Biology subjects

WANG, X.

Publications and source records attributed to WANG, X..

At least 19 recordsLinked to original sources

bioRxiv2026

Lysine acetylation-mediated regulation of ferredoxin and ferredoxin reductase redox-active proteins in Haloferax volcanii

Lysine acetylation is an evolutionarily conserved, post-translational modification that regulates metabolism and protein function, yet its role in archaeal electron transfer systems remains poorly understood. Here, we investigated lysine acetylation of the 2Fe-2S ferredoxin HvFdx (HVO_2995) and its flavin-dependent oxidoreductase HvFdR (HVO_2345) partner in the halophilic archaeon Haloferax volcanii. Genetic and biochemical analyses established HvFdx as an essential 2Fe-2S ferredoxin with a midpoint redox potential of -385 mV. Lysine acetylation of HvFdx was found to occur primarily at K119, a residue positioned near the [Fe-S] cluster interface, and to modulate electron transfer capacity without impacting Fe-S cluster incorporation, midpoint potential, or protein abundance. In contrast, HvFdR was found lysine acetylated at multiple sites in a manner consistent with a non-enzymatic mechanism that resulted in altered flavin binding, enzymatic activity, and thermal stability. Lysine acetylation of HvFdx was found to stimulate electron flow from HvFdR as measured by an anaerobic NADPH [->] HvFdR [->] HvFdx [->] DCIP assay. 3D structural modeling, proteomic, biochemical, and genetic assays suggest the haloarchaeal GNAT-family acetyltransferase homolog HVO_2874 as a candidate enzyme associated with HvFdx lysine acetylation and optimal growth of H. volcanii. Together, these findings demonstrate that lysine acetylation differentially regulates archaeal redox-active proteins and functions as an important mechanism coordinating redox metabolism in H. volcanii.

microbiology↗

bioRxiv2026

Discovery of A Multi-Class Antibiotic Potentiator Against Resistant Klebsiella pneumoniae

The rapid rise of multidrug-resistant (MDR) bacterial infections has severely limited treatment options, particularly for Gram-negative pathogens such as Klebsiella pneumoniae, a leading contributor to pneumonia, bloodstream, urinary tract, and surgical-site infections. One strategy to restore antibiotic efficacy is the use of resistance-mitigating agents (RMAs), compounds that re-sensitize bacteria to existing antibiotics without displaying independent antibacterial activity. Herein, we report the results of a high-throughput screen of a 3,200-compound fragment-based library against an MDR K. pneumoniae isolate in the presence of subinhibitory ciprofloxacin. This screen identified a tetrahydrocarbazole-containing compound, 1, as a ciprofloxacin potentiator. Subsequent structure-activity relationship studies yielded a difluorinated analog, compound 5, which potentiated multiple antibiotic classes in MDR K. pneumoniae, reducing MICs up to [≥]16 fold. Further testing demonstrated synergistic interactions between compound 5 and ciprofloxacin, ceftriaxone, cefoxitin, and tetracycline across four genetically diverse MDR K. pneumoniae strains. These findings suggest that tetrahydrocarbazole-containing compounds constitute a promising new class of RMAs with potential for future development as therapies against MDR K. pneumoniae infections.

microbiology↗

bioRxiv2026

Extracellular salicylic acid activates immune signaling through cell-surface receptors

Salicylic acid (SA) is a central immune hormone that accumulates in both intracellular and extracellular compartments during pathogen infection. While intracellular SA signaling is well established, whether extracellular SA (eSA) directly activates immune responses remains unknown. Here we show that eSA functions as an extracellular signal potentially perceived by the plasma membrane-localized lectin receptor kinases LecRK-I.8 and LecRK-VI.2 in Arabidopsis. The extracellular domains of both receptors bind SA with micromolar affinity, SA rapidly induces LecRK-I.8 phosphorylation, and the kinase activities of LecRK-I.8 and LecRK-VI.2 are required for downstream signaling. Moreover, mutagenesis of a computationally predicted binding pocket in LecRK-VI.2 abolishes SA binding and immune function, providing evidence for receptor-mediated perception. Genetic analyses further demonstrate that LecRK receptors are required for SA-induced resistance, transcriptional reprogramming, and phosphoproteomic responses. Together, these findings expand current models of SA signaling by revealing a potential receptor-mediated cell-surface perception mechanism for a classical immune hormone.

plant biology↗

bioRxiv2026

IL-36γ Drives Th9 cell Differentiation via IκBζ to Sustain Antitumor Immunity

Th9/Tc9 cells polarized with TGF-{beta} and IL-4 exhibit superior antitumor efficacy, prompting extensive efforts to optimize their differentiation protocols and augment therapeutic potency. In the current study, we identified IL-36{gamma} as a potent cytokine that synergizes with TGF-{beta} to robustly drive Th9 differentiation both in the presence and absence of IL-4. IL-36{gamma}-programmed Th9 cell subsets exhibited phenotypic and transcriptional profiles identical to classic Th9 cells. Mechanistically, IL-36{gamma} drove Th9 cell differentiation through amplifying key signaling pathways such as STAT6, STAT5, and NF-{kappa}B that are essential for classic Th9 programming. Notably, we uncovered a novel regulatory axis wherein IL-36{gamma} upregulates the transactivation factor I{kappa}B{zeta}, which directly governs Th9 lineage specification. In in adoptive cell therapy (ACT) models, IL-36{gamma}-polarized Th9 cell subsets demonstrated enhanced antitumor efficacy, attributable to their sustained persistence, reduced exhaustion markers and stem-like/memory properties. Collectively, this study elucidates a previously unrecognized I{kappa}B{zeta}-dependent mechanism underpinning Th9 differentiation and highlights the translational potential of IL-36{gamma}-engineered Th9 cells as a valuable ACT strategy for refractory tumors.

immunology↗

bioRxiv2026

Aberrant GPX4 processing reveals its critical roles in maintaining ROS homeostasis in Citrus

Glutathione peroxidases (GPXs) are key antioxidant enzymes that contribute to cellular redox homeostasis through reactive oxygen species (ROS) detoxification and modulation of redox signaling pathways. Although GPX functions have been studied in many annual plants, their roles in woody perennial crops remain poorly understood. Here, we characterized the GPX gene family in Citrus sinensis and investigated the function of CsGPX4, the closest homolog of Arabidopsis thaliana AtGPX8 because of its potential role in mediating oxidative stress signaling. Overexpression of CsGPX4 induced an oxidative stress phenotype that includes chlorosis, growth inhibition, cellular degeneration, and elevated intracellular ROS accumulation. Immunoblot and MALDI-TOF analyses showed that CsGPX4 overexpression resulted in a truncated proteoform, while the full length CsGPX4 was able to accumulate in Nicotiana benthamiana, indicating a species-specific post-translational truncation. The truncated CsGPX4 proteoform exhibited an altered subcellular localization shifting from cytoplasmic and nuclear localization to membrane-associated compartment in citrus cells. The truncated form of CsGPX4 had a reduced glutathione peroxidase activity compared to the full-length protein. Proteomic profiling suggested reprogramming of pathways associated with redox detoxification, cytoskeleton organization, hormone signaling, and stress responses. Our study identifies a citrus-specific post-translational regulatory mechanism that modulates CsGPX4 localization and enzymatic activity. This suggests that citrus may employ a species-specific proteolysis processing as a protective mechanism to maintain redox homeostasis during oxidative stress.

plant biology↗

bioRxiv2026

A spatial-temporal atlas of human islet pathophysiology identifies a size-dependent trajectory from compensation to decompensation

Type 2 diabetes (T2D) is characterized by progressive islet dysfunction, yet the transition from functional adaptation to failure remains poorly defined within the native tissue architecture. Using multiplex imaging mass cytometry, we systematically analyzed human pancreatic islets across a spectrum of non-diabetic (ND), prediabetic (PreD), and T2D donors, revealing that pathological remodeling is profoundly size-dependent. This remodeling is manifested as a coordinated evolution of subpopulation abundance, endocrine cell proportions, structural integrity, and protein expression profiles, revealing that islets of different sizes undergo divergent fates during disease progression. We identified a size-dependent vulnerability spectrum where medium-and large-sized islets (>100 m in diameter) serve as the primary histopathological correlates of glycemic failure (HbA1c), exhibiting early density loss and structural disintegration. In contrast, small islets (30-100 {micro}m in diameter) exhibited compensatory hormone upregulation during PreD. Notably, diverging from the death of the small paradigm in Type 1 Diabetes, our data reveal a significant expansion of extra-islet endocrine clusters (EECs) that initiates during the compensatory stage, effectively preceding the onset of overt hyperglycemia. Finally, t-SNE clustering reconstructed a continuous trajectory of islet remodeling, capturing the phenotypic evolution of islets from normoglycemia through compensation to clinical decompensation. This study provides a high-resolution atlas of islet pathophysiology, offering new insights into T2D progression. HighlightsO_LIIslet remodeling during T2D progression is critically dependent on islet size. C_LIO_LIMedium and large islets density negatively correlates with HbA1c. C_LIO_LISmall islets exhibit resilience to metabolic stress during T2D progression. C_LIO_LIEECs expansion suggests a process of -cell-biased neogenesis. C_LIO_LIt-SNE maps the islet trajectory from compensation to decompensation. C_LI

pathology↗

bioRxiv2025

Hedyotis Diffusae Herba Mitigates Rotenone-Induced Neurotoxicity via Akt Pathway in SH-SY5Y Cells

Hedyotis Diffusae Herba (HDH), known in traditional Chinese medicine for its heat-clearing and detoxifying properties, has been widely used to manage inflammation-related conditions. However, its neuroprotective potential and mechanism in the context of Parkinsons disease (PD) remain unclear.Network pharmacology and molecular docking were applied to predict the interactions between HDH components and PD-associated targets. Molecular dynamics simulations assessed the binding stability of major compounds to core targets. Rotenone-induced SH-SY5Y cell injury served as an in vitro PD model to evaluate HDHs biological effects. Cell viability, reactive oxygen species (ROS), IL-6 secretion, and Akt phosphorylation were assessed by CCK-8 assay, ROS detection kit, ELISA, and western blot, respectively. MK2206, an Akt inhibitor, was used to validate pathway involvement.Seven bioactive compounds were identified in HDH, among which stigmasterol and quercetin exhibited strong binding affinities with AKT1, IL-6, and JUN. Simulations confirmed stable interactions. HDH significantly increased cell viability and decreased intracellular ROS and IL-6 levels in rotenone-treated SH-SY5Y cells. Akt phosphorylation was restored by HDH, and the effect was blocked by MK2206, indicating Akt pathway participation.HDH exerts neuroprotective effects against rotenone-induced toxicity via antioxidant and anti-inflammatory activities and Akt pathway activation. These findings provide mechanistic insight and pharmacological support for HDH as a potential candidate in complementary therapy for PD.

cell biology↗

bioRxiv2025

PHbinder and PSGM: A Cascaded Framework for Epitope Prediction and HLA-I Allele Identification

The presentation of antigens by Human Leukocyte Antigen class I (HLA-I) molecules is a cornerstone of adaptive immunity. Although existing prediction tools such as NetMHCpan and MHCflurry exhibit high accuracy in predicting binding affinity between peptides and specific HLA-I alleles, they are constrained to a preset set of alleles. Consequently, they can neither directly determine whether a peptide is an epitope nor provide a holistic binding profile across the entire HLA-I allelic landscape. To overcome these challenges, we introduce two synergistic models: PH-binder (Peptide-HLA-I Binder) and PSGM (Pseudo Sequence Generation and Mapping). PHbinder integrates features from a fine-tuned ESM2 language model with Low-Rank Adaptation (LoRA), processing them through parallel CNN and Transformer branches to capture local and global patterns, which are then fused using a Cross-Multi-Head Attention mechanism. In the epitope prediction task, PHbinder achieved an accuracy of prediction of 85. 12%, significantly exceeding established benchmark models. Complementing this, the PSGM model employs a Generative Adversarial Network(GAN) architecture to generate the corresponding HLA-I pseudo sequences. These are then mapped to the known alleles using a Hamming distance-based nearestneighbor search. PSGM achieved 49.26% average coverage in its predictions of the Top-50 alleles. Furthermore, orthogonal validation with MHCflurry revealed that 63% of the highest affinity binding partners within its Top-50 list were new experimentally unverified HLA-I alleles. Together, PHbinder and PSGM establish a cascaded framework that enables a precise "Peptide [->] Epitope Determination [->] HLA-I Alleles List" pipeline. This work accelerates the screening of immunogenic epitopes and provides a powerful upstream preprocessor for traditional prediction tools.

bioinformatics↗

bioRxiv2025

Ketone Bodies-mediated Cysteine Modifications Discovered by Chemical Proteomics

All the studies of ketone body-dependent post-translational modifications (PTMs), notably those mediated by ketone bodies, {beta}-hydroxybutyrate (Bhb) and acetoacetate (Acac), have focused on lysine acylations. However, given the chemically diverse and reactive nature of metabolites generated, it remains unclear whether non-lysine modifications can also happen. Here, we report the synthesis of an acetoacetate-alkyne (Acac-alkyne) chemical probe that enables efficient metabolic labeling, robust fluorescent visualization, and mass spectrometry-based identification of Acac-modified proteins. By combining chemical proteomics with open-search strategy, we showed that Acac will induce previously uncharacterized cysteine modifications in mammalian cells. Notably, cysteine S-crotonation (Ccr) is validated by employing both probe-based and standard peptide-based co-elution assays. Metabolic pathway tracing further identifies BDH1 and ECHS1 as key enzymes that generate Ccr formation. Together, these findings establish ketone metabolism as a novel source of cysteine modifications and provide an alternative mechanistic pathway to explain the profound biological effects of ketone body.

biochemistry↗

bioRxiv2025

Two independent translocation modes drive neural stem cell dissemination into the human fetal cortex

The strong size increase of the human neocortex is supported both by the amplification and the basal translocation of a neural stem cell population, the basal radial glial cells (or bRG cells). Using live imaging of second trimester human fetal tissue and cortical organoids, we identify two independent translocation modes for bRG cell colonization of the human neocortex. On top of an actomyosin-dependent movement called mitotic somal translocation (MST), we identify a microtubule-dependent motion occurring during interphase, that we call interphasic somal translocation (IST). We show that IST is driven by the LINC complex, through the nuclear envelope recruitment of the dynein motor and of its activator LIS1. Consequently, IST severely altered in LIS1 patient-derived cortical organoids. We also demonstrate that MST occurs during prometaphase and is a mitotic spindle translocation event. MST is controlled by the mitotic cell rounding molecular pathway, via Moesin and Vimentin, driving translocation. We report that 85% of bRG cell translocation is due to IST, for a total movement of 0,67 mm per month of human fetal gestation. Our work identifies how bRG cells colonize the human fetal cortex, and further shows that IST and MST are conserved in bRG-related migrating glioblastoma cells.

neuroscience↗

bioRxiv2024

Dimorphic Neural Network Architecture Prioritizes Sexual-related Behaviors in Male C.elegans

Neural network architecture determines its functional output. However, the detailed mechanisms are not well characterized. In this study, we focused on the neural network architectures of male and hermaphrodite C. elegans and the association with sexually dimorphic behaviors. We applied graph theory and computational neuroscience methods to systematically discern the features of these two neural networks. Our findings revealed that a small percentage of sexual-specific neurons exerted dominance throughout the entire male neural net-work, suggesting males prioritized sexual-related behavior outputs. Based on the structural and dynamical characteristics of two complete neural networks, sub-networks containing sex-specific neurons and their immediate neighbors, or sub-networks exclusively comprising sex-shared neurons, we predicted dimorphic behavioral outcomes for males and hermaphrodites. To verify the prediction, we performed behavioral and calcium imaging experiments and dissected a circuit that is specific for the increased spontaneous local search in males for mate-searching. Our research sheds light on the neural circuits that underlie sexually dimorphic behaviors in C. elegans, and provides significant insights into the inter-connected relationship between network architecture and functional outcomes at the whole-brain level.

neuroscience↗

bioRxiv2024

Chemically Induced Nuclear Pore Complex Protein Degradation via E3 Ligase TRIM21

Despite the exciting progress of the bifunctional degrader molecules, also known as proteolysis-targeting chimeras (PROTACs), the rapidly expanding field is still significantly hampered by the lacking of available E3 ligase ligands. Our research bridges this gap by uncovering a series of small-molecule ligands to the E3 ligase TRIM21 through DNA-Encoded Library (DEL) technology. We confirmed their interaction with TRIM21 using crystallography and demonstrated their anti-proliferative effects across various cancer cell types. Furthermore, proteomic studies identified that the mRNA Export Factor GLE1, and the Nuclear Pore Complex Protein NUP155, were significantly down-regulated upon TRIM21 ligand treatment. This degradation required TRIM21 and was ubiquitin-proteasome-dependent. More specifically, NUP155 was the primary target for the TRIM21 ligands, while GLE1 was considered a passenger target upon the initial degradation of NUP155. Using immunofluorescence techniques, we further demonstrated that the degradation of GLE1 and NUP155 proteins impaired the integrity of the nuclear envelope, leading to cell death. Highlighted by this research, a novel mode of action has been discovered for the TRIM21 E3 ligase ligand, acting as a monovalent degrader that triggers de novo interaction with functional complex proteins and induces their degradation.

cell biology↗

bioRxiv2024

DCX knockout ferret reveals a neurogenic mechanism in cortical development

Doublecortin (DCX) is one of the major causal proteins leading to lissencephaly and subcortical band heterotopia in human patients. However, our understanding of this disease, as well as the function of DCX during neurogenesis, remains limited due to the absence of suitable animal models that accurately represent human phenotypes. Here, we conducted a comprehensive examination of the neocortex at different stages in DCX knockout ferrets. We corroborated the neurogenic functions of DCX in progenitors. Loss of function of DCX led to the over-proliferation of neural progenitors and the truncation of basal processes of radial glial cells, which contributed to the thickening of cortices and the stalling of neurons underneath the cortical plate during neurogenic stages, respectively. We also present the first-ever cell atlas of the lissencephaly disease model, which embraces an almost reversed neuronal lamination distribution in the neocortex compared to the normal controls. Furthermore, we discovered alterations in molecular signatures tied to epilepsy, a condition frequently observed in lissencephaly patients. We also provided compelling evidence that the distribution of GABAergic inhibitory neurons in the cortex is intricately linked to glutamatergic excitatory neurons in a subtype-specific manner. In conclusion, our research offers new insights to expand our understanding of DCXs functions and enrich our comprehension of lissencephalys intricacies. HighlightsDCX ferrets phenocopy human lissencephaly and subcortical band heterotopia syndrome DCX is required for NPC proliferation and radial glial basal fiber extension The atlas of lissencephalic cortex is illustrated using snRNA-seq and spatial transcriptome Inhibitory neurons couple to excitatory neurons in a cell-type specific manner

neuroscience↗

bioRxiv2024

Fibronectin 1 is a novel biomarker of obstetric antiphospholipid syndrome

ObjectiveTo investigate novel biomarkers and the mechanism of obstetric antiphospholipid syndrome (OAPS). MethodsHTR8/SVneo cells line were treated with plasma from OAPS (OAPS group) and healthy (NC group) pregnant women, respectively. The changes induced by plasma treatment at the transcriptome level were examined by RNA sequencing of the cells. Results were analyzed with bioinformatics tools to elucidate the potential biomarkers. Reverse-transcription quantitative polymerase chain reaction (RT-qPCR), western blotting, hematoxylin and eosin (HE), immunohistochemistry (IHC), and immunofluorescence (IF) were used for subsequent validation. ResultsBioinformatic analysis revealed the expression of Fibronectin 1 (FN1) was significantly increased in OAPS group. On analyzing molecular function, OAPS plasma exposure mainly affected the expression of the genes related to extracellular matrix (ECM) structural constituent. Compared to the NC group, differently expressed genes were mainly annotated to the collagen-containing ECM matrix and the ECM organization. In OAPS group, the protein expression of FN1 was also increased in blood (p <0 .05). The mRNA and protein expression of FN1 in placenta tissue were increased (p <0 .05) in OAPS group. Massive degeneration and atrophy can be seen in placental villi, with a significant reduction or disappearance of syncytiotrophoblasts and excessive fibrinoid deposition in the villous stroma of OAPS placenta. Both IHC and IF results showed the staining area and intensity of FN1 in the placental villi and stroma were significantly higher in OAPS group. ConclusionsFN1 may play a potential role in the pathogenic mechanisms of OAPS. Highlights

developmental biology↗

bioRxiv2023

Zbtb46 coordinates angiogenesis and immunity to control tumor outcome

Tumor-angiogenesis and -immunity play critical roles in cancer progression and outcome. An inverse correlation of these two1 hints at common regulatory mechanism(s). Here, we report that Zbtb46, a repressive transcription factor and a widely accepted marker for classical dendritic cells (DCs)2, 3, constitutes one such regulatory mechanism. Zbtb46 was downregulated in both DCs and endothelial cells (ECs) by tumor-derived factors to facilitate robust tumor growth. Zbtb46 downregulation led to a hallmark pro-tumor microenvironment (TME), including dysfunctional vasculature and immunosuppressive cell accumulation. Analysis of cancer patient data revealed a similar association of low ZBTB46 expression with an immunosuppressive TME and a worse prognosis. In contrast, enforced Zbtb46 expression mitigated the pro-tumor TME features and restricted tumor growth. Mechanistically, Zbtb46-deficient ECs were highly angiogenic, and Zbtb46-deficient bone-marrow progenitors upregulated Cebpb and diverted the DC program to myeloid lineage output, potentially explaining the myeloid lineage skewing phenomenon in cancer4-7. Conversely, enforced Zbtb46 expression normalized tumor vessels and, by suppressing Cebpb, skewed bone-marrow precursors towards more DC generation over macrophages, leading to an immune-hot TME. Remarkably, Zbtb46 mRNA treatment synergized with anti-PD1 immunotherapy to improve tumor management in pre-clinical models. These findings identify Zbtb46 as a common regulatory mechanism for angiogenesis and for myeloid lineage skewing in cancer and suggest that maintaining its expression could have therapeutic benefits.

cancer biology↗

bioRxiv2022

Single cell sequencing reveals microglia induced angiogenesis by specific subsets of endothelial cells following spinal cord injury

Spinal cord injury (SCI) results in dynamic alterations of the microenvironment at the lesion site, which inevitably leads to neuron degeneration and functional deficits. The prominent deterioration of the milieu, derived from the destruction of spinal vascular system, not only activates innate immunity but also makes cells in the lesion lose nutrient supports. Limited endogenous angiogenesis happens after SCI, but the cell events at the lesion site underpinning this process have not been delineated so far. Here, we conducted single-cell RNA sequencing (scRNA-seq) of tissues in the spinal lesion at different time points after rat SCI. After performing clustering and cell-type identification, we focused on the vascular endothelial cells (ECs), which play a pivot role in angiogenesis, and drew a comprehensive cellular and molecular atlas for endogenous angiogenesis after SCI. We found that microglia and macrophage promote endogenous angiogenesis by regulating EC subsets through SPP1 and IGF1 signal pathways. Our results indicated that immune cells promotes angiogenesis by the regulation of specific cell subsets of vascular ECs, which provides new clues for the development of interventions for SCI.

neuroscience↗

bioRxiv2021

The Mesodiencephalic Junction as a Central Hub for Cerebro-Cerebellar Communication

Most studies investigating the impact of cerebral cortex (CC) onto the cerebellum highlight the role of the pontine mossy fibre system. However, cerebro-cerebellar communication may also be mediated by the olivary climbing fibres via a hub in the mesodiencephalic junction (MDJ). Here, we show that rostromedial and caudal parts of mouse CC predominantly project to the principal olive via the rostroventral MDJ and that more rostrolateral CC regions prominently project to the rostral medial accessory olive via the caudodorsal MDJ. Moreover, transneuronal tracing results show that the cerebellar nuclei innervate the olivary-projecting neurons in the MDJ that receive input from CC, and that they adhere to the same topographical relations. By unravelling these topographic and dense, mono- and disynaptic projections from the CC through the MDJ and inferior olive to the cerebellum, this work establishes that cerebro-cerebellar communication can be mediated by both the mossy fibre and climbing fibre system.

neuroscience↗

bioRxiv2021

An awareness-dependent saliency map in the human visual system

The bottom-up contribution to the allocation of exogenous attention is a saliency map. However, how the saliency map is distributed when multiple salient stimuli are presented simultaneously and how this distribution interacts with awareness remain unclear. These questions were addressed here using visible and invisible stimuli that consisting of two salient foregrounds: the high one served as the target and the low one served as the distractor, which did or did not interfere the target saliency, indicating a gradient or winner-take-all manner, respectively. By combining psychophysics, fMRI, and effective connectivity analysis, we found that the saliency map was distributed as a gradient or winner-take-all manner with and without awareness, respectively. Crucially, we further revealed that the gradient manner was derived by feedback from pIPS, whereas the winner-take-all manner was constructed in V1. Together, our findings indicate an awareness-dependent saliency map and reconcile previous, seemingly contradictory findings on the saliency map.

neuroscience↗