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Vidal, E.

Publications and source records attributed to Vidal, E..

At least 19 recordsLinked to original sources

Interpreting graph neural networks reveals microbial association patterns in inflammatory bowel diseases

Traditional machine learning models trained on gut microbiome abundance profiles can distinguish individuals with inflammatory bowel disease (IBD) from non-IBD individuals. However, their interpretation typically considers taxa in isolation, making it difficult to understand how associations between taxa contribute to predictions. Here, we inferred individual-specific microbial association networks from longitudinal metagenomics data of 106 individuals in HMP2/iHMP and used them to train and interpret graph neural network (GNN) models, which we compared with abundance-based models such as Random Forest (RF). Although RF achieved higher predictive performance (AUPRC ~0.59 vs 0.446), interpreting the GNNs revealed that their predictions relied on a densely connected module of co-abundant Bacteroidales species. Unlike the taxa prioritized by RF, these species were not differentially abundant between conditions. In an independent cohort, this module carried most of the predictive signal, and removing its associations reduced performance to near chance. These results show that coordinated association structure, rather than abundance shifts alone, is a feature of the IBD gut microbiome, and that interpreting GNNs can uncover such patterns that complement abundance-based analyses.

bioinformatics↗

First outbreak of Lumpy Skin disease in Catalonia, Spain, 2025-2026

Lumpy skin disease (LSD) is an emerging cattle disease caused by lumpy skin disease virus (LSDV), with major impacts on the industry, being classified as a Category A disease. Although it was historically confined to Africa, LSD has expanded into the Middle East, Asia and Europe. Here, we report two LSDV genomes from the first outbreak detected in Catalonia, Spain, in October 2025. The genomes were assembled from high-throughput sequencing data generated from two homogenized skin nodules. Comparative phylogenetic analyses were performed using all available complete LSDV genomes and rpo30 gene sequences. These analyses placed the LSDV isolates detected in Catalonia within clade 1.2, closely related to the isolates recently reported in Sardinia, Italy. Our findings also support a connection between recent south-western Europe and central African strains, possibly through northern Africa, and highlight the need for more complete genomes to clarify the origin and connections among recent LSDV outbreaks.

genomics↗

CysK2 couples copper sensing to metabolic and redox adaptation in Mycobacterium tuberculosis

Copper is increasingly recognized as a host-derived cue encountered by Mycobacterium tuberculosis and other microbes during infections, yet the magnitude, intracellular distribution, and physiological consequences of this exposure remain incompletely understood. Here, we combined high-resolution imaging, transcriptomic profiling, intracellular reporter assays, isotope tracing, and mouse infection models to define how M. tuberculosis responds to physiologically relevant copper levels during macrophage infection. NanoSIMS analysis showed that copper reaches intracellular bacilli and accumulates in discrete phosphorus-rich foci in bacteria. Exposure to physiological copper concentrations in vitro triggered a highly specific transcriptional response dominated by the copper-inducible CsoR and RicR regulons. The RicR-regulated gene cysK2 gene, encoding the S-sulfocysteine synthase CysK2, was one of the most strongly induced loci. In infected macrophages, cysK2 expression was modulated by extracellular copper availability, host copper transport pathways, and hypoxia. In vitro, an H37Rv cysK2-deficient mutant showed reduced amino acid biosynthesis in response to copper exposure. In vivo, the mutant was impaired in long-term persistence in mice and displayed a higher oxidation status. Together, these findings identify CysK2 as a copper-responsive metabolic effector that couples host-derived copper sensing to redox homeostasis and intracellular adaptation in M. tuberculosis. IMPORTANCESuccessful infection by Mycobacterium tuberculosis depends on its ability to detect and adapt to host-imposed changes in the phagosomal environment. Our work shows that copper contributes to this adaptation not simply by imposing toxicity, but by triggering a metabolic response that helps sustain bacterial fitness within host cells. We identify CysK2 as a key component of this response, linking copper sensing to sulfur metabolism, redox balance, and persistence during infection. These findings shift the view of copper from a purely antimicrobial factor to a host-derived environmental signal that remodels M. tuberculosis physiology, and they uncover a new mechanism by which the pathogen maintains intracellular survival.

microbiology↗

Environmental complexity constrains evolutionary adaptation across taxa

Complex environments combining multiple stressors are the new norm worldwide. Adaptive evolution will be critical to population persistence under these combined challenges, but how environmental complexity affects the pace of evolution remains poorly understood. Using a meta-experimental evolution approach, we exposed 14 species, from bacteria to unicellular eukaryotes and plants, to single stressors and their pairwise combinations for multiple generations, while keeping the overall stress level comparable. Populations evolving under combined stressors tended to have lower fitness increase in the selective environments, higher fitness reductions in the control environment, and shallower relation between initial maladaptation and fitness gain, than under single stressors. However, these responses varied with species and stressor type. Accounting for such constraints on evolutionary dynamics should prove crucial for the management of biodiversity. Significance StatementA pressing challenges for modern science and society in the face of ongoing global change is understanding what limits the capacity of living organisms to adapt to complex environments combining multiple stressors. To answer to this question, we conducted a large-scale meta-experimental evolution design across a diversity of organisms, exposing them for multiple generations to either single or combined-stress treatments. Combined stressors led to less adaptive fitness gain than single stressors, and imposed additional costs through reduced fitness in non-stressful conditions. This unique combination of meta-experimental approach with a careful distinction between environmental complexity and overall stress allowed us to gain robust quantitative evidence on how environmental complexity can impact the pace of evolution.

evolutionary biology↗

The alarmin Interleukin-33 modulates platelet proteome, function and biogenesis

Platelets, traditionally recognized for their involvement in hemostasis and wound healing, also play a central role in immune regulation and inflammation. Their function and production adapt in response to inflammatory cues such as cytokines and danger-associated molecular patterns. Interleukin-33 (IL-33), an alarmin released during tissue damage, particularly in lung inflammation, has been implicated in influencing platelet biology, though its exact effects remain poorly understood. To clarify IL-33s role, we examined its impact on platelet production, proteome, adhesion, secretion, and aggregation using platelets from IL-33-deficient (IL-33KO) mice and IL-33 stimulation in vivo. Our results reveal that while platelets themselves do not express IL-33, platelets isolated from IL-33KO mice display altered proteomic signatures and reduced adhesion to fibrinogen, podoplanin, and laminin, alongside impaired thrombus formation under shear stress. IL-33 administration in vivo led to proteomic remodeling characterized by increased expression of inflammatory proteins, as well as changes in platelet morphology, including increased size, typically associated with de novo production. Using lung intravital microscopy, we visualized platelet fragmentation within the lung vasculature in real time, and observed enhanced fragmentation following IL-33 stimulation. Interestingly, ST2, the receptor for IL-33, is expressed in subsets of mouse and human megakaryocytes and hematopoietic progenitors, particularly those involved in a non-canonical pathway of thrombopoiesis that enables the rapid replenishment of platelets during inflammation, infection, and aging. Together, these findings identify IL-33 as a pivotal regulator of platelet function and production, linking inflammatory signaling to the dynamic regulation of thrombopoiesis. Key PointsIL-33 impacts platelet inflammation-related proteins and adhesion IL-33 receptor is expressed by subsets of MK progenitors in mouse and human

immunology↗

The Bone Morphogenetic Pathway Controls the Uptake of Infectious Prions

Prions propagate through cycles of intracellular replication, release, and uptake by host cells. Each of these steps is required for disease progression. Here, we used dCAS9-VP64 mediated transactivation to screen for determinants of prion uptake. We transduced PRNP-/- SH-SY5Y cells with a post-pooled human quadruple-guide-RNA library targeting all transcription start sites of the protein-coding genome, exposed them to synthetic infectious prions, and identified modifiers of prion internalization. Specificity was tested by counterscreens with other neurodegeneration-related aggregates and endocytic probes. Surprisingly, the Bone Morphogenetic Protein (BMP) signaling pathway emerged as a strong modulator. Prion uptake was increased by transcriptional activation of the BMPR1B, BMPR2 and ACVRL1 receptors, by the BMP effector SMAD1 and by exposure to BMP ligands. Conversely, prion uptake was reduced by activation of the BMP inhibitor SMAD6. Pharmacological inhibition of BMP signaling by the antagonistic ligand noggin and by the BMP kinase inhibitor dorsomorphin decreased prion internalization, reduced the number of prion-carrying cells, and suppressed the accumulation of proteinase-resistant prion protein in a panel of chronically infected human cell lines. Hence, cell-autonomous and non-autonomous BMP signaling components regulate prion uptake, and their manipulation provides a framework for interfering with the early steps of prion propagation.

neuroscience↗

ABaCo: Addressing Heterogeneity Challenges in Metagenomic Data Integration with Adversarial Generative Models

The rapid advancement of high-throughput metagenomics has produced extensive and heterogeneous datasets with significant implications for environmental and human health. Integrating these datasets is crucial for understanding the functional roles of microbiomes and the interactions within microbial communities. However, this integration remains challenging due to technical heterogeneity and the inherent complexity of these biological systems. To address these challenges, we introduce ABaCo, a generative model that combines a Variational Autoencoder (VAE) with an adversarial discriminator specifically designed to handle the unique characteristics of metagenomic data. Our results demonstrate that ABaCo effectively integrates metagenomic data from multiple studies, corrects technical heterogeneity, outperforms existing methods, and preserves taxonomic-level biological signals. We have developed ABaCo as an open-source, fully documented Python library to facilitate, support and enhance metagenomics research in the scientific community.

bioinformatics↗

Real time monitoring of hydrogenotrophic methanogenesis under deep saline aquifers conditions

To investigate the microbial response to deep underground gas injection, specifically CO2 and H2, a new optically transparent high-pressure reactor was developed to monitor autotrophic microbial growth via in situ and ex situ characterization techniques. The main advantages rely on avoiding any decompression phases during the entire process, thanks to direct optical access. Here, we monitored the growth of the model methanogenic strain Methanothermococcus thermolithotrophicus by applying different H2/CO2 partial pressures at a total pressure of 100 bar, which is representative of the deep underground storage environment. Additionally, we measured the methane production of the strain at the end of the incubation, which resulted in an increase in methane production with increasing CO2 and H2 partial pressures until a certain point. These reactors can be used to investigate deep microbial strains under pressure conditions close to their natural environments, eliminating decompression biases.

bioengineering↗

EWS-FLI1 Expression in Human Embryonic MSCs Leads to Transcriptional Reprograming, Defective DNA Damage Repair and Ewing Sarcoma

Ewing sarcoma (ES) is an aggressive bone and soft tissue neoplasm characterized by EWSR1/ETS rearrangements and whose cellular origin remains unclear. EWS-FLI1 expression in human pediatric mesenchymal stem cells (hpMSCs) induces a quantitatively and qualitatively different transcriptional response than its expression in human adult MSCs (haMSCs), but fails to form tumors in vivo. ES cells have early developmental lineage signatures distinct from postnatal MSCs. Here, we have generated MSCs from experimental teratomas out of human embryonic stem cells (heSCs). Transduction of these human embryonic mesenchymal stem cells (heMSCs) with EWS-FLI1 results in the acquisition of an ES transcriptome, although the oncogene does not preferentially bind to promoters, but to intronic and intergenic microsatellites with >10 CA dinucleotides and GGAA repeats, respectively. In heMSCs, EWS-FLI1 directly regulates BRCA1 expression, although EWS-FLI1-expressing cells show defects in DNA damage repair. Xenografting of EWS-FLI1-transduced heMSCs resulted in the formation of tumors expressing characteristic ES markers. In summary, EWS-FLI1 enforces an aberrant transcriptome and endows in vivo transforming capacity when expressed in an undifferentiated early heMSC. Our approach represents an innovative experimental method for understanding critical aspects of the biology of developmental tumors, from leukemia to sarcomas, in which few (even single) genetic alterations are able to transform a fetal stem cell.

cancer biology↗

The Plantae Visualization Platform: a comprehensive web-based tool for the integration, visualization, and analysis of omic data across plant and related species

The increasing availability of omics data from non-model plant species has created a pressing need for centralized, user-friendly platforms that maximize the utility of these datasets in a FAIR manner. Here, we introduce PlantaeViz, a web-based tool designed for the integration, visualization, and analysis of multi-omics data across a wide range of plant species. PlantaeViz offers advanced functionalities, including gene catalogues built from curated literature, transcriptomic meta-analyses presented as gene expression atlases, gene co-expression and regulatory networks with on-the-fly ontology analyses, cistrome visualization and metabolomics-transcriptomics integration, among other tools, providing a robust framework for hypothesis generation and biological interpretation. Gene Cards applications, tailored to each plant species, provide both community-curated and automatically generated functional annotation information. One of the platforms core features is its big data approach: over 58,000 publicly available SRA transcriptomic samples have been processed and visualized to date. Significant efforts have been made in orthology assessment using multiple layers of evidence, as well as in the automatic classification and standardization of omics metadata through regular expressions and data mining. As a result, around 90% of transcriptomic runs have been successfully classified according to sample tissue. These data have been used to construct gene networks via computationally intensive methods based on diverse algorithms. We present a study case to illustrate the platforms integration and exploratory capabilities. PlantaeViz bridges genomics and functional knowledge between model and non-model plant species and aims to expand its species catalogue of species in the future, democratizing access to large-scale plant omics data. Further developments will include the incorporation of additional data types, and the implementation of new tools to further support plant research across diverse biological contexts.

bioinformatics↗

Chromosome Compartments on the Inactive X Guide TAD Formation Independently of Transcription during X-Reactivation

A hallmark of chromosome organization is the partition into transcriptionally active A and repressed B compartments and into topologically associating domains (TADs). Both structures were regarded absent from the inactive X chromosome, but to be re-established with transcriptional reactivation and chromatin opening during X-reactivation. Here, we combine a tailor-made mouse iPSC-reprogramming system and high-resolution Hi-C to produce the first time-course combining gene reactivation, chromatin opening and chromosome topology during X-reactivation. Contrary to previous observations, we uncover A/B-like compartments on the inactive X harboring multiple subcompartments. While partial X-reactivation initiates within a compartment rich in X-inactivation escapees, it then occurs rapidly along the chromosome, coinciding with acquisition of naive pluripotency, leading to downregulation of Xist. Importantly, we find that TAD formation precedes transcription, suggesting them to be causally independent. Instead, TADs form first within Xist-poor compartments, establishing Xist as common denominator, opposing both gene reactivation and TAD formation through separate mechanisms. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=188 SRC="FIGDIR/small/177790v2_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@1e5ba28org.highwire.dtl.DTLVardef@120ad95org.highwire.dtl.DTLVardef@64264borg.highwire.dtl.DTLVardef@10e168a_HPS_FORMAT_FIGEXP M_FIG Graphical Summary C_FIG

genomics↗

Transcription factor TGA2 is essential for UV-B stress tolerance controlling oxidative stress in Arabidopsis

Plants possess a diversity of Reactive Oxygen Species (ROS)-processing enzymes involved in sensing and controlling ROS levels under basal and stressful conditions. There is little information on the transcriptional regulators that control the expression of these ROS-processing enzymes, particularly at the onset of the defense response to abiotic stress. Filling this gap, this paper reports a critical role for Arabidopsis TGA class II factors (TGA2, TGA5, and TGA6) in the tolerance response to UV-B light and photooxidative stress, by activating the expression of genes with antioxidative roles. We identified two clusters of genes responsive to UV-B and activated by TGA2/5/6 were identified using RNAseq and clustering analysis. The GSTU gene family, which encodes glutathione transferase enzymes from the Tau subclass, was overrepresented in these clusters. We corroborated the TGA2-mediated activation in response to UV-B for three model genes (GSTU7, GSTU8, and GSTU25) using RT-qPCR and ChIP analyses. Interestingly, using tga256 mutant and TGA2- and GSTU7-complemented mutant plants, we demonstrated that TGA2-mediated induction of GSTU genes is essential to control ROS levels and oxidative damage after UV-B and MeV treatments. This evidence positions TGA class II factors, particularly TGA2, as a key players in the redox signaling network of Arabidopsis plants. HighlightArabidopsis TGA2 transcription factor is part of the redox-signaling network controlling ROS levels and oxidative damage in tolerance response to UV-B and photooxidative stress, via activation of antioxidant GSTU genes.

plant biology↗

Monolingual and bilingual infants rely on the same brain networks: Evidence from resting-state functional connectivity

This study examines whether bilingual exposure has a profound effect on the functional organization of the developing human brain during infancy. Recent behavioural research attests that monolingual vs. bilingual experience affects cognitive and linguistic processes already during the first months of life. However, to what extent the intrinsic organization of the infant human brain adapts to monolingual vs. bilingual environments is unclear. We measured spontaneous hemodynamic brain activity using functional near-infrared spectroscopy (fNIRS) in a large cohort (N=99) of 4-month-old monolingual and bilingual infants. We implemented well-established analysis approaches of functional brain imaging that enabled us to reveal the functional organization of the infant brain in large-scale cortical networks, and to perform group-level comparisons (i.e., monolingual vs. bilingual groups) in a reliable manner. Our results revealed no differences between the intrinsic functional organization of the developing monolingual and bilingual infant brain at 4 months of age.

neuroscience↗

The amino acid residue in position 163 of canine PrPC is critical to the exceptional resistance of dogs to prion infections: evidence from transgenic mouse models

Unlike other species, such as cattle, cats or humans, prion disease has never been described in dogs, even though they were similarly exposed to the bovine spongiform encephalopathy (BSE) agent. This resistance prompted a thorough analysis of the canine PRNP gene and the presence of a negatively charged amino acid residue in position 163 was readily identified as potentially fundamental as it differed from all known susceptible species. Furthermore, recent results from our group demonstrated that mouse PRNP with the dog substitution N158D (mouse equivalent to position 163) rendered mice resistant to prion infection. In the present study, a transgenic mouse model was generated expressing dog prion protein (with glutamic acid at position 163) and challenged intracerebrally with a panel of prion isolates (including cattle BSE, sheep scrapie, atypical sheep scrapie, atypical BSE-L, sheep-BSE and chronic wasting disease, among others) none of which could infect them. The brains of these mice were subjected to in vitro prion amplification and failed to find even minimal amounts of misfolded prions providing definitive experimental evidence that dogs are resistant to prion disease. Subsequently, a second transgenic model was generated in which aspartic acid in position 163 was substituted for asparagine (the most common amino acid in this position in prion susceptible species) and this mutation resulted in susceptibility to BSE-derived isolates.\n\nThese findings strongly support the hypothesis that the amino acid residue at position 163 of canine PrPC is a major determinant of the exceptional resistance of the canidae family to prion infection and establish this as a promising therapeutic target for prion diseases.\n\nAUTHOR SUMMARYCats, cattle, people and dogs were all exposed to mad cow disease but, unlike the other three, dogs never succumbed to the disease. We generated a mouse model expressing canine prion protein (instead of mouse prion protein) to provide experimental evidence that dogs are resistant to prion infection by challenging the mice with a panel of prion isolates. None of the prions could infect our transgenic mice that expressed dog prion protein. When the prion protein amino acid sequence of dogs was compared to that of other susceptible species, one amino acid in a specific position was found to be different to all the prion-susceptible animals. To determine if this amino acid was the one responsible for dogs resistance to prions, a second mouse model was generated with the canine prion protein but the critical amino acid was substituted for the one susceptible species have. When this model was challenged with the same panel of prions it could be infected with at least one of them. These results demonstrate the relevance of this amino acid position in determining susceptibility or resistance to prions, and this information can be used to design preventative treatments for prion diseases.

neuroscience↗

Time-resolved systems analysis reveals a critical role of XCR1+ 1 dendritic cells in the maintenance of effector T cells during chronic viral infection

Upon a viral infection, the host immune system attempts to eradicate the virus. However, once the infection threat seems overwhelming, the infected host actively shuts down effector responses to reduce immunopathology. The price to pay for this is the establishment of a chronic infection that is only partially controlled by a lower level immune response. The genetic networks underlying this infection fate decision and the immune adaptation to the lower level response are not well understood. Here we used an integrated approach of gene coexpression network analysis of time-resolved splenic transcriptomes and immunological analysis to characterize the host response to acute and chronic lymphocytic choriomeningitis virus (LCMV) infections. We found first, an early attenuation of inflammatory monocyte/macrophage prior to the onset of T cell exhaustion and second, a critical role of the XCL1-XCR1 communication axis during the functional adaptation of the T cell response to the chronic infection state. These findings not only reveal an important feedback mechanism that couples T cell exhaustion with the maintenance of a lower level of effector T cell response but also suggest therapy options to better control virus levels during the chronic infection phase.\n\nAuthor SummaryThe outcomes of viral infections are the result of dynamic interplays between infecting viruses and induced host responses. They can be categorized as either acute or chronic depending on temporal virus-host relationships. Chronic infections are associated with immune exhaustion, a partial shut-down of effector responses. The processes underlying infection fate decisions are incompletely understood. Here we analyzed, on a systems level, infection-fate-specific gene signatures and the resulting adaptive processes of the host. We used the well-established lymphocytic choriomeningitis virus infection mouse model which has been instrumental to detect many fundamental processes in the virus-immune system crosstalk that are also relevant in human infections. We show an early attenuation of macrophage-mediated inflammation and an involvement of cross-presenting dendritic cells in the maintenance of an antiviral cytotoxic T cell response and virus control in the chronic infection phase. Together our data demonstrate a delicate adaptation process towards a chronic virus infection with both immunosuppressive and immunostimulatory processes. We fill a knowledge gap regarding the mechanisms of effector T cell maintenance and provide a new rational for targeted therapeutic vaccination.

immunology↗

TFIIIC dynamically binds Alu elements to control gene expression through chromatin looping

Folding of the mammalian genome is governed by architectural proteins, such as CTCF. TFIIIC, a RNA polymerase III transcription factor, has been identified as an insulator but its role in genome topology is totally unknown. Here, we show that TFIIIC establishes long-range genomic interactions that affect gene expression. Upon serum starvation (SS), TFIIIC occupancy increases at Alu elements (AEs) near promoters of cell cycle-related genes. Bound AEs become H3K18 hyper-acetylated and fold to contact distal pre-loaded CTCF sites near other cell cycle genes. The promoters of these genes also become hyper-acetylated ensuring their basal transcription during SS and their increased expression during serum re-exposure. Ablation of TFIIIC or deletion of the TFIIIC-bound AE that loops to the G2/M cycling F (CCNF) locus affects its expression and nuclear positioning. These results illustrate a novel function of human TFIIIC in changing 3D genome topology through the epigenetic state of AEs.\n\nHighlightsO_LISerum starvation enhances TFIIIC binding to Alu Elements (AEs) near cell cycle genes\nC_LIO_LIBinding of TFIIIC increases H3K18 acetylation over the bound AE\nC_LIO_LITFIIIC-mediated looping to distal genes favors their reactivation upon serum addition\nC_LIO_LILong-range TFIIIC interactions tune cell cycle genes expression through nuclear repositioning\nC_LI\n\nGraphical abstract\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=64 SRC=\"FIGDIR/small/455733_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (22K):\norg.highwire.dtl.DTLVardef@917ee4org.highwire.dtl.DTLVardef@21d0fborg.highwire.dtl.DTLVardef@1f1a17org.highwire.dtl.DTLVardef@1e9df24_HPS_FORMAT_FIGEXP M_FIG C_FIG

genomics↗

Comparative Analysis of Linear and Nonlinear Dimension Reduction Techniques on Mass Cytometry Data

Mass cytometry, also known as CyTOF, is a newly developed technology for quantification and classification of immune cells that can allow for analysis of over three dozen protein markers per cell. The high dimensional data that is generated requires innovative methods for analysis and visualization. We conducted a comparative analysis of four dimension reduction techniques - principal component analysis (PCA), isometric feature mapping (Isomap), t-distributed stochastic neighbor embedding (t-SNE), and Diffusion Maps by implementing them on benchmark mass cytometry data sets. We compare the results of these reductions using computation time, residual variance, a newly developed comparison metric we term neighborhood proportion error (NPE), and two-dimensional visualizations. We find that t-SNE and Diffusion Maps are the two most effective methods for preserving relationships of interest among cells and providing informative visualizations. In low dimensional embeddings, t-SNE exhibits well-defined phenotypic clustering. Additionally, Diffusion Maps can represent cell differentiation pathways with long projections along each diffusion component. We thus recommend a complementary approach using t-SNE and Diffusion Maps in order to extract diverse and informative cell relationship information in a two-dimensional setting from CyTOF data.

bioinformatics↗

Hormone Control Regions mediate opposing steroid receptor-dependent genome organizations

In breast cancer cells, topologically associating domains (TADs) behave as units of hormonal gene regulation with transcripts within hormone responsive TADs changing coordinately their expression in response to steroid hormones. Here we further described that responsive TADs contain 20-100 kb-long clusters of intermingled estrogen receptor (ER) and progesterone receptor (PR) binding sites, hereafter called Hormone-Control Regions (HCRs). We identified more than 200 HCRs, which are frequently bound by ER and PR even in the absence of hormones. These HCRs establish steady long-distance inter-TAD interactions between them and organize characteristic looping structures with promoters even in the absence of hormones. This organization is dependent on the expression of the receptors and is further dynamically modulated in response to steroid hormones. HCRs function as platforms integrating different signals resulting in some cases in opposite transcriptional responses to estrogens or progestins. Altogether, these results suggest that steroid hormone receptors act not only as hormone-regulated sequence-specific transcription factors, but also as local and global genome organizers.\n\nHighlightsHormone responsive TADs are organized around conserved large regulatory regions (HCRs) enriched in ER and PR.\nHCR contact promoters within their TADs and engaged long-range inter-TADs contacts between them.\nBinding of the receptors in absence of hormones maintains global HCR-HCR interactions and intra-TADs regulatory loops.\nHCRs can integrate the hormone signals in divergent ways leading to opposite restructuration of TADs in response to Estrogens or Progestins.

genomics↗