jiang, J..

At least 55 records · Page 3Linked to original sources

A low-dimensional transcriptional code enables decoding of BMP/TGFβ signaling from single-cell transcriptomes

Cells interpret complex extracellular environments through signaling pathways that compress diverse ligand inputs into a limited set of intracellular mediators. How this information is encoded in transcriptional responses, and whether it can be decoded to infer the original signaling environment, remains unclear. Here, we systematically map BMP/TGF{beta} transcriptional responses using single-cell RNA sequencing across 48 ligand-concentration conditions, generating a multi-ligand dose-response atlas. We find that, for each ligand, transcriptional responses collapse onto a one-dimensional, highly coordinated program in which concentration modulates response amplitude without altering gene identity. Across ligands, we find a small number of distinct, ligand-dependent transcriptional programs. We leverage this structured encoding to define a quantitative perception score that captures pathway activity at single-cell resolution. Finally, we train a machine learning model to decode extracellular ligand concentrations from single-cell transcriptomes. The model further generalizes to in vivo intestinal epithelium, where it reconstructs the spatial BMP gradient profile. Together, these results reveal a low-dimensional transcriptional code in BMP/TGF{beta} signaling that constrains cellular responses and enables quantitative inference of extracellular signaling environments from gene expression.

systems biology↗

TMEM106B C-terminal fragments drive nucleocytoplasmic transport failure and TDP-43 mislocalization in the aging human brain

TMEM106B is a lysosomal membrane protein and major genetic modifier of multiple neurodegenerative diseases, including frontotemporal lobar degeneration, Alzheimers disease, and amyotrophic lateral sclerosis. Proteolytically generated C-terminal fragments of TMEM106B assemble into amyloid fibrils that accumulate in the brains of individuals with neurodegenerative disease and in cognitively normal aged adults, yet how these fibrils produce neuronal dysfunction has remained unclear. Here, we show that cytosolic and lysosome-directed TMEM106B C-terminal fragments (CTF and gCTF) form detergent-insoluble amyloid aggregates, drive redistribution of endogenous TDP-43 from the nucleus to the cytoplasm, and accelerate neuronal death. Unbiased proximity proteomics identified the inner nuclear membrane LAP1-TorsinA axis as a fragment-specific interactome, and co-immunoprecipitation confirmed a direct physical interaction between gCTF and LAP1 that was not observed with full-length TMEM106B. Fragment expression disrupted Lamin B1 organization, mislocalized the nuclear import machinery KPNB1 and RanGAP1, and impaired importin-dependent nuclear transport in primary cortical neurons. Critically, neurons harboring endogenous TMEM106B fibrillar pathology in aged human frontal cortex exhibited the same phenotypes, namely disrupted Lamin B1 and LAP1 localization and cytoplasmic redistribution of TDP-43, whereas fibril-negative neurons from the same cases and younger control tissue retained intact nuclear envelope organization. These findings define TMEM106B proteinopathy as an upstream driver of nuclear envelope disruption and nucleocytoplasmic transport failure, linking a widespread feature of brain aging to a central mechanism of neurodegeneration.

neuroscience↗

CAD variants act through ox-LDL-induced enhancer remodelling to alter VSMC gene programmes

BackgroundVascular smooth muscle cells (VSMCs) play a central role in atherosclerotic coronary artery disease (CAD). Oxidised low-density lipoprotein cholesterol (ox-LDL) induces VSMCs dysfunction but the underlying molecular mechanisms are unclear. CAD genome-wide association studies (GWAS) have identified hundreds of disease-associated loci but their biological roles remain poorly defined. We hypothesised that ox-LDL drives pro-atherogenic changes in VSMCs by altering gene regulatory programs involving causal CAD variants. MethodsEx-vivo human coronary VSMCs were exposed to ox-LDL and profiled using RNA-seq, ATAC-seq, and H3K27ac ChIPmentation. Enhancer-gene links were inferred by integrating these data with Hi-C using the Activity-by-Contact (ABC) model. Variant effect predictions were done using AlphaGenome and key target genes functionally tested by CRISPR/Cas9 knockout. ResultsOx-LDL induced widespread transcriptional reprogramming in coronary VSMCs, with 1,487 upregulated and 1,864 downregulated genes (FDR < 0.05). Single-cell RNA-seq meta-analysis demonstrated that ox-LDL-associated programmes enriched in pro-inflammatory and synthetic-inflammatory VSMC clusters in vivo. ATAC-seq identified [~]22k differentially accessible regions following ox-LDL exposure (FDR < 0.05). Integration of ATAC-seq, H3K27ac, and Hi-C using the ABC framework showed that ox-LDL-driven chromatin remodelling was concentrated at distal enhancers, which linked to 2,008 differentially expressed genes via 4,243 peak-gene connections. ABC enhancers were significantly enriched for CAD variants compared with non-vascular disease controls, with stronger enrichment in dynamically accessible enhancers. AlphaGenome predicted larger regulatory effects of prioritised CAD variants in smooth muscle cells than in a non-vascular comparator, and motif analyses indicated allele-dependent transcription factor binding at prioritised enhancer variants. Locus-level prioritisation nominated candidate enhancer-mediated mechanisms at the SPECC1L and MAP1S loci, and CRISPR knockout of the target genes GUCD1 and BACH1 rescued ox-LDL-induced growth arrest/senescence phenotypes in human coronary artery VSMCs. ConclusionsOur unbiased multi-omics framework shows that ox-LDL rewires VSMC regulatory programmes that influence CAD genetic risk. Enhancer-gene mapping refines effector-gene assignment at CAD loci and prioritises regulatory targets in coronary VSMCs.

genomics↗

OneGenomeRice (OGR): A Genomic Foundation Model for Rice

The transition of genomics to a predictive intelligence discipline is driven by the advent of genomic foundation models. While substantial progress has been observed in all-life and human-centric models, plant species, particularly for the staple crops, remains hindered by a lack of models. Here we introduce OneGenome-Rice (OGR), a rice (Oryza sativa) genomic foundation model pre-trained on a genomic dataset comprising 422 high-quality genomes of cultivated and wild rice. OGR is engineered upon a Mixture of Experts (MoE) transformer architecture with 1.25-billion parameters and supports an ultra-long context window of up to 1 million base (Mb) pairs at single-nucleotide resolution. A comprehensive benchmark demonstrated that OGR significantly outperforms existing state-of-the-art multi-plant or all-life genome models in 11 categories (e.g. motif identification, sweep detection, etc). We further demonstrated the utility of OGR in several downstream applications, such as indica-japonica subspecies introgression analysis, identification of agronomy trait-associated functional loci and prediction of gene expression from DNA sequences. These results establish OGR as a promising foundational computational infrastructure for rice functional genomics and precision breeding. The OGR and its fine-tuned models, including pretrained weights, training code and the rice genomic benchmark suit, have been fully opened.

genomics↗

Spatiotemporal profiling reveals the role of inflammatory niche in driving prostate cancer

Prostate cancer (PCa) is a lethal malignancy that displays profound resistance to immune checkpoint blockade (ICB), via mechanisms that are poorly understood. Here, we investigate the causes of CD8 T cell exhaustion and mechanisms of tumor progression in a PCa animal model, by single cell and spatial profiling, along a time course, following orthotopic transplantation of RB1/TP53/PTEN-deficient mouse organoids, competent to express neoantigens. The resulting tumors were castration resistant, consisting of largely basal and L2 malignant cells with upregulated inflammatory gene programs, and a specific spatial distribution of macrophages, cancer associated fibroblast (CAF) subtypes, and CD8 T-cells that was not previously reported. Using Zman-seq, we demonstrate that the effector function of tumor-infiltrating CD8 T cells was rapidly impaired as early as 24hrs after their infiltration, likely driven by signals from proinflammatory macrophages, Ccl2-Jak2+ inflammatory CAFs, and malignant basal cells, thus driving resistance to ICB. Interestingly, dual blockade of JAK1/2 and PD1 induced potent anti-tumor effects in tumor epithelial cells, decreased malignant epithelial cells and pro-inflammatory macrophages, and increased the proportion of normal (Pi16+) fibroblasts in the TME. Our results underscore the therapeutic potential of targeting JAK1/2 to enhance the efficacy of ICB, providing a rationale for clinical investigation of this combination in PCa.

cancer biology↗

Frontoparietal Hub Connectivity Integrates Information from Multiple Sources

Frontoparietal connector hubs are thought to support information integration across the brain, but this role has largely been inferred from static connectivity, leaving unclear how computational processes shape inter-regional connectivity during behavior. Here, we address this question using a model-based functional connectivity approach in human fMRI data. Thirty-Eight participants (males and females) performed a task requiring the integration of sensory evidence with an internally maintained state belief to guide behavior. We developed a computational model that combines these information sources into an integrated representation and generates distinct variables at successive stages of integration: uncertainty before choice (entropy), the inferred task representation guiding action (task belief), and feedback-driven updating (task inference error). We then tested how these variables modulate the connectivity of frontoparietal connector hubs. Entropy increased coupling between hubs and regions encoding task-relevant inputs and outputs during cue processing, suggesting enhanced communication under uncertainty. During task selection, task belief selectively modulated hub connectivity with motor regions according to the selected task. During feedback, task inference errors increased coupling with regions supporting task-relevant inputs and internal state, while reducing coupling with motor regions, consistent with updating internal representations. Together, our findings show that frontoparietal connector hubs implement integrative control by using an integrated representation to generate distinct computational signals that selectively and dynamically reconfigure inter-regional communication. SignificanceFlexible behavior depends on combining different kinds of information, but how the brain coordinates this integration remains unclear. The frontoparietal cortex is well positioned to support this process because it is broadly connected with many other systems. Here, we combined a computational model with functional MRI to test how integrating information changes patterns of functional connectivity. We find that a common set of signals is associated with dissociable changes in how frontoparietal regions couple with systems involved in perception, action, and internal updating. These findings reveal that integration generates multiple control signals that dynamically reconfigure brain-wide interactions to support goal-directed behavior.

neuroscience↗

Mapping Slow Speckle Dynamics to Probe Cellular Metabolic Activity In Vivo using Laser Speckle Contrast Imaging

SignificanceLaser speckle contrast imaging (LSCI) is widely used to measure blood flow, but speckle fluctuations may also encode biologically meaningful dynamics beyond perfusion. Foundational studies in dynamic light scattering (DLS) and micro-optical coherence tomography (OCT) have also demonstrated that slow coherent signal fluctuations can arise from energy-dependent intracellular motion in in vitro and ex vivo systems. Building upon these advances, recent work has shown that LSCI has the potential to detect slow speckle dynamics (SSD) correlated with cellular dynamics in vivo. However, the biophysical mechanisms underlying SSD in intact brain tissues remain insufficiently validated. Establishing a mechanistic bridge from controlled ex vivo and in vitro conditions to in vivo brain measurements is critical for translating speckle-based imaging beyond perfusion measurements to enable label-free assessment of cellular and metabolic activity in disease models. AimThe objective of this study is to investigate the biophysical origin of the SSD in vivo and evaluate its sensitivity to intracellular metabolic activity in brain tissue. ApproachWe utilize an epi-illumination LSCI system to measure speckle contrast as a function of camera exposure time and extract characteristic decorrelation time constants. SSD was investigated in acute mouse brain slices, where blood flow is absent, to eliminate vascular confounds. Cellular metabolism was systematically modulated using 2-deoxyglucose and glucose. Complementary in vivo measurements were performed to reveal SSDs response to hyperoxia and normoxia after ischemic stroke. ResultsSSD signals persisted in acute brain slices in the absence of blood flow. Inhibition of glycolysis significantly reduced SSD, while restoration of metabolic substrates partially recovered the signal. In in vivo measurements, SSD increased during hyperoxia compared to normoxia after ischemic stroke, suggesting increased oxygen-supported cellular metabolic activity. ConclusionsThese results indicate that SSD is sensitive to energy-dependent cellular processes closely tied to metabolic activity. SSD represents a previously uncharacterized, label-free in vivo optical contrast that enables assessment of cellular metabolic activity as well as vascular dynamics. This work establishes a mechanistic foundation for using SSD as a general optical marker of cellular viability in in vivo measurements.

neuroscience↗

Pi16+ fibroblast-derived Csf1 shapes skin topography

Peptidase inhibitor 16 (Pi16)-expressing fibroblasts are found across tissues and species, but their functional role is unclear. As fibroblasts and macrophages have been proposed to exist in a reciprocal circuit, we hypothesized Pi16+ fibroblasts may regulate macrophage homeostasis. Flow cytometry revealed [~]80% of skin fibroblasts express Pi16, leading us to investigate the role of these cells in maintaining a macrophage niche in this tissue. We generated an in vivo system where fibroblast-derived Colony Stimulating Factor 1 (Csf1) was constitutively eliminated in Pi16+ fibroblasts by crossing animals with a Csf1fl/fl allele to mice in which the gene Pi16 drives an IresCre cassette. Deletion of Csf1 in Pi16+ fibroblasts resulted in significant diminishment of CD64+ and CD11c+ macrophages alongside expansion of PDPN+YFP+ fibroblasts. Alterations in cell population dynamics coincided with thickening of both the dermis and fascial compartments of the skin. Deletion of Csf1 in Pi16+ fibroblasts delayed early wound healing in a unsplinted mouse model. Loss of PI16+ fibroblasts was observed in individuals with limited (lSSc) and diffuse (dSSc) systemic Scleroderma compared to healthy controls. These findings suggest that loss of Csf1 in Pi16+ fibroblasts elicit changes in the population dynamics of skin macrophages and modifications to tissue architecture.

immunology↗

Integrated analysis of stemness-associated immune modulatory circuits in squamous cell carcinomas

Emerging evidence indicates that a subset of cancer cells enriched for stemness-related gene signatures possess distinct immunomodulatory capacities, enabling these tumor-initiating stem cells (tSCs) to more effectively evade or resist anti-tumor immunity. Despite these advances, the tSC-specific molecular circuits orchestrating their specialized immune privilege program are not well defined. Here, in squamous cell carcinomas of the skin and oral cavity, we comprehensively delineate the unique immune-evasive properties of tSCs and dissect the transcriptional regulation shaping their immunomodulatory programs. By integrating transcriptome profiling, chromatin landscape mapping, genetic perturbation, and single-cell RNA sequencing, we found that the tSC-specific immune program is broadly governed by SOX2, a stemness-associated transcription factor. We demonstrate that SOX2 enables tSCs to sustain immature tumor-associated neutrophils (TANs) and subsequently trigger these myeloid cells to foster the development of tumor-associated macrophages (TAMs). This SOX2-directed tSC-TAN-TAM axis establishes a localized immunosuppressive niche for protecting tSC. SIGNIFICANCEHere, we uncover SOX2 as a master regulator that orchestrates conserved immune modulatory circuits in tSCs to sustain pro-tumor myeloid cell states. These findings place tSCs at the apex of immune landscape remodeling, asserting a central role of stemness-associated program in organizing the immunosuppressive tumor microenvironment.

cancer biology↗

Suppression of de novo lipogenesis and dietary PUFA supplementation inhibit prostate cancer progression

Prostate cancer progression is characterized by dysregulated lipid metabolism, with activation of fatty acid synthase (FASN), the rate-limiting step in de novo lipogenesis (DNL), resulting in significant accumulation of saturated lipids. Here, we show that pharmacologic FASN inhibition creates a metabolic state that increases reliance on exogenous polyunsaturated fatty acids (PUFAs). Inhibition of FASN profoundly alters membrane phospholipid composition, driving compensatory incorporation of PUFAs into membrane phospholipids, thus increasing susceptibility to lipid peroxidation and oxidative damage. Combined FASN inhibition and PUFA exposure induce mitochondrial hyperpolarization and enhance lipid peroxidation in both hormone-sensitive and castration-resistant prostate cancer models, resulting in increased reactive oxygen species production, ferroptosis, as well as apoptosis. Marked inhibition of growth in castration-resistant human and murine prostate cancer organoids is achieved ex vivo. In genetically engineered, DNL-reliant Hi-Myc mice, a diet enriched in PUFAs significantly inhibited invasive carcinoma compared to a saturated fat-enriched diet. Thus, environmental PUFAs modulate and enhance the therapeutic efficacy of FASN-targeted strategies. These findings set the stage for pharmacologic and dietary intervention in prostate cancer patients.

cancer biology↗

Unified Multi-Cohort Harmonisation and Normative Modelling of Neuroimaging Data via Hierarchical GAMLSS

Large-scale neuroimaging studies increasingly pool data across multiple cohorts, scanners, and acquisition protocols, introducing technical between-cohort variation that must be addressed before meaningful biological inference can be drawn. Existing harmonisation methods, particularly ComBat-based approaches, have been widely adopted for this purpose. However, they remain limited by Gaussian assumptions and by their focus on location or location-scale correction. In this study, we propose a unified hierarchical Generalised Additive Models for Location, Scale and Shape (GAMLSS) framework for multi-cohort harmonisation and normative modelling of structural neuroimaging data. The framework models cohort effects directly within all fitted distributional parameters, accommodates any parametric family for which exact inverse mapping is available, and returns harmonised values on the original measurement scale through centile-based quantile mapping. Normative deviation scores are obtained as a direct by-product of the same fitted model, enabling harmonisation and normative inference to be conducted jointly. The method was evaluated in a pooled longitudinal dataset comprising 88,126 observations across 237 structural neuroimaging features from six cohorts spanning childhood to late life: ABCD, IMAGEN, NCANDA, LIFE, UK Biobank, and MAS. Harmonisation performance was compared with ComBat, ComBat-GAM, and ComBat-LS using complementary criteria assessing data retention, residual batch effects, preservation of age-related and sex-related biological signal, and coherence of post-harmonisation lifespan trajectories. GAMLSS achieved near-complete removal of residual cohort effects, retained almost all valid observations post-harmonisation, and showed the strongest overall preservation of biological signal across validation metrics. In particular, it better preserved biologically plausible age trajectories for distributionally complex features such as white matter hypointensity volume, while simultaneously providing harmonised native-scale values and normative deviation scores within a single framework. These findings suggest that hierarchical GAMLSS offers a flexible and practical alternative to existing ComBat-based methods for large-scale neuroimaging harmonisation, particularly for features with non-Gaussian residual distributions and settings where cohort effects extend beyond differences in mean and variance.

neuroscience↗

Parallelised detection of bacteria viability using an electrode array and the Exeter Multiscope

Antimicrobial resistance remains a global existential threat. Given that antimicrobial therapy commonly starts before pathogen identification, rapid and scalable methods capable of determining effective antimicrobial compounds are needed. In this paper, we demonstrate a 2 x 2 array of parallelised microscopes that uses low numerical aperture (NA=0.25) detection optics and LED excitation to determine bacterial viability based on their fluorescence response to an electrical stimulus. Following a 2-hour incubation, the fluorescent viability readout requires less than one minute. We use K-means clustering to classify pixels in a time lapse sequence of widefield fluorescence images and extract changes seen within bacterial clusters. We demonstrate sufficient sensitivity to measure fluorescence changes after electrical stimulation in a bacterial monolayer. To capture these subtle fluorescence changes at high signal-to-background ratios, we place a limit on the minimum optical density of the bacterial sample. This novel approach is scalable to 96-well formats using a suitable consumable electrode array.

microbiology↗

A Novel Glycoproteomics Platform for High-Throughput Identification of Disease-Associated Glycoforms

Glycosylation is a critical post-translational modification, and its aberrant forms are potent disease biomarkers; however, the comprehensive, site-specific identification of all glycosites and glycoforms across an entire proteome remains prohibitively slow and computationally demanding. To address this bottleneck and accelerate biomarker discovery, we introduce the Glycoproteomics Data Analysis Software (GDAS), a novel, high-throughput platform designed to provide confident, proteome-scale identification of disease-specific glycoforms. GDAS streamlines the analysis through a core, multi-step workflow: it initially employs an ultrafast open search (e.g., MSFragger-Glyco) on mass spectrometry data to rapidly screen and statistically reduce the vast proteome database to a manageable subset of significantly regulated glycoproteins, conserving computational resources for subsequent, in-depth, targeted N- and O-glycosylation analysis using specialized tools (e.g., GlycReSoft and O-Pair). Furthermore, a unique Final Analysis Module utilizes an advanced statistical and machine learning pipeline (incorporating Bootstrap/Bayesian methods, XGBoost, and Random Forest) to integrate quantitative results and generate a robust, comprehensive glycosylation score. We demonstrate GDASs power to recognize biologically relevant glycosylation changes in targeted proteins by validating it using published Alzheimers disease data. GDAS can be downloaded from https://github.com/yang-lab/GDAS. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=92 SRC="FIGDIR/small/708406v1_ufig1.gif" ALT="Figure 1"> View larger version (19K): org.highwire.dtl.DTLVardef@189b270org.highwire.dtl.DTLVardef@1221045org.highwire.dtl.DTLVardef@15a3f50org.highwire.dtl.DTLVardef@1f2d43f_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗

Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

PurposeEndothelial cell (EC) activation, characterized by upregulation of adhesion molecules that drive monocyte recruitment, contributes to plaque progression while also providing an opportunity for targeted therapeutic delivery. Leveraging the cell membrane cloaking strategy, we recently developed a monocyte-mimetic nanoparticle (MoNP) platform that exploits the natural inflammatory tropism of monocytes for site-specific delivery to atherosclerotic vessels. Recognizing that integrin activation is a key determinant of monocyte adhesion to ECs, this study investigates whether pre-activating integrins on MoNP enhances their binding affinity and accumulation at atherosclerotic lesions. MethodsMouse bone marrow-derived monocytes were pretreated with CCL2 or Mn2{square} to activate membrane integrins. Isolated monocyte plasma membranes were cloaked onto fluorescently labeled polymeric cores to generate integrin-activated MoNPs (IA@MoNPs). The targeting capability of IA@MoNPs toward endothelial ligands, inflamed ECs, and atherosclerotic lesions was evaluated using in vitro and in vivo models. ResultsIA@MoNPs exhibited markedly enhanced binding to VCAM1, the primary endothelial ligand mediating integrin-dependent monocyte adhesion, and significantly increased uptake by ECs under atheroprone conditions compared to standard MoNPs. In vivo, IA@MoNPs demonstrated enhanced accumulation in atherosclerotic arteries without increasing nonspecific binding, and blocking {beta}1-integrins on IA@MoNPs abolished this targeting effect. Importantly, integrin activation on IA@MoNPs did not compromise circulatory stability or induce immune or organ toxicity. ConclusionIntegrin activation represents a simple yet effective strategy to enhance MoNP targeting to inflamed ECs and atherosclerotic lesions. This mechanism-driven approach improves targeting performance while maintaining specificity and safety, advancing the translational potential of the biomimetic nanomedicine platform for atherosclerosis.

bioengineering↗

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↗

Distributed neural signatures of discomfort induced by transcranial magnetic stimulation

Transcranial magnetic stimulation (TMS) is a cornerstone tool for causal inference in human brain function and an increasingly used neuromodulation therapy, yet it induces well-recognized discomfort that may systematically bias measured outcomes. Despite its ubiquity, a critical gap remains in understanding how TMS-induced discomfort is represented across the brain and to what extent it contributes to TMS-evoked neural responses. Using concurrent TMS-fMRI across 11 cortical targets, we collected an unprecedented dataset (165 participants; 1,535 runs) spanning healthy participants and those with elevated affective symptoms. Cross-validated multivariate modeling revealed that TMS-induced discomfort engages distributed cortical and subcortical regions across sensorimotor, attentional, default mode, and limbic networks, with both shared and group-specific patterns. Discomfort-related activity accounted for approximately 12% and 25% of TMS-evoked responses in healthy and elevated-symptom groups, respectively, and varied systematically across stimulating sites. These findings identify TMS-induced discomfort as a substantial and previously under-characterized component of TMS-evoked neural responses, underscoring the need to explicitly measure and model it. By providing a whole-brain map of regional contributions associated with TMS-induced discomfort and an analytic framework to dissociate direct neuromodulatory effects from discomfort-related responses, this work improves the interpretability of TMS-evoked signals and supports more rigorous causal inference and therapeutic applications.

neuroscience↗

CsFDL1-CsFTL3 complex represses CsFTL3 via negative feedback to fine-tune flowering in Chrysanthemum seticuspe

In many flowering plants, the transition from vegetative growth to reproductive development is regulated by seasonal changes in photoperiod. Under inductive photoperiods, leaves produce the florigen FT (FLOWERING LOCUS T), which is transported to the shoot apex to promote flowering. The photoperiod is known to have a major effect on the flowering of chrysanthemum. In the perennial short-day (SD) plant Chrysanthemum seticuspe, the expression of CsFTL3 (FT-like gene) does not increase immediately after shifting from long-day (LD) to SD conditions but gradually accumulates under continuous SD conditions, peaking during inflorescence development. However, the underlying mechanism remains elusive. We show that CsFDL1 (an ortholog of FD) and CsFTL3 exhibit a significant inverse expression pattern in leaves during the initial stage of short-day inductions. Furthermore, the expression of CsFTL3 is upregulated in the leaves of CsFDL1-knockdown transgenic lines. CsFDL1 is expressed in leaves and forms a complex with CsFTL3 to recognize several TCGA- and ACGT-containing motifs in the CsFTL3 promoter. The CsFTL3-CsFDL1 complex downregulates CsFTL3 expression, thereby preventing its excessive induction by SD signals and inhibiting precocious floral transition. This study reveals that CsFDL1 acts as a key early repressor in the photoperiodic flowering pathway of chrysanthemum leaf, mediating negative feedback regulation by forming a complex with CsFTL3 to achieve precise temporal control of short-day-dependent flowering responses.

plant biology↗

Disruption of the SYNGAP1 PDZ ligand motif accelerates differentiation of human iPSC-derived GABAergic neurons

SYNGAP1 haploinsufficiency is a leading genetic cause of neurodevelopmental disorders (NDD), including intellectual disability and epileptic encephalopathy. While most studies on SYNGAP1 function have focused on glutamatergic neurons, its role in GABAergic neurons and during early neuronal development is unclear. Using human iPSC-derived GABAergic neurons, we demonstrate that SYNGAP1 haploinsufficiency accelerates neuronal maturation, characterized by increased dendritic length, synaptic density, and maturation of synaptic structures. Disruption of the isoform-specific SYNGAP1 PDZ binding motif reproduces these phenotypes, highlighting the critical role of PDZ-mediated interactions in regulating GABAergic neuronal differentiation. Proteomic and phosphoproteomic analyses reveal significant dysregulation of synaptic proteins, RNA processing, and transcriptional control, with a significant increase in postsynaptic density proteins content. RNA-seq analysis suggest that the acceleration in neuronal differentiation starts few hours after neuronal induction setting a path to a faster neuronal and synapse maturation. These findings establish that SYNGAP1 acts as a key regulator of neuronal differentiation across both excitatory and inhibitory neurons. Our work underscores the importance of the SYNGAP1 PDZ ligand motif for normal neuronal development and suggests translational strategies targeting SYNGAP1 alpha1 isoform levels to mitigate SYNGAP1-related NDD.

neuroscience↗