bioRxiv Science⌕ Search

Biology subjects

Ning, W.

Publications and source records attributed to Ning, W..

At least 19 recordsLinked to original sources

Four genome assemblies of new wild Gossypium hirsutum accessions from the Yucatan Peninsula, the center of domestication

Gossypium hirsutum is a leading source of natural cotton fiber, accounting for most of the market share. While domestication and improvement have led to significant gains in fiber quantity and quality, the narrow germplasm base of modern cultivars creates vulnerabilities, including to emerging pests. Wild populations provide a reservoir for genetic diversity that may be valuable in identifying and transferring resistance or stress-adaptation alleles to modern breeding lines. Here we report four new genome assemblies of G. hirsutum representing distinct populations from its center of diversity in Yucatan, Mexico. These chromosome-level assemblies are highly contiguous and structurally similar to existing G. hirsutum genomes; however, comparative analyses highlight their distinctiveness, suggesting they form a valuable reservoir of untapped diversity. Preliminary analyses of nucleotide-binding leucine-rich repeat (NLR) immune receptor genes underscore this variation, suggesting presence-absence variation may exist among populations. These findings demonstrate the potential of these new genomic resources for discovery of novel disease resistance alleles and, generally, for expanding the narrow germplasm base of the modern cotton cultivars.

genomics↗

TRIP6 condensates constrain Hippo pathway hyperactivation under osmotic stress

The Hippo pathway integrates mechanical and chemical cues to regulate cell proliferation and tissue homeostasis, whereas its dysregulation contributes to impaired regeneration and tumorigenesis. Liquid-liquid phase separation has emerged as an organizing principle for Hippo signal transduction, but how cells constrain excessive pathway activation under stress remain poorly defined. Here we demonstrate that TRIP6, a LIM-domain scaffold and tension-sensitive Hippo inhibitor, undergoes intrinsic phase separation both in vitro and in living cells. Osmotic stress triggers rapid redistribution of TRIP6 condensates from large cortical assemblies to dispersed cytoplasmic puncta. Domain mapping shows that the N-terminal IDR2 drives TRIP6 phase separation, whereas the C-terminal LIM domains negatively regulate condensate fluidity. Mechanistically, TRIP6 condensates selectively recruit the LATS1 inhibitor AJUBA and the MST1 scaffold SAV1 while excluding MST1 itself. The phase-separation-deficient {Delta}IDR2 mutant fails to undergo stress-induced condensate redistribution, exhibits weakened LATS1 binding, and shows increased YAP phosphorylation and cytoplasmic retention under osmotic stress, with reduced cell proliferation and stress resilience. Finally, TRIP6 condensates disassemble in a mouse model of elevated epidermal tissue tension, identifying them as mechanosensitive platforms that link phase transitions to Hippo-dependent growth control. Together, these findings establish TRIP6 condensates as a negative regulatory node that buffers excessive Hippo activation to preserve cellular homeostasis under hyperosmotic conditions.

cell biology↗

Molecular architecture of the tumor microenvironment caused by BRCA1 and BRCA2 somatic mutations in lung adenocarcinoma

ObjectivesHomologous recombination repair (HRR) deficiency is associated with improved immunotherapy responses in non-small cell lung cancer (NSCLC) patients. The HRR genes BRCA1/2 are key regulators of DNA repair, yet their impact on the tumor microenvironment (TME) in lung adenocarcinoma (LUAD) remains unclear. MethodsUsing single-cell sequencing and multi-omics data, we characterized BRCA1/2 mutation-associated transcriptional programs, immune cell composition, and functional alterations in T cells, investigating the molecular and immune architecture of BRCA-mutant LUAD patients. ResultsBRCA1/2 mutations were associated with increased genomic instability and poor prognosis in LUAD patients, but predicted better clinical outcomes following immune checkpoint blockade (ICB) treatment. BRCA1 mutations correlated with an upregulated type I IFN/IFN-{gamma} signature and CD8+ T cell activation. BRCA2 mutations were associated with alveolar/stress/inflammatory responses and enhanced MHC-II antigen presentation, linked to CD4+ T cell differentiation. Both alterations coincided with reduced CD28 co-stimulation and CTL activity, hinting of immune evasion. We identified two tissue-resident memory T cell (Trm) subsets as predictors of clinical outcomes and ICB response. BRCA1 mutations were associated with CD8+ Trm expansion, whereas BRCA2 mutations linked to tumor CD4+ Trm expansion and peripheral T/NK cell cytotoxicity. Furthermore, a cancer-promoting program activated by BRCA1 mutation was vulnerable to histone deacetylase inhibitors, which inhibited LUAD tumor growth. ConclusionsThis study provides a preliminary characterization of the BRCA-mutant TME in LUAD patients, revealing distinct transcriptional and immune patterns that highlight differences in BRCA1/2-associated molecular architecture and offer a framework for improving therapy efficacy in LUAD.

cancer biology↗

Enriched experience increases reciprocal synaptic connectivity and coding sparsity in higher-order cortex

The integration of new information during sleep reshapes cortical representations that support categorical knowledge. Auto-associative attractor network theories predict that reciprocal excitatory connections help form stable categorical attractors, but direct evidence is missing. We tested this using ten weeks of enriched experience (ENR) in mice as a model for knowledge accumulation and recorded single-unit activity across hippocampus and neocortex. ENR induced significant remodeling in high- but not low-level neocortex, with a shift from unidirectional to bidirectional excitatory-excitatory connections, suggestive of increased cell assemblies. This was accompanied by increased inhibitory-to-excitatory connections and sparser, more orthogonal population activity during awake rest and slow-wave sleep, particularly in deep layers. Thus, ENR reorganizes cortical circuits into a symmetric, inhibition-balanced network that improves coding efficiency, supporting long-standing attractor network predictions.

neuroscience↗

Systemic translocation of S. aureus Drives Anti-CD4 Autoimmunity in Treated HIV Infection

BackgroundIn 2017, our group first demonstrated that autoimmunity contributes to HIV pathogenesis, even without autoimmune disease. This concept is now broadly recognized, exemplified by the role of autoimmunity in severe COVID-19. In people with HIV (PWH) on suppressive ART, anti-CD4 autoantibodies may impair CD4+ T cell recovery, though the mechanisms driving their production remain unclear. Building on evidence from our group and others that Staphylococcus aureus and its peptidoglycan (PGN) promote autoimmunity, we investigated their contribution to anti-CD4 IgG in HIV. MethodsPlasma from 32 ART-naive PWH, 53 ART-treated PWH, and 32 HIV-negative controls was analyzed for IgG autoantibodies and markers of S. aureus translocation using protein array, ELISA, and microarray. EcoHIV mice were injected intraperitoneally with saline, S. aureus PGN, or Bacillus subtilis PGN. PGN structures were compared by mass spectrometry. ResultsAmong 87 autoantibodies, 40% were elevated in ART-naive PWH and largely normalized by ART; however, anti-CD4 IgGs remained elevated in PWH on ART. Anti-CD4 IgG levels inversely correlated with CD4+ T cell counts in ART-treated PWH and positively with S. aureus translocation. In mice, S. aureus PGN induced anti-CD4 IgGs, reduced gut CD4+ T cells, and promoted surface IgG binding and apoptosis in CD4+ T cells. ConclusionS. aureus and its PGN translocation may drive anti-CD4 autoimmunity and hinder immune recovery in PWH on suppressive ART, highlighting S. aureus colonization as a therapeutic target and supporting the development of competitive probiotic interventions such as Bacillus subtilis.

immunology↗

Population Genomics Informs Conservation Strategies for Critically Endangered Kokia Species in Hawaii

Island endemic species are particularly vulnerable to extinction due to their limited geographic ranges and small population sizes. Kokia is a genus found exclusively in the Hawaiian Islands, whose species were once major components of local forests but have experienced significant population reductions due to habitat destruction and the consequences of invasive species. Although conservation of Kokia species has been an ongoing topic for over a century, records regarding historical efforts are sparse. Recently generated genomes for each of the three extant species provide the foundation for understanding genetic diversity and population structure for future conservation work. Whole genome resequencing of K. cookei (n = 23 samples), K. drynarioides (n = 92), and K. kauaiensis (n = 45) suggests that K. drynarioides has the lowest overall diversity, reflecting propagation from a limited part of the remaining gene pool, whereas K. kauaiensis exhibits the most diversity. Diversity in the primarily graft-propagated K. cookei is higher than expected, and slightly higher than in the free-living K. drynarioides. Notably, our analyses identified a source of novel variation in K. cookei in a cultivated plant historically labeled K. drynarioides. Population structure analyses reveal a single population for K. cookei, but three groups for each of the other two species. Importantly, our analyses identify clusters of related individuals, reflected in genetic distance and clustering metrics, which provide valuable information for increasing diversity in managed populations and in ex situ conservation collections. These results provide a genomic framework for ongoing efforts in restoring and maintaining diversity in these critically endangered Hawaiian species.

genomics↗

Comparative population genomics of relictual Caribbean island Gossypium hirsutum

Gossypium hirsutum is the worlds most important source of cotton fiber, yet the diversity and population structure of its wild forms remain largely unexplored. The complex domestication history of G. hirsutum combined with reciprocal introgression with a second domesticated species, G. barbadense, has generated a wealth of morphological forms and feral derivatives of both species and their interspecies recombinants, which collectively are scattered across a large geographic range in arid regions of the Caribbean basin. Here we assessed genetic diversity within and among populations from two Caribbean islands, Puerto Rico (n = 43, five sites) and Guadeloupe (n = 25, one site), which contain putative wild and/or introgressed forms. Using whole-genome resequencing data and a phylogenomic framework derived from a broader genomic survey, we parsed individuals into feral derivatives and truly wild forms. Feral cottons display uneven levels of genetic and morphological resemblance to domesticated cottons, with diverse patterns of genetic variation and heterozygosity. These patterns are inferred to reflect a complex history of interspecific and intraspecific gene flow that is spatially highly variable in its effects. Wild cottons in both Caribbean islands appear to be relatively inbred, especially the Guadeloupe samples. Our results highlight the dynamics of population demographics in relictual wild cottons that experienced profound genetic bottlenecks associated with repeated habitat destruction superimposed on a natural ecogeographical distribution comprising widely scattered populations. These results have implications for conservation and utilization of wild diversity in G. hirsutum.

evolutionary biology↗

A novel tool for labeling intermediary proteins between two non-interacting proteins

Decoding the complexities of signaling pathways is fundamental for deciphering the mechanisms underlying tissue development, homeostasis, and disease pathogenesis. Proximity labeling tools have been instrumental in identifying upstream or downstream effectors of specific proteins within signaling pathways. However, currently, there are no tools available to directly label and capture intermediary proteins that bridge two non-interacting proteins. Here, we developed STUPPIT (Split-TurboID and PUP-IT based Protein Identification Tool), a novel method combining split-TurboID and PUP-IT to biotinylate intermediary proteins of two non-interacting proteins through a two-step enzymatic reaction. Two approaches of STUPPIT were validated using three well-characterized protein triad, including YAP1/AMOT/{beta}-actin, YAP1/LATS1/MOB1A, and {beta}-catenin/-catenin/{beta}-actin. Combining STUPPIT and proteomics, we identified novel intermediary proteins including RNF20, ERC1, USP7 and TRIM33, which interact both with {beta}-catenin and SMAD4, key components of the Wnt and BMP signaling pathways. In conclusion, STUPPIT represents a powerful tool for labeling and capturing intermediary proteins between non-interacting partners, offering new insights into protein-protein interactions and advancing signal transduction research.

cell biology↗

Single-cell alternative polyadenylation analysis reveals mechanistic insights of COVID-19-associated neurological and psychiatric effects

COVID-19 is associated with increased risks of neurological and psychiatric sequelae. Alternative polyadenylation (APA) is ubiquitous in human genes, resulting in mRNA diversity, and has been validated to play a pivotal regulatory role in the onset and progression of a variety of diseases, including viral infections. Here, we analyzed the APA usage across different cell types in frontal cortex cells from non-viral control group and COVID-19 patients, and identified functionally related APA events in COVID-19. According to our study, the poly(A) site (PAS) usage is different among cell types and following SARS-COV-2 infection. Moreover, we found the genes with significant PAS level changes affected pathways related to RNA splicing, and neuronal development and function, suggesting that survivors of COVID-19 will have a high risk of these diseases and that alternative splicing functions cause these changes. Additionally, APA usage and its correlation with gene expression levels varied across genes, some prefer short isoform that is more stable to produce more proteins, while others may be regulated by different mechanisms. A total of 267 risk genes targeted by microRNAs for common neurological and psychiatric disorders were found to undergo significant changes in APA following infection. In conclusion, our comprehensive analysis of APA in neural cells from COVID-19 patients at the single-cell level elucidated changes in APA levels in the brains of SARS-COV-2-infected patients and confirmed that these changes impair the function of the nervous system, providing important insights for COVID-19-associated sequelae. HighlightsO_LIWe analyzed the changes in single-cell APA level in the frontal cortex after SARS-COV-2 infection and found that PAS usage is different among cell types and changed after infection. C_LIO_LIWe find that APA changes are related to RNA splicing, and neuronal development and function, such as synaptic plasticity, nervous system development, learning or memory and cognition, and the brain function may be impaired due to global gene expression and APA changes. C_LIO_LIA total of 267 risk genes for common neurological and psychiatric disorders were found to undergo significant changes in APA following infection, implying that APA alterations in specific genes could be a potential therapeutic target and predictive biomarker for neurological and psychiatric disease. C_LIO_LIAPA in infection samples results in the removal/addition of miRNA target sites in the 3'-UTR of genes. A total of 2404 miRNAs were predicted which suggests that the miRNAs target site information can indicate the impact of APA events and has the potential to be used as a predictive biomarker. C_LI

bioinformatics↗

Molecular and Mechanical Signatures Contributing to Epidermal Differentiation and Barrier Formation

Formation of the skin barrier requires rapid proliferation coupled with differentiation and stratification of the embryonic epidermis. Basal progenitors give rise to progeny throughout development - first to intermediate cells, a transient proliferative suprabasal cell population, and later to spinous cells. Neither the function nor the differentiation trajectory of intermediate cells has been documented. We generated transcriptomes of intermediate and spinous cells and identified specific markers that distinguish these two populations. Further, we found that intermediate cells express a subset of genes in common with granular cells of the epidermis - the terminal living cell type that helps establish the barrier. Lineage tracing revealed that most intermediate cells directly transition to granular cells without expressing markers specific to spinous cells, thus revealing a distinct lineage pathway leading to granular fate. In addition to their transcriptional similarities, intermediate and granular cells both had hallmarks of increased actomyosin contractility. We found that rather than simply lying downstream of cell fate pathways, contractility was sufficient to suppress spinous fate and promote granular gene expression. Together, these data establish the molecular and mechanical characteristics of the developing epidermis that allow this tissue to rapidly develop barrier activity.

developmental biology↗

ARHGAP32 as a novel RhoGAP interacting with desmoplakin is required for desmosomal organization and assembly

Desmosomes are specialized cell-cell junctions that play a critical role in maintaining tissue barrier integrity, particularly in mechanically stressed tissues. The assembly of desmosomes is regulated by the cytoskeleton and its regulators, and desmosomes also function as a central hub for regulating F-actin. However, the specific mechanisms underlying the crosstalk between desmosomes and F-actin, particularly involving RhoGAP or RhoGEF proteins, remain unclear. In our study, we identified that ARHGAP32, a Rho GTPase-activating protein, is located in desmosomes through its interaction with DSP via its GAB2-interacting domain. Using CRISPR-Cas9 gene knockout system, we confirmed that ARHGAP32 is required for proper desmosomal organization, maturation, and length regulation. Notably, the loss of ARHGAP32 resulted in increased formation of F-actin stress fibers and phosphorylation of MYOSIN at T18/S19, indicating enhanced actomyosin contractility. Furthermore, inhibition of ROCK1 kinase activity using Y27632 effectively restored desmosomal organization. Moreover, we demonstrated that the regulation of desmosomes by ARHGAP32 is crucial for maintaining the integrity of epithelial cell sheets. Collectively, our study unveils ARHGAP32 as a RhoGAP present at desmosomes, potentially facilitating the crosstalk between desmosomes and F-actin. Its presence is indispensable for desmosomal assembly and the preservation of epithelial cell sheet integrity by regulating actomyosin contractility.

cell biology↗

Compartment specific responses to contractility in the small intestinal epithelium

Tissues are subject to multiple mechanical inputs at the cellular level that influence their overall shape and function. In the small intestine, actomyosin contractility can be induced by many physiological and pathological inputs. However, we have little understanding of how contractility impacts the intestinal epithelium on a cellular and tissue level. In this study, we probed the cell and tissue-level effects of contractility by using mouse models to genetically increase the level of myosin activity in the two distinct morphologic compartments of the intestinal epithelium, the crypts and villi. We found that increased contractility in the villar compartment caused shape changes in the cells that expressed the transgene and their immediate neighbors. While there were no discernable effects on villar architecture, even low levels of transgene induction in the villi caused non-cell autonomous hyperproliferation of the transit amplifying cells in the crypt, driving increased cell flux through the crypt-villar axis. In contrast, induction of increased contractility in the proliferating cells of the crypts resulted in nuclear deformations, DNA damage, and apoptosis. This study reveals the complex and diverse responses of different intestinal epithelial cells to contractility and provides important insight into mechanical regulation of intestinal physiology. Author SummaryThe small intestine epithelium is comprised of two main compartments: the villi which contain differentiated cells that function in nutrient absorption, and the crypts which are made up of undifferentiated cells which serve to replenish cells of the villi. Because of their physical location within the tissue, villi and crypts are subjected to different types of insults and mechanical forces. We sought to directly test how villi and crypts respond to mechanical changes in the epithelia by genetically inducing actomyosin contraction. Increasing contractility in villar cells resulted in cell shape changes without affecting their overall polarity or organization. However, it led to a non-autonomous increase in proliferation of the undifferentiated cells of the intestine. In contrast, increased contractility in the proliferative cells of the crypt resulted in nuclear shape changes, DNA damage and ultimately a rapid cell death. Thus, our work demonstrates that the crypt and villi epithelia respond differently to mechanical changes and highlights long-range regulation between villi and crypt compartments.

cell biology↗

The TRIP6/LATS1 complex constitutes the tension sensor of α-catenin/vinculin at both bicellular and tricellular junctions

Cell-cell mechanotransduction regulates tissue development and homeostasis. -catenin, the core component of adherens junctions, functions as a tension sensor and transducer by recruiting vinculin and transducing the signals to influence cell behaviors. However, little is known about the components, distributions, and dynamics of the -catenin based tension sensors at the cell junctions. Here, we uncovered the TRIP6/LATS1 complex locates at the tension sites where -catenin/vinculin is at both the bicellular junctions (BCJs) and tricellular junctions (TCJs). Vinculin/TRIP6/LATS1 are prone to form as puncta in the cytoplasm without -catenin participation. Furthermore, the tension sensing complex distributed stronger at TCJs and exhibited a discontinuously button-like pattern on BCJs. The -catenin/vinculin BiFC-based mechanosensor further proved the discontinuous distribution of the tension at BCJs, and was more motile than the TCJs. In summary, our study revealed that TRIP6 and LATS1 are novel compositions of the tension sensor, together with the core complex of -catenin/vinculin, at both the BCJs and TCJs. This work gives insights and improvements in exploring the molecular mechanism that mediates cell-cell mechanotransduction at cell junctions.

cell biology↗

The repertoire of copy number alteration signatures in human cancer

Copy number alterations (CNAs) are a predominant source of genetic alterations in human cancer and play an important role in cancer progression. However comprehensive understanding of the mutational processes and signatures of CNA is still lacking. Here we developed a mechanism-agnostic method to categorize CNA based on various fragment properties, which reflect the consequences of mutagenic processes and can be extracted from different types of data, including whole genome sequencing (WGS) and SNP array. The 14 signatures of CNA have been extracted from 2778 pan-cancer analysis of whole genomes (PCAWG) WGS samples, and further validated with 10851 the cancer genome atlas (TCGA) SNP array dataset. Novel patterns of CNA have been revealed through this study. The activities of some CNA signatures consistently predict cancer patients prognosis. This study provides a repertoire for understanding the signatures of CNA in cancer, with potential implications for cancer prognosis, evolution, and etiology.

bioinformatics↗

Pan-cancer quantification of neoantigen-mediated immunoediting in cancer evolution

Immunoediting, which includes three temporally distinct stages, termed elimination, equilibrium, and escape, has been proposed to explain the interactions between cancer cells and the immune system during the evolution of cancer. However the status of immunoediting in cancer remains unclear, and the existence of neoantigen depletion signal in untreated cancer has been debated. Here we developed a distribution pattern based method for quantifying neoantigen mediated negative selection in cancer evolution. Our method provides a robust and reliable quantification for immunoediting signal in an individual cancer patient. The prevalence of immunoediting signal in immunotherapy untreated cancer genome has been demonstrated with this method. Importantly, the elimination and escape stages of immunoediting can be quantified separately, tumor types with strong immunoediting-elimination tend to have weak immunoediting-escape signal, and vice versa. Quantified immunoediting-elimination signal predicts cancer immunotherapy clinical response. Immunoediting quantification provides an evolutional perspective for evaluating the antigenicity of neoantigen, and reveals a potential biomarker for cancer precision immunotherapy.

cancer biology↗

Environmental response in gene expression and DNA methylation reveals factors influencing the adaptive potential of Arabidopsis lyrata

Understanding what factors influence plastic and genetic variation is valuable for predicting how organisms respond to changes in the selective environment. Here, using gene expression and DNA methylation as molecular phenotypes, we study environmentally induced variation among Arabidopsis lyrata plants grown at lowland and alpine field sites. Our results show that gene expression is highly plastic, as many more genes are differentially expressed between the field sites than between populations. These environmentally responsive genes evolve under strong selective constraint - the strength of purifying selection on the coding sequence is high, while the rate of adaptive evolution is low. We find, however, that positive selection on cis-regulatory variants has likely contributed to the maintenance of genetically variable environmental responses, but such variants segregate only between distantly related populations. In contrast to gene expression, DNA methylation at genic regions is largely insensitive to the environment, and plastic methylation changes are not associated with differential gene expression. Besides genes, we detect environmental effects at transposable elements (TEs): TEs at the high-altitude field site have higher expression and methylation levels, suggestive of a broad-scale TE activation. Compared to the lowland population, plants native to the alpine environment harbor an excess of recent TE insertions, and we observe that specific TE families are enriched within environmentally responsive genes. Together, our findings provide insight into selective forces shaping plastic and genetic variation. We also highlight how plastic responses at TEs can rapidly create novel heritable variation in stressful conditions.

evolutionary biology↗

Extrachromosomal DNA is associated with decreased immune cell infiltration and antigen presentation, represents a potential cancer immune evasion mechanism

Extrachromosomal DNA (ecDNA) is a type of circular and tumor specific genetic element. EcDNA has been reported to display open chromatin structure, facilitate oncogene amplification and genetic material unequal segregation, and is associated with poor cancer patients prognosis. The ability of immune evasion is a typical feature for cancer progression, however the tumor intrinsic factors that determine immune evasion remain poorly understood. Here we show that the presence of ecDNA is associated with markers of tumor immune evasion, and obtaining ecDNA could be one of the mechanisms employed by tumor cells to escape immune surveillance. Tumors with ecDNA usually have comparable TMB and neoantigen load, however they have lower immune cell infiltration and lower cytotoxic T cell activity. The microenvironment of tumors with ecDNA shows increased immune desert, decreased immune enriched fibrotic types. Both MHC class I and class II antigen presentation genes expression are decreased in tumors with ecDNA, and this could be the underlying mechanism for ecDNA associated immune evasion. This study provides evidence that the presence of ecDNA is an immune escape mechanism for cancer cells.

cancer biology↗

Sharing happy stories increases interpersonal closeness mediated by enhancing interpersonal brain synchronization

Our lives revolve around sharing stories with others. Expressing emotion (i.e., happy and sad) is an essential characteristic of sharing stories and could enhance the similarity of story comprehension across speaker-listener pairs. The Emotions as Social Information Model (EASI) suggests that emotional communication may influence interpersonal closeness, but the effect of sharing emotional (happy/sad) stories on interpersonal closeness remains poorly understood. Here, one speaker watched emotional videos and communicated the content of the videos to thirty-two listeners (happy/sad/neutral group). Both speaker and listeners neural activities were recorded using EEG. After listening, we assessed the interpersonal closeness between the speaker and listeners. Compared to the sad group, sharing happy stories showed a better recall quality and a higher rating of interpersonal closeness. Meanwhile, the happy group showed higher interpersonal brain synchronization (IBS) in the prefrontal cortex (PFC) and temporal cortex (specifically TPJ) than the sad group. Moreover, such IBS mediated the relationship between the quality of sharing stories and interpersonal closeness, and happy emotion moderated this mediation model. The magnitude of IBS differentiated high interpersonal closeness from low interpersonal closeness. Exploratory analysis using support vector regression showed that the IBS could also predict the ratings of interpersonal closeness in left-out subjects. These results suggest that IBS could serve as an indicator of whether sharing emotional stories facilitate interpersonal closeness. These findings improve our understanding of sharing emotional information among individuals that guide behaviors during interpersonal interactions.

neuroscience↗