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Cai, D.

Publications and source records attributed to Cai, D..

At least 19 recordsLinked to original sources

SLAFIT: Viral fitness inference and structural variant detection from TGS data

Evolution is driven by genetic variation at multiple scales, from single-nucleotide variants (SNVs) to structural variants (SVs). Within populations, nonrandom associations among SNVs, quantified by linkage disequilibrium (LD), must be considered when inferring fitness from sequencing data. Characterizing SVs, SNVs, and the LD between SNVs therefore provides complementary insights into the genetic basis of evolutionary change. Although third-generation sequencing technologies facilitate the characterization of genomic variation, finite read lengths often limit the resolution of LD across entire genomes. Here, we present SLAFIT, a pipeline for linkage-aware fitness inference and SV detection from third-generation sequencing data. The pipeline reconstructs genome-wide haplotypes and their frequencies from third-generation sequencing reads to infer SNVs and estimate LD. When time-series data are available, it also infers fitness. An established SV detection tool is incorporated into the same workflow. Simulations support accurate LD and fitness inference under tested conditions, with reduced computation time through parallelization. Applications to enterovirus C104 and herpes simplex virus 1 reveal selection signals in predicted epitopes and recover a known inversion, respectively. Together, these results demonstrate the utility of SLAFIT for studying viral evolution through complementary analyses of fitness and structural variation.

bioinformatics↗

ASC specks and α-synuclein amplify microglial NLRP3 inflammasome activation and co-localize with Lewy body pathology

Neuroinflammation is a hallmark of several chronic neurodegenerative disorders, including Parkinson's disease (PD) and other synucleinopathies, and is closely associated with microglial activation. The inflammasome adaptor protein apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC) undergoes oligomerization upon inflammasome activation, resulting in the formation of ASC specks. These structures are recognized by microglia as damage-associated molecular patterns (DAMPs), thereby promoting inflammatory signaling. Recent studies have demonstrated that extracellular ASC specks associate with amyloid-{beta} (A{beta}), and that uptake of ASC-A{beta} composites by microglia amplifies pro-inflammatory responses. Although ASC specks have also been shown to potentiate -synuclein (Syn) preformed fibril-induced pathology, their interaction with monomeric Syn and their effects on inflammasome activation remain poorly understood. Here, we co-stimulated murine SIM-A9 microglia with ASC-Syn assemblies and evaluated their effects on NLRP3 inflammasome activation. Electron microscopy revealed a close association between ASC fibrils and Syn monomers. Exposure of microglia to ASC-Syn enhanced NLRP3 inflammasome activation, as evidenced by increased ASC speck formation, caspase-1 activation, and secretion of IL-1{beta} and IL-18, when compared to ASC or Syn alone. In addition, immunohistochemical analyses of post mortem brain tissue from patients with dementia with Lewy bodies demonstrated ASC expression in regions exhibiting Syn pathology and showed ASC co-localization with Syn within Lewy bodies. Collectively, these findings identify ASC-Syn assemblies as potent amplifiers of NLRP3 inflammasome signaling and suggest a mechanism through which they may contribute to sustained neuroinflammation in synucleinopathies.

neuroscience↗

A transcriptomic and spatial map of serotonin autoreceptor expression in Drosophila

Serotonin is an evolutionarily ancient neurotransmitter that modulates an array of behaviors such as mood, sleep, and appetite across species. Serotonin acts primarily by binding to serotonin receptors, which are expressed in post-synaptic neurons (heteroreceptors) and serotonergic neurons themselves (autoreceptors). Serotonin autoreceptors modulate serotonergic tone, the foundational principles of which have been excellently demonstrated in vertebrate and invertebrate models. However, many aspects of the mechanisms and contexts in which this modulation occurs are still unclear. Drosophila melanogaster is a powerful model organism that can provide unique insights into autoreceptor function by the ability to perform precise spatial and temporal genetic manipulation with structural and functional readouts / behaviors of serotonin systems. However, a systematic characterization of serotonin autoreceptor expression in Drosophila has not been conducted. Here we use single-cell sequencing and genetic labeling to show that all five serotonin receptors are expressed in serotonergic neurons and map their expression at both the larval and adult stages of development. This is the first evidence of 5-HT2A and 5-HT7 expression in serotonergic neurons in any organism. Moreover, the unique combinations of autoreceptor expression in specific neuronal clusters will aid in the development of novel hypotheses for autoreceptor function, and demonstrates the utility of Drosophila as a model organism to study the function of serotonin autoreceptors.

neuroscience↗

Novel bile salt analogs reduce lipid accumulation in liver cells with potential to treat both metabolic dysfunction-associated steatotic liver disease and Clostridioides difficile infection

Metabolic dysfunction-associated steatotic liver disease (MASLD) and Clostridioides difficile (C. difficile) infection (CDI) are clinically associated, yet there is limited effective treatment for both diseases. Bile salt analogs (BSAs) have demonstrated potential in treating either MASLD or CDI. We screened a library of BSAs (n=112) previously synthesized as potential inhibitors of C. difficile spore germination, for their therapeutic potential in reducing intracellular accumulation of fatty acids in HepG2 cells as candidates for prevention and treatment of both MASLD and CDI. The screening was based on an in vitro model established by incubating HepG2 cells with free fatty acids, with obeticholic acid (OCA), a known BSA with anti-MASLD activity as a control. Gene and protein expressions were quantified to validate the treatment effect. We found that compounds C13, C24, C25, C74, C98, and C101 demonstrated significant effectiveness in both preventing the intracellular accumulation of lipids and removing pre-loaded cellular lipids. Gene expression analysis showed that C24, C25, and C74 produced a similar pattern characterized by a robust induction of FGF21 expression, while C13, C98, and C101 produced a transcription pattern that mirrors the effect of OCA. Structurally, while C13, C24, and C25 do not display drug-like properties, C74, C98, and C101 are drug-like and share a similar structure. Interestingly, C101 is a potent inhibitor of C. difficile spore germination. OCA shows a weak anti-gemination effect. Our study identified lead compound candidates for the development of novel therapeutics capable of treating both MASLD and CDI. Significance statementThe clinical association between MASLD and CDI remains an unmet need for dual acting therapeutic strategies. Given the reported potential of BSA, we screened 112 previously synthesized as potential inhibitors of C. difficile spore germination, for their therapeutic potential in reducing intracellular accumulation of fatty acids in HepG2 cells. Our study identified compounds that effectively reduce intracellular lipid accumulation and inhibit C. difficile spore germination. These results nominate lead candidates for developing dual-acting therapeutics targeting both MASLD and CDI.

pharmacology and toxicology↗

The hedonic evaluation of neurofeedback stimuli is fast, automatic and implicit: An ERP study on stimulus design.

Introduction - Neurofeedback (NFB) has demonstrated efficacy in treating various disorders, often achieving substantial symptom reductions. Despite its effectiveness, a significant percentage of users (non-responders), fail to benefit from NFB. Addressing this issue, the study at hand investigates the role of NFB design on neuro-physiological responses. Method - event related potentials (ERPs) are examined in response to the application of different aesthetic principles in the context of NFB stimulus design. Drawing from Self-Determination Theory and ERP studies in the field of web design, 16 feedback stimuli were developed according to specific design principles. Stimulus design effects were inspected by means of ERPs allowing for the assessment of implicit and fast electroencephalogram (EEG) reactions. Results of n = 38 participants indicated distinct ERP response patterns at time window of interest 1 (TWOI-1; 100-200 ms) and TWOI-2 (200-300 ms), predicted by beholder-based liking and complexity of stimuli. The findings align with the proposed hypotheses suggesting that aesthetic evaluation of NFB stimuli occurs rapidly and implicitly. In response to the aesthetic vs. non-aesthetic categories, the findings were mixed. The results underscore the importance of further exploration of aesthetic design guidelines in the context of NFB applications. It is discussed how NFB aesthetics relate to Processing Fluency and Affective Prediction Error Theory, while the theoretical methodological issue of the Fixed Effect Fallacy is taken into consideration. The study contributes to the broader understanding of how design elements can affect therapeutic efficacy and engagement in NFB and Human Computer Interaction in therapeutic contexts in general.

neuroscience↗

Simultaneous brain-wide single-cell recording resolves spatiotemporal memory architecture

Many fundamental mammalian brain functions emerge from the coordinated activity of cells distributed across large, brain-wide networks. To understand these processes in healthy and diseased states, ideally one would simultaneously measure and analyze single-cell activity at the brain-wide scale, an enduring challenge for live-measurement approaches that often face an inherent tradeoff between spatial resolution and scale. Here, we present GLOBE (sinGle-cell spatiotemporaL recOrding Brain-widE), a technology for brain-wide single-cell recording of cellular activity in vivo with spatiotemporal resolution, physiological sensitivity, and parallelization-accelerated readout. GLOBE leverages genetically encoded intracellular protein tape recorders and a high-throughput computational platform for integrated image and signal analysis. GLOBE records analog signal amplitudes across a continuous time axis, requires only standard light microscopy for in situ readout, and is compatible with expansion microscopy and RNA readouts. We applied GLOBE to simultaneously record transcriptional activity of the immediate early gene Fos in up to 219,703 neurons simultaneously across a single mouse brain over 5.5 continuous days, with a timestamp precision of 3.1-6.7 hours (median absolute error), a local recording density of 69-90% of neurons per imaging field of view, and a post-mortem imaging readout speed of 2.9 seconds per neuron on average. GLOBE resolves the brain-wide spatiotemporal structure of single-cell activity, revealing that Fos transcriptional dynamics associated with fear learning and memory retrieval are distributed across the brain with region-specific temporal heterogeneity, and that the variance of this structure scales down as the number of sampled cells increases. We envision GLOBE to have broad applications for dissecting and decoding physiological and pathological processes at the brain-wide scale.

neuroscience↗

A graph-based pangenome reveals the genetic basis of climate-resilient and horticultural traits in pear

Climate change poses an increasing threat to the cultivation of deciduous fruit trees, placing greater demands on modern pear breeding. Using pear germplasm adapted to diverse environments, we assembled 11 chromosome-level genomes. In combination with 13 publicly accessible pear genomes, we analyzed presence-absence variations (PAVs) and constructed a graph-based pangenome for pear. By performing a PAV-eQTL analysis of the fruit of 123 pear accessions, we identified PAVs significantly associated with expression levels of genes that may be involved in regulating agronomic traits. Population analysis of 268 pear accessions revealed two stop-gained variants in DAM1 of independent origin, which may function in advancing the blooming date and reducing the chilling requirement. We detected complex PAVs at the NOR1 locus, including two copy-number variations and one deletion. These PAVs contributed to the rapid diversification of the NOR1 locus and the fruit development period through regulating ARF5 and other ripening-related genes. We revealed the selection history of the NOR1 locus and developed novel pear individuals that accumulated alleles for low chilling requirement, early blooming date, and short fruit development period. The results provide valuable resources for pear genomics research and offer a guideline for breeding modern pears with climate resilience.

plant biology↗

Detergent-Free Nuclear-Cytoplasmic Fractionation Enables Spatially Resolved PELSA for Enhanced Nuclear Drug Target Identification

Accurate identification of drug target proteins remain major challenges in proteomics-based target discovery, particularly for low-abundance nuclear proteins that are difficult to detect because of the complexity of whole-cell lysates. Here, we developed a detergent-free nuclear-cytoplasmic fractionation strategy compatible with peptide-centric local stability analysis (PELSA), which markedly improves detection of nuclear drug targets. Using K562 cells, we demonstrated that mild detergent-free fractionation enables high-fidelity nuclear-cytoplasmic separation with minimal cross-contamination. When coupled with PELSA, this workflow significantly increases the number of detected nuclear targets relative to whole-cell analysis. Benchmarking with well-characterized nuclear drugs, including the histone deacetylase inhibitor panobinostat and the RNA polymerase II inhibitor -amanitin, our results showed improved identification of canonical nuclear targets. Broad profiling of staurosporine target further revealed expanded kinase target coverage by combining the results of nuclear and cytoplasmic fraction, with the CLK family kinases detected exclusively in the nuclear fractions. Additionally, we showed that PELSA can also be performed on intact nucleus level. Collectively, these findings establish detergent-free nuclear-cytoplasmic fractionation-PELSA as a robust and scalable strategy for spatially resolved drug target identification, improving sensitivity for nuclear and low-abundance proteins.

biochemistry↗

Retrotransposons Promote Clonal Hematopoiesis Through Aging-Related Stromal Inflammation

Clonal hematopoiesis (CH) is an age-related phenomenon driven by the expansion of mutant hematopoietic stem cell (HSC) clones, most commonly harboring mutations in DNMT3A. While inflammation is known to promote CH, the upstream triggers of this inflammatory state remain unclear. We show that aging selectively upregulates retrotransposons in the non-hematopoietic cell compartment of the murine bone marrow, particularly in mesenchymal stromal cells. Using in vivo competitive transplant models, we demonstrate that retrotransposon-induced inflammation cell-extrinsically promotes Dnmt3a-mutant HSC expansion. This competitive advantage arises from mutant HSC resistance to inflammation-driven cell cycle perturbations. Mechanistically, we show that retrotransposon activation induces type I interferon signaling via viral mimicry, such that stromal knockdown of either Irf3 or Sting abrogates the competitive advantage of Dnmt3a-mutant HSCs. Our findings establish stromal-selective retrotransposon reactivation as a previously unrecognized, non-cell-autonomous source of inflammation that contributes to age-associated CH. Key PointsO_LIRetrotransposons remodel the aging niche through viral mimicry pathways to promote Dnmt3a-mutant clonal hematopoiesis. C_LIO_LIRetrotransposon-mediated inflammation impairs wild-type HSC fitness, while Dnmt3a-mutant HSCs resist inflammatory changes. C_LI

cancer biology↗

Histone H2BK120 ubiquitination modulates PRC1 activity and H2AK119ub deposition on nucleosomes

Polycomb group and Trithorax group complexes antagonistically regulate developmental gene expression, yet the mechanisms coordinating their interplay remain poorly understood. Here, we uncover a synergistic histone crosstalk in which H2BK120ub (histone H2B ubiquitination at lysine 120), a Trithorax-associated active mark, enhances Polycomb repressive complex 1 (PRC1) activity by directly binding specific PCGF subunits of PRC1 on the nucleosome surface, as shown in cryo-electron microscopy (cryo-EM) analysis. Beyond regulating enzymatic activity, H2BK120ub also modulates the competitive binding between the catalytic RNF2-BMI1 module and the RYBP subunit of noncanonical PRC1.4 complexes to nucleosomes, potentially restricting H2AK119ub (histone H2A ubiquitination at lysine 119) spreading to neighboring nucleosomes. In mouse embryonic stem cells, H2BK120ub directs the deposition of H2AK119ub within the gene bodies of a subset of developmental genes, which exhibit more rapid activation compared to canonical H3K4me3/H3K27me3 bivalent genes. These findings reveal a previously unrecognized mechanism that links active and repressive histone modifications, providing new insights into the intricate chromatin regulation of gene expression during development.

molecular biology↗

Stress-induced loss of CTCF reveals an alternative, promoter-based mode of cohesin looping

Cells continually face environmental stressors that challenge homeostasis, yet how three-dimensional (3D) chromatin structure contributes to these stress responses remains unclear under hyperosmotic conditions. To investigate this, we map 3D chromatin structure, its molecular drivers, and transcriptional outcomes during sorbitol-induced hyperosmotic stress. Within 1 hour of sorbitol treatment, pre-existing loops and domains collapse, while several hundred de novo sorbitol-induced loops emerge. These loops are punctate, longer-range, and transient. 3D chromatin structure largely returns to baseline conditions by 24 hours. Loop reorganization is consistent across cell types and hyperosmotic stimuli. Sorbitol-induced loops require cohesin but not CTCF, and anchors are enriched at active promoters harboring GC-rich transcription factor motifs. Genes at these anchors show delayed activation following loop formation, consistent with loops acting upstream of transcription. Together, hyperosmotic stress triggers rapid, reversible, CTCF-independent chromatin reorganization that correlates with transcriptional adaptation.

genomics↗

Monitor individual health and improve breeding success in Crested ibis (Nipponia nippon)

Biodiversity loss has become a pressing issue, requiring effective conservation measures. Drawing lessons from successful examples is essential. The Crested ibis (Nipponia nippon), once critically endangered but now recovering through intensive conservation programs, provides an informative model for evaluating and improving conservation practices. Using 17 years of monitoring data from a captive population spanning eight generations, we applied quantitative genetic tools (Animal Model) to characterize individual growth and improve breeding success of this endangered species. We found that body weight from Day 0 to Day 42 exhibited significant heritability (h2 = 0.195, 95% HPD 0.139 [~] 0.250). As for growth curve parameters, growth time-scale parameter a (h2 = 0.33, 95% HPD: 0.14 [~] 0.55) and growth-rate coefficient b (h2 = 0.22, 95% HPD: 0.10 [~] 0.34) were also significantly heritable, while the heritability of potential maximum weight M was relatively low (h2 = 0.023, 95% HPD: 0.00 [~] 0.16). We further estimated the breeding values of these phenotypical traits to inform future breeding and selections. Intergenerational analyses showed the estimated breeding values for body weight exhibited a tendency to increase, accompanied by a slower growth rate, though trends did not differ significantly from expectations under genetic drift. Comparison of parental and offspring growth trajectories revealed that healthy offspring closely follow parental growth trajectories, whereas unhealthy individuals display reduced growth. Given the multiple breeding times of this long-lived species, this approach enables effective monitoring of individual growth and health, allowing timely veterinary interventions so to enhance conservation efficiency.

zoology↗

Carbohydrate adaptation drives liver-brain axis maturation

Mammalian postnatal life requires adaptation to a carbohydrate-rich diet, yet how metabolic programs are coordinated within and across organs is unclear. Using time-resolved transcriptomic and metabolomic analyses from the neonatal period through adulthood, we show that mouse liver rapidly acquires oxidative and detoxification capacity after weaning. This transition enables the brain to establish energy-sufficient, low-toxicity metabolic environment for neuronal development. This maturation process is marked by progressive activation of the hepatic electron transport chain (ETC), with the mitochondrial RNA endoribonuclease LACTB2 acting as a key regulator. LACTB2 prevents the accumulation of mitochondrial RNAs and sustains expression of mtDNA-encoded ETC subunits, thereby preserving mitochondrial competence for oxidative metabolism. LACTB2 is postnatally induced in hepatocytes, and its loss causes defective glucose utilization, systemic metabolic toxicity, and impaired brain metabolism and myelination, leading to prepubertal lethality, particularly in males. Restoring ETC function through liver-targeted expression of yeast NADH dehydrogenase NDI1, inhibiting the integrated stress response or ammonia scavenging improved survival. Our findings identify LACTB2-dependent hepatic mitochondrial maturation as a central mechanism that aligns carbohydrate adaptation with the liver-brain metabolic coordination to support early-life development.

developmental biology↗

Molecular determinants underlying functional divergence of TBP homologs

The TATA-box binding protein (TBP) is a highly conserved basal transcription factor and a core component of the pre-initiation complex (PIC) for all three eukaryotic RNA polymerases (RNA Pols). Despite this conservation, TBP function diverges across species. In yeast, TBP is required for all three RNA Pols, whereas in mammals, it is essential only for RNA Pol III, but not RNA Pol I or II. To examine the evolutionary divergence of TBP homologs in different species, we determined the ability of murine TBP and its paralogs to complement endogenous TBP in Saccharomyces cerevisiae. Despite their highly conserved DNA-binding domains, murine TBP homologs were unable to fully rescue the lethality caused by TBP inactivation in yeast. This incomplete complementation correlates with a failure to fully support binding by RNA Pols II and III. Furthermore, we show that the divergent N-terminal domain (NTD) of TBP contributes to species-specific activity and modulates RNA Pol II binding changes in stress-induced response. Lastly, we demonstrate a negative correlation between the length of the intrinsically disordered NTD of TBP family proteins and the gene density in different species, suggesting that the NTD may have contributed to increasingly complex gene regulation during evolution.

molecular biology↗

Repurpose of Ritlecitinib Reduces Neointima Formation and Enhances Endothelial Recovery Following Vascular Injury

BackgroundNeointimal hyperplasia after vascular injury reflects excess smooth muscle cell (SMC) proliferation with impaired endothelial recovery. We tested the hypothesis that selective Janus kinase 3 (JAK3) inhibition with the FDA-approved drug Ritlecitinib limits neointima while accelerating reendothelialization. MethodsWe used mouse carotid wire injury and a human internal mammary artery (IMA) xenograft model to evaluate effects of genetic JAK3 loss in SMCs or oral Ritlecitinib in vascular remodeling. Mechanistic studies in SMCs assessed JNK/c-Jun signaling and its regulation of thrombospondin-1 (TSP-1) and vascular endothelial growth factor A (VEGF-A) using RNA-seq and CUT&RUN. Rescue experiments tested whether VEGF-A neutralization or exogenous TSP-1 reversed the antineointimal effects. Patient-derived IMA SMCs were analyzed for variabilities in drug responses. ResultsGenetic JAK3 loss in SMCs or oral Ritlecitinib reduced neointimal area and intima/media ratio and increased luminal CD31+ coverage in both models. In SMCs, Ritlecitinib suppressed JNK/c-Jun signaling, downregulated TSP-1, and restored VEGF-A, shifting the milieu toward endothelial regeneration. RNA-seq and CUT&RUN corroborated JNK/c-Jun- dependent control of TSP-1 and VEGFA. VEGF-A neutralization or exogenous TSP-1 abrogated the anti-neointimal phenotype. In patient-derived IMA SMCs, variable drug response was linked to the JAK3 Pro893Asn variant and a VEGFA promoter SNP. ConclusionSelective JAK3 inhibition by Ritlecitinib simultaneously restrains SMC proliferation and promotes endothelial repair through modulating TSP-1 and VEGF-A activities. Ritlecitinib merits clinical evaluation as a precision therapy to prevent restenosis, with genetic stratification to identify responders.

pathology↗

Hypobaric hypoxia drives citrate cycle reprogramming to suppress tumor progression

High altitude residents present lower tumor incidence and mortality than plain residents, suggesting that hypobaric hypoxia displays protective effect against tumor development. The results of our studies showed that hypobaric hypoxia exposure significantly suppressed tumor progression in subcutaneous bearing and lung metastasis tumor models. With single-cell transcriptome analysis, we identified HIF-1 pathway was significantly downregulated in tumor tissues with high altitude hypoxia, leading to decreased glycolysis and angiogenesis and improved antitumor immune response. Mechanistically, systemic hypoxia rewired citric acid cycle, with enhanced CS and IDH2 expression and reduced OGDH and SUCLG2 expression, to induce -ketoglutarate accumulation and succinate decline in tumor microenvironment, further mediating HIF-1 pathway inhibition. Moreover, hypobaric hypoxia treatment significantly improved the antitumor effects of adjuvant therapies (including chemotherapy, anti-angiogenic therapy and immunotherapy). Our findings reveal the role and mechanism of hypobaric hypoxia for tumor regression and yield new insights into tumor therapy.

cancer biology↗

A parallelly distributed microscope and software system for scalable high-throughput multispectral 3D imaging

Recent advances in high throughput optical microscopy have achieved whole-organism scale imaging at diffraction-limited resolutions. Current microscopes, however, require making compromises between achieving the optimal resolution, imaging depth, multispectral capability, and data throughput due to limitations in optical design and data stream handling. We have created a parallel-line scanning confocal microscope (plSCM) which provides 1.1 Gigavoxels/second high speed imaging while achieving an optical resolution of [~]180 x 220 x 650 nm with 2 millimeters of imaging depth in 3 simultaneous spectral channels. To handle such a massive imaging data stream, we have engineered a scalable network-distributed image acquisition/processing framework (SNDiF), which allows continuous capture, real-time processing, and cluster storage of petabyte-scale single image datasets in days. Together, our parallelly distributed microscope and software system presents a general solution for large-scale high-throughput and high-resolution multicolor imaging which can operate for days at a time.

bioengineering↗

Rainbow Nucleus Charts Dynamic Interactome of Membrane-less Organelles

Membrane-less organelles (MLOs) perform diverse cellular functions, but how they interact to coordinate these processes remains poorly understood. Here we constructed a "Rainbow Nucleus" cell line to simultaneously visualize five nuclear MLOs using multi-spectral live-cell imaging. We find that MLO interactions are not random: nuclear speckles serve as hubs, and functionally related MLOs interact more frequently than unrelated MLOs. While some interactions are stable, such as those between the histone locus bodies and Cajal bodies, others are transient, such as those between PML nuclear bodies and Cajal bodies. Single particle tracking revealed that stable contacts between Cajal bodies and nuclear speckles are functional, promoting the outward trafficking of small nuclear ribonucleoproteins from Cajal bodies. Finally, RNA Polymerase II-mediated transcription is required to organize the MLO interactome. Our study reveals a structured, transcription-dependent contact network among nuclear MLOs, laying the foundation for future cellular engineering efforts to modulate the MLO interactome.

cell biology↗