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Jeong, D.

Publications and source records attributed to Jeong, D..

At least 19 recordsLinked to original sources

Fine-Grained and Reliable Cell Classification from Pathology Images

Molecular assays such as spatial transcriptomics facilitate fine-grained identification of cell types for analyzing tumor microenvironments. However, they are expensive to acquire in routine clinical practice compared to hematoxylin and eosin (H&E) images. With molecular guidance, such images can distinguish cell lineages, yet often fail to resolve closely related subtypes. To overcome this, we introduce CellBridge, a multi-modal contrastive learning framework pretrained on 16M cells with paired H&E and spatial profiles, for transferring molecular information into morphological representations. CellBridge further incorporates a Cell-Ontology-aware conformal prediction module that assigns labels at different levels of specificity: leaf-level cell types when morphology alone provides sufficient evidence, and broader ancestor categories when distinguishing among more specific cell types would require molecular information. Across in-domain and out-of-domain benchmarks, CellBridge outperforms leading pathology foundation models in macro F1 by up to 16 percentage points, with the largest gains on the most fine-grained label spaces. It consistently achieves smaller prediction sets, while reducing class-wise coverage gaps. We envision CellBridge as a step toward extracting cellular information that currently requires costly molecular assays from routinely acquired pathology images, while explicitly identifying where such assays remain necessary. Our code is available at https://github.com/Lotfollahi-lab/cellbridge.

bioinformatics↗

Chromatin accessibility–transcription coupling is dynamically reconfigured during Arabidopsis embryo maturation

Chromatin accessibility (CA) is widely profiled alongside transcription because it is generally associated with transcriptional activity. How directly the two layers are linked remains unclear. We addressed this in Arabidopsis thaliana embryos. We profiled CA and transcription across the torpedo, bent-cotyledon, and mature-green stages using stage-resolved nicking enzyme-assisted sequencing (NicE-seq) and nanopore RNA sequencing. To test whether their relationship is genetically regulated, we also analyzed ld-1, a mutant of LUMINIDEPENDENS (LD) linked to global transcriptional repression. Transcriptomes formed discrete stage-specific programmes, but CA did not. Accessibility at both promoters and transcription-factor motifs largely followed a common developmental trajectory that peaked at the bent-cotyledon stage and declined thereafter, rather than mirroring module-specific expression patterns. Loss of LD preserved promoter architecture but extensively remodelled motif accessibility, increasing its concordance with module-specific expression timing and strengthening CA-transcription coupling. Chromatin accessibility and transcription are subject to partly independent regulation during embryo maturation. The ability of LD loss to strengthen accessibility-transcription concordance demonstrates that their coupling is a regulated rather than fixed property of developmental chromatin.

Developmental Biology↗

Fructose utilization by GM-CSF-differentiated macrophages aggravates autoimmune inflammation via MG-derived AGE-RAGE signaling

Excessive fructose intake is increasingly associated with metabolic and inflammatory pathologies; however, the direct impact of fructose metabolism on immune cell function remains insufficiently understood. Here, we demonstrate that GM-CSF-differentiated macrophages markedly upregulate the fructose-specific transporter GLUT5, enabling efficient fructose utilization through two complementary metabolic pathways. Using 13C-fructose tracing, we identified distinct carbon fluxes via a hexokinase (HK)-dependent glycolytic route and a ketohexokinase (KHK)-ALDOB-mediated fructolytic route. The HK-dependent pathway sustains glycolytic activity under glucose-limiting conditions, stabilizing HIF-1 and preserving pro-inflammatory gene expression. Conversely, the KHK-ALDOB axis increases dihydroxyacetone phosphate (DHAP) production, leading to methylglyoxal-derived advanced glycation end-products (MG-AGEs) that engage receptor for AGE (RAGE) signaling. This activation enhances MMP9 expression in macrophages and drives Th17 differentiation in CD4 T cells, amplifying inflammatory and tissue-remodeling processes. In vivo, fructose intake exacerbates autoimmune arthritis in SKG mice, and elevated fructose-driven glycolysis and MG-AGE accumulation are observed in monocytes from patients with rheumatoid arthritis. These results link fructose-driven carbonyl stress to macrophage effector programs and downstream T cell polarization. Collectively, these findings uncover a dual fructose metabolic program that integrates nutrient stress with persistent inflammation via the MG-AGE-RAGE axis and underscore the immunometabolic risks of excessive fructose exposure.

immunology↗

Ubiquitin Receptor-Induced Proximity is Sufficient for Ubiquitin-Independent Targeted Protein Degradation via the 26S Proteasome

The 26S proteasome engages with ubiquitinated substrates primarily through its constituent ubiquitin (Ub) receptors, which initiates a cascade of proteolytic processes. Leveraging this recognition mechanism, we developed a targeted protein degradation (TPD) strategy that recruits substrates directly to the proteasome, thereby bypassing the ubiquitination step. Our proteasome-targeting chimera, Protea-Tac, is a heterobifunctional protein degrader composed of a Ub receptor and an intracellular antibody. This chimera integrates into 26S proteasomes without altering their functional integrity. Localization of target proteins, including c-Fos, BRD4, Flag-TDP43, HA-tau, and GFP-ODC, to the proteasome via Protea-Tac with cognate antibodies resulted in their induced degradation. We demonstrated that this platform is 1) modular, allowing facile switching between targets; 2) Ub-independent; and 3) highly target-specific. Protea-Tac exhibited in vivo anti-tumor efficacy, degrading c-Fos and substantially delaying tumor growth. Overall, these findings identify Protea-Tac as a distinct TPD modality capable of directly degrading intracellular proteins via engineered 26S proteasomes. TeaserProtea-Tac is a heterobifunctional protein degrader that enables Ub-independent TPD, exhibits high specificity and modularity, and demonstrates in vivo applicability.

biochemistry↗

Scaling Large Language Models for Next-Generation Single-Cell Analysis

AO_SCPLOWBSTRACTC_SCPLOWSingle-cell RNA sequencing has transformed our understanding of cellular diversity, yet current single-cell foundation models (scFMs) remain limited in their scalability, flexibility across diverse tasks, and ability to natively integrate textual information. In this work, we build upon the Cell2Sentence (C2S) framework, which represents scRNA-seq profiles as textual "cell sentences," to train Large Language Models (LLMs) on a corpus comprising over one billion tokens of transcriptomic data, biological text, and metadata. Scaling the model to 27 billion parameters yields consistent improvements in predictive and generative capabilities and supports advanced downstream tasks that require synthesis of information across multi-cellular contexts. Targeted fine-tuning with modern reinforcement learning techniques produces strong performance in perturbation response prediction, natural language interpretation, and complex biological reasoning. This predictive strength enabled a dual-context virtual screen that nominated the kinase inhibitor silmitasertib (CX-4945) as a candidate for context-selective upregulation of antigen presentation. Experimental assessment in human cell models unseen during training supported this prediction, demonstrating that C2S-Scale can effectively guide the discovery of context-conditioned biology. C2S-Scale unifies transcriptomic and textual data at unprecedented scales, surpassing both specialized single-cell models and general-purpose LLMs to provide a platform for next-generation single-cell analysis and the development of "virtual cells."

bioinformatics↗

Acetate metabolism during xylose fermentation enhances 3-hydroxypropionic acid production in engineered acid-tolerant Issatchenkia orientalis

Efficient bioconversion of acetate-rich lignocellulosic biomass into value-added chemicals remains a major challenge due to the toxicity of acetic acid. In this study, we engineered an acid-tolerant Issatchenkia orientalis strain (IoDY01H) capable of producing 3-hydroxypropionic acid (3-HP), a key bioplastic precursor, from glucose, xylose, and acetate. Using a Cas9-based genome editing system with a hygromycin B resistance marker, we introduced heterologous genes encoding xylose utilization and {beta}-alanine-based 3-HP biosynthetic pathways into the I. orientalis genome. Metabolomic analysis revealed that acetate supplementation redirected metabolic flux toward amino acid and lipid metabolism while reducing TCA cycle intermediates. Acetate enhanced 3-HP production by promoting accumulation of {beta}-alanine, but also revealed {beta}-alanine-pyruvate aminotransferase as a metabolic bottleneck under acidic conditions. Using pretreated hemp stalk hydrolysate as a feedstock, the engineered strain achieved a 3-HP titer of 8.7 g/L via separate hydrolysis and fermentation (SHF), outperforming simultaneous saccharification and fermentation (SSF). These findings demonstrate the feasibility of producing 3-HP from acetate-rich biomass using engineered non-conventional yeast and highlight I. orientalis as a promising microbial chassis for industrial bioconversion. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=90 SRC="FIGDIR/small/649204v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@c04442org.highwire.dtl.DTLVardef@c16b4aorg.highwire.dtl.DTLVardef@6af6d9org.highwire.dtl.DTLVardef@743029_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIEngineered I. orientalis co-utilized xylose and acetate to produce 3-HP. C_LIO_LIAcetate addition enhanced 3-HP production during xylose fermentation. C_LIO_LIAcetate redirected metabolic flux toward 3-HP biosynthesis pathways. C_LIO_LIEngineered I. orientalis achieved 8.7 g/L 3-HP from hemp stalk hydrolysate via SHF. C_LI

synthetic biology↗

Long-term innovative potential of genetic research and its suppression

Long-term innovation depends not only on discovering new elements but also on facilitating new recombination at the time of their co-availability. This notion of combinatorial innovation raises the question about whether scientific exploration and industry research persist over similar time horizons to meet innovative opportunities. Here, we analyze about 20 million papers and US, Chinese, and European patents to compare the courses of scientific and industrial activities in genetic research, a domain of far-reaching societal importance. We observe that research on new genes has declined since the early 2000s, but the exploration of novel gene combinations remains active for biotechnology innovation. Yet, fields of highly practical or commercial focus are less likely to test novel gene combinations. Furthermore, industry R&D on each gene tends to decline earlier than scientific interest in that gene. After this decline of the industrial momentum, continuous scientific research still sustains exploratory and innovative opportunities, involving novel gene combinations, clinical trials, and technologically-impactful work. Based on a hypothetical scenario of over-aligned science and industry, we estimate that up to 42.2-74.4% of the combinational opportunities would be unexplored if scientific research becomes hindered due to industrys retreat. This study suggests the potential complementary roles of scientific and industrial research with different temporal modes in innovation cycles, calling for balanced policies to foster innovation ecosystems.

scientific communication and education↗

Neuronal LAG3 facilitates pathogenic α-synuclein neuron-to-neuron propagation

Lymphocyte activation gene 3 (LAG3) is a key receptor involved in the propagation of pathological proteins in Parkinsons disease (PD). This study investigates the role of neuronal LAG3 in mediating the binding, uptake, and propagation of -synuclein (Syn) preformed fibrils (PFFs). Using neuronal LAG3 conditional knockout mice and human induced pluripotent stem cells-derived dopaminergic (DA) neurons, we demonstrate that LAG3 expression is critical for pathogenic Syn propagation. Our results show that the absence of neuronal LAG3 significantly reduces Syn pathology, alleviates motor dysfunction, and inhibits neurodegeneration in vivo. Electrophysiological recordings revealed that Syn PFFs induce pronounced neuronal hyperactivity in wild-type (WT) neurons, increasing firing rates in cell-attached and whole-cell configurations, and reducing miniature excitatory postsynaptic currents. In contrast, neurons lacking LAG3 resisted these electrophysiological effects. Moreover, treatment with an anti-human LAG3 antibody in human DA neurons inhibited Syn PFFs binding and uptake, preventing pathology propagation. These findings confirm the essential function of neuronal LAG3 in mediating Syn propagation and associated disruptions, identifying LAG3 as a potential therapeutic target for PD and related -synucleinopathies.

neuroscience↗

Long-term Immunity of a Microneedle Array Patch of SARS-CoV-2 S1 Protein Subunit Vaccine Irradiated by Gamma Rays in Mice

COVID-19 vaccines effectively prevent symptomatic infection and severe disease, including hospitalization and death. However, unequal vaccine distribution during the pandemic, especially in low- and middle-income countries, has led to the emergence of vaccine-resistant strains. This underscores the need for alternative, safe, and thermostable vaccine platforms, such as dissolved microneedle array patches (MAP) delivering a subunit vaccine, which eliminate the need for cold chain and trained healthcare personnel. This study demonstrates that the SARS-CoV-2 S1 monomer with RS09, a TLR-4 agonist peptide, serves as an optimal protein subunit immunogen. This combination stimulates a stronger S1-specific immune response, resulting in binding to the membrane-bound spike on the cell surface and ACE2-binding inhibition, compared to the monomer S1 alone or trimer S1, regardless of RS09. MAP delivery of the rS1RS09 subunit vaccine elicited higher and longer-lasting immunity compared to conventional intramuscular injection. S1-specific IgG levels remained significantly elevated for up to 70 weeks post-administration. Additionally, different doses of 5, 15, and 45 g of MAP vaccines induced robust and sustained Th2-prevalent immune responses, suggesting a dose-sparing effect and inducing significantly high neutralizing antibodies against the Wuhan, Delta, and Omicron variants at 15 and 45 g dose. Moreover, gamma irradiation as a terminal sterilization method did not significantly affect immunogenicity, with irradiated vaccines maintaining comparable efficacy to non-irradiated ones. The stability of MAP vaccines was evaluated after long-term storage at room temperature and refrigeration for 19 months, showing minimal protein degradation. Further, after an additional one-month of storage at elevated temperature (42{degrees}C), rS1RS09 in both non-irradiated and irradiated MAP degraded less than 3%, while the liquid subunit vaccine degraded over 23%. Overall, these results indicate that gamma irradiation sterilized MAP-rS1RS09 vaccines maintain stability during extended storage without refrigeration, supporting their potential for mass production and widespread use in global vaccination efforts.

microbiology↗

Single-cell multidimensional profiling of tumor cell heterogeneity in supratentorial ependymomas

Supratentorial ependymomas are aggressive childhood brain cancers that retain features of neurodevelopmental cell types and segregate into molecularly and clinically distinct subgroups, suggesting different developmental roots. The developmental signatures as well as microenvironmental factors underlying aberrant cellular transformation and behavior across each supratentorial ependymoma subgroup are unknown. Here we integrated single cell- and spatial transcriptomics, as well as in vitro and in vivo live-cell imaging to define supratentorial ependymoma cell states, spatial organization, and dynamic behavior within the neural microenvironment. We find that individual tumor subgroups harbor two distinct progenitor-like cell states reminiscent of early human brain development and diverge in the extent of neuronal or ependymal differentiation. We further uncover several modes of spatial organization of these tumors, including a high order architecture influenced by mesenchymal and hypoxia signatures. Finally, we identify an unappreciated role for brain-resident cells in shifting supratentorial ependymoma cellular heterogeneity towards neuronal-like cells that co-opt immature neuronal morphology and invasion mechanisms. Collectively, these findings provide a multidimensional framework to integrate transcriptional and phenotypic characterization of tumor heterogeneity in supratentorial ependymoma and its potential clinical implications.

cancer biology↗

Chaperonin-mediated Winter Cold Response via Circadian Clock Components in Arabidopsis

Vernalization and cold acclimation are plant strategies that evolved to enhance their fitness during the winter season. The molecular mechanisms behind these processes in Arabidopsis have been intensively studied. However, how plants measure the duration of long-term cold exposure has not been fully understood. Our research shows that cytosolic chaperonin is crucial for appropriate long-term cold responses by regulating plant circadian clocks. Furthermore, one of the clock components, REVEILLE4 (RVE4) and RVE8 directly activate VERNALIZATION INSENSITIVE 3 (VIN3) and the C-REPEAT BINDING FACTOR (CBF)/DEHYDRATION-RESPONSIVE ELEMENT BINDING 1 (DREB1) family genes, which are key regulators of vernalization and cold acclimation, respectively. The activation of the VIN3 and CBF/DREB1 genes was specific to the time of day, indicating that cold exposure during the day is critical for long-term cold responses. Our research delves deeper into understanding the regulatory mechanism governing these two distinct long-term cold responses.

plant biology↗

Self-Assembled Origami Neural Probes for Scalable, Multifunctional, Three-Dimensional Neural Interface

Flexible intracortical neural probes have drawn attention for their enhanced longevity in high-resolution neural recordings due to reduced tissue reaction. However, the conventional monolithic fabrication approach has met significant challenges in: (i) scaling the number of recording sites for electrophysiology; (ii) integrating of other physiological sensing and modulation; and (iii) configuring into three-dimensional (3D) shapes for multi-sided electrode arrays. We report an innovative self-assembly technology that allows for implementing flexible origami neural probes as an effective alternative to overcome these challenges. By using magnetic-field-assisted hybrid self-assembly, multiple probes with various modalities can be stacked on top of each other with precise alignment. Using this approach, we demonstrated a multifunctional device with scalable high-density recording sites, dopamine sensors and a temperature sensor integrated on a single flexible probe. Simultaneous large-scale, high-spatial-resolution electrophysiology was demonstrated along with local temperature sensing and dopamine concentration monitoring. A high-density 3D origami probe was assembled by wrapping planar probes around a thin fiber in a diameter of 80[~]105 m using optimal foldable design and capillary force. Directional optogenetic modulation could be achieved with illumination from the neuron-sized micro-LEDs (LEDs) integrated on the surface of 3D origami probes. We could identify angular heterogeneous single-unit signals and neural connectivity 360{degrees} surrounding the probe. The probe longevity was validated by chronic recordings of 64-channel stacked probes in behaving mice for up to 140 days. With the modular, customizable assembly technologies presented, we demonstrated a novel and highly flexible solution to accommodate multifunctional integration, channel scaling, and 3D array configuration.

neuroscience↗

Unveiling the influence of tumor and immune signatures on immune checkpoint therapy in advanced lung cancer

This study investigates the variability among patients with non-small cell lung cancer (NSCLC) in their responses to immune checkpoint inhibitors (ICI). Recognizing that patients with advanced-stage NSCLC rarely qualify for surgical interventions, it becomes crucial to identify biomarkers that influence responses to ICI therapy. We conducted an analysis of single-cell transcriptomes from 33 lung cancer biopsy samples, with a particular focus on 14 core samples taken before the initiation of palliative ICI treatment. Our objective was to link tumor and immune cell profiles with patient responses to ICI. We discovered that ICI non-responders exhibited a higher presence of CD4+ regulatory T cells, resident memory T cells, and TH17 cells. This contrasts with the diverse activated CD8+ T cells found in responders. Furthermore, tumor cells in non-responders frequently showed heightened transcriptional activity in the NF-kB and STAT3 pathways, suggesting a potential inherent resistance to ICI therapy. Through the integration of immune cell profiles and tumor molecular signatures, we achieved an discriminative power (AUC) exceeding 95% in identifying patient responses to ICI treatment. These results underscore the crucial importance of the interplay between tumor and immune microenvironment, including within metastatic sites, in affecting the effectiveness of ICIs in NSCLC.

bioinformatics↗

Single cell approaches define forebrain neural stem cell niches and identify microglial ligands that enhance precursor-mediated remyelination

Here we used single cell RNA-sequencing and single cell spatial transcriptomics to characterize the forebrain neural stem cell (NSC) niche under homeostatic and injury conditions. We define the dorsal and lateral ventricular-subventricular zones (V-SVZ) as two distinct neighborhoods, and show that following white matter injury, dorsal NSCs are locally activated to make oligodendrocytes for remyelination. This activation is coincident with a robust increase in transcriptionally-distinct microglia in the dorsal V-SVZ niche. We modeled ligand-receptor interactions within this changing niche and identified two remyelination-associated microglial ligands, IGF1 and OSM, that promote precursor proliferation and oligodendrogenesis in culture. Infusion of either ligand into the lateral ventricles also enhanced oligodendrogenesis, even in the lateral V-SVZ, where NSCs normally make neuroblasts. These data support a model where gliogenesis versus neurogenesis is determined by the local NSC neighborhood and where injury-induced niche alterations promote NSC activation, local oligodendrogenesis, and likely contribute to myelin repair.

neuroscience↗

Fourth dose of Microneedle Array Patch of SARS-CoV-2 S1 Protein Subunit Vaccine Elicits Robust Long-lasting Humoral Responses in mice

The COVID-19 pandemic has underscored the pressing need for safe and effective booster vaccines, particularly in considering the emergence of new SARS-CoV-2 variants and addressing vaccine distribution inequalities. Dissolving microneedle array patches (MAP) offer a promising delivery method, enhancing immunogenicity and improving accessibility through the skins immune potential. In this study, we evaluated a microneedle array patch-based S1 subunit protein COVID-19 vaccine candidate, which comprised a bivalent formulation targeting the Wuhan and Beta variant alongside a monovalent Delta variant spike proteins in a murine model. Notably, the second boost of homologous bivalent MAP-S1(WU+Beta) induced a 15.7-fold increase in IgG endpoint titer, while the third boost of heterologous MAP-S1RS09Delta yielded a more modest 1.6-fold increase. Importantly, this study demonstrated that the administration of four doses of the MAP vaccine induced robust and long-lasting immune responses, persisting for at least 80 weeks. These immune responses encompassed various IgG isotypes and remained statistically significant for one year. Furthermore, neutralizing antibodies against multiple SARS-CoV-2 variants were generated, with comparable responses observed against the Omicron variant. Overall, these findings emphasize the potential of MAP-based vaccines as a promising strategy to combat the evolving landscape of COVID-19 and to deliver a safe and effective booster vaccine worldwide.

immunology↗

Pathological Tau transmission initiated by binding lymphocyte-activation gene 3

The spread of prion-like protein aggregates is believed to be a common driver of pathogenesis in many neurodegenerative diseases. Accumulated tangles of filamentous Tau protein are considered pathogenic lesions of Alzheimers disease (AD) and related Tauopathies, including progressive supranuclear palsy, and corticobasal degeneration. Tau pathologies in these illnesses exhibits a clear progressive and hierarchical spreading pattern that correlates with disease severity1, 2. Clinical observation combined with complementary experimental studies3, 4 have shown that Tau preformed fibrils (PFF) are prion-like seeds that propagate pathology by entering cells and templating misfolding and aggregation of endogenous Tau. While several receptors of Tau are known, they are not specific to the fibrillar form of Tau. Moreover, the underlying cellular mechanisms of Tau PFF spreading remains poorly understood. Here, we show that the lymphocyte-activation gene 3 (Lag3) is a cell surface receptor that binds to PFF, but not monomer, of Tau. Deletion of Lag3 or inhibition of Lag3 in primary cortical neurons significantly reduces the internalization of Tau PFF and subsequent Tau propagation and neuron-to-neuron transmission. Propagation of Tau pathology and behavioral deficits induced by injection of Tau PFF in the hippocampus and overlying cortex are attenuated in mice lacking Lag3 selectively in neurons. Our results identify neuronal Lag3 as a receptor of pathologic Tau in the brain, and for AD and related Tauopathies a therapeutic target. One Sentence SummaryLag3 is a neuronal receptor specific for Tau PFF, and is required for uptake, propagation and transmission of Tau pathology.

neuroscience↗

Post-weaning parvalbumin expression in left orbitofrontal cortex shapes sociability in female mice

The adolescent social experience is essential for the maturation of the prefrontal cortex in mammalian species. However, it still needs to be determined which cortical circuits mature with such experience and how it shapes adult social behaviors in a sex-specific manner. Here, we examined social approaching behaviors in male and female mice after post-weaning social isolation (PWSI), which deprives social experience during adolescence. We found that the PWSI, particularly isolation during late adolescence, caused an abnormal increase in social approaches (hypersociability) only in female mice. We further found that the PWSI female mice showed reduced parvalbumin (PV) expression in the left orbitofrontal cortex (OFCL). When we measured neural activity in the female OFCL, a substantial number of neurons showed higher activity when mice sniffed other mice (social sniffing) than when they sniffed an object (object sniffing). Interestingly, the PWSI significantly reduced both the number of activated neurons and the activity level during social sniffing in female mice. Similarly, the CRISPR/Cas9-mediated knock-down of PV in the OFCL during late adolescence enhanced sociability and reduced the social sniffing-induced activity in adult female mice via decreased excitability of PV+ neurons and reduced synaptic inhibition in the OFCL. Moreover, optogenetic activation of excitatory neurons or optogenetic inhibition of PV+ neurons in the OFCL enhanced sociability in female mice. Our data demonstrate that the adolescent social experience is critical for the maturation of PV+ inhibitory circuits in the OFCL; this maturation shapes female social behavior via enhancing social representation in the OFCL. Significance StatementAdolescent social isolation often changes adult social behaviors in mammals. Yet, we do not fully understand the sex-specific effects of social isolation and the brain areas and circuits that mediate such changes. Here, we found that adolescent social isolation causes three abnormal phenotypes in female but not male mice: hypersociability, decreased PV+ neurons in the OFCL, and decreased socially evoked activity in the OFCL. Moreover, PV deletion in the OFCL in vivo caused the same phenotypes in female mice by increasing excitation compared with inhibition within the OFCL. Our data suggest that adolescent social experience is required for PV maturation in the OFCL, which is critical for evoking OFCL activity that shapes social behaviors in female mice.

animal behavior and cognition↗

VRK1 is required in VRK2-methylated cancers of the nervous system

Collateral lethality occurs when loss of one paralog renders cancer cells dependent on the remaining paralog. Combining genome scale CRISPR/Cas9 screens coupled with RNA-sequencing in over 900 cancer cell lines, we found that cancers of nervous system lineage, including adult and pediatric gliomas and neuroblastomas, required the nuclear kinase Vaccinia-Related Kinase 1 (VRK1) for their survival. VRK1 dependency was inversely correlated with expression of its paralog VRK2. VRK2 knockout (KO) sensitized cells to VRK1 suppression, and conversely, VRK2 overexpression increased cell fitness in the setting of VRK1 suppression. DNA methylation of the VRK2 promoter was associated with low VRK2 expression in human neuroblastomas, and adult and pediatric gliomas. Mechanistically, depletion of VRK1 reduced Barrier-to-Autointegration Factor (BAF) phosphorylation during mitosis, resulting in DNA damage and apoptosis. Together, these studies identify VRK1 as a synthetic lethal target in VRK2 promoter-methylated adult and pediatric gliomas and neuroblastomas. Statement of SignificanceWe credential VRK1 as a target in adult and pediatric gliomas, and neuroblastomas with VRK2 promoter methylation. This demonstrates the utility of paralog-driven synthetic lethal interactions for biomarker-linked, targeted therapeutics.

cancer biology↗