Biology subjects

Kim, N.

Publications and source records attributed to Kim, N..

At least 19 recordsLinked to original sources

bioRxiv2026

Visual experience-driven switch in endothelial metabolic transporters is essential for cerebrovascular maturation

Angiogenesis and blood-brain barrier (BBB) maturation are tightly regulated by coordinated interactions among neuronal, glial, and endothelial cells. Although neuronal activity is essential for postnatal cerebrovascular development, how it is translated into endothelial programs that coordinate vascular maturation remains unknown. Here, we show that visual experience drives metabolic reprogramming in brain endothelial cells by decreasing the lactate transporter MCT1 while increasing the glucose transporter GLUT1, a switch that is essential for proper vascular development. Sustained endothelial expression of MCT1 impaired vascular development and BBB maturation, resulting in vascular leakage. Mechanistically, the developmental decline in TGF-beta signaling drives the endothelial MCT1-to-GLUT1 transition. Endothelial-derived TGF-beta1 further reinforces the immature angiogenic state through a lactate-dependent autocrine positive feedback loop, whereas sensory experience promotes astrocyte maturation, which attenuates endothelial TGF-beta signaling, potentially by altering the perivascular environment. Together, our findings identify a neuron-astrocyte-endothelial metabolic signaling axis that links sensory experience to endothelial metabolic reprogramming and coordinates the transition from angiogenesis to BBB maturation.

neuroscience↗

bioRxiv2026

Dynamic Filament Assembly Regulates the Prolyl Aminopeptidase Activity of Plant Immune Protein DM3

The alpha/beta hydrolase DANGEROUS MIX 3 (DM3), a proline aminopeptidase in Arabidopsis thaliana, contributes to stress resilience through both metabolic regulation and immune signaling. Its functions are partitioned within its oligomeric structure as a trimer-of-dimers, in which the immune regulatory switch resides at the dimer interface. While the enzymatic activity of DM3 is not necessary for immune response, its activity to free prolines is critical to promote tolerance to salt and drought stress. However, how this activity is regulated has remained unclear. Here, we show that DM3 undergoes dynamic and reversible assembly into higher-order filaments in a salt-sensitive manner. The cryo-electron microscopy (EM) structure of filamentous DM3 reveals that the three-stranded helical filament arises from rearrangements of a planar hexamer into a tilted hexameric configuration. Notably, within these filaments, one of the catalytic residues is flipped out to disrupt the catalytic geometry, rendering the enzyme inactive. These findings establish filament assembly as a mechanism to sequester DM3 in an inactive state and suggest that the transition between distinct oligomeric states enables DM3 to coordinate its roles in biotic and abiotic stress responses.

plant biology↗

bioRxiv2026

Aberrant 3'UTR splicing drives FUS-dependent mRNA condensates and prevents β-catenin from adherens junctions to promote cancer aggressiveness

The protein-coding sequence has long been considered the primary determinant of protein function. Alternative splicing within 3'UTRs (AS-3'UTRs) generates multiple transcript isoforms from a single gene, yet their roles in protein function and disease relevance remain largely unexplored. Through systematic transcriptome-wide identification of cancer-associated AS-3'UTRs, we uncover that AS-3'UTRs of {beta}-catenin mRNA direct distinct subcellular localization of {beta}-catenin mRNA isoforms. Specifically, an aberrantly spliced 3'UTR isoform promotes cytoplasmic mRNA condensate formation through FUS binding to a cancer-associated alternative exon (Exon 16A). Because {beta}-catenin function is exquisitely dependent on its subcellular distribution between adherens junctions and the nucleus, this aberrant 3'UTR isoform reprograms {beta}-catenin localization. By sequestering {beta}-catenin in the cytoplasm, the aberrant 3'UTR isoform prevents its incorporation into E-cadherin-based adherens junctions, thereby inducing epithelial-mesenchymal transition (EMT)-associated transcriptional programs. Notably, the expression signature of the aberrant 3'UTR isoform robustly correlates with poor clinical outcomes in colorectal cancer patients. Together, our findings reveal that AS-3'UTRs operate as a previously unrecognized post-transcriptional regulatory mechanism through which the untranslated region of mRNA, without altering a single amino acid, reprograms protein subcellular fate to drive oncogenic phenotypes.

cell biology↗

bioRxiv2026

IscR-mediated morphological regulation confers virulence and stress resistance by reducing stress molecule uptake in Acinetobacter baumannii

Living organisms must adequately respond to stress to survive and proliferate. Bacterial pathogens face multiple stressors during infections, including oxidative stress from host innate immune cells and antibiotic treatment from clinical therapy. The pathogenic bacterium Acinetobacter baumannii is considered the most critical threat to public health due to its broad antibiotic resistance. However, it is poorly known how A. baumannii properly responds to antibiotics and stress molecules during infection. Here, we investigate the mechanisms by which A. baumannii regulates its morphology to reduce the uptake of stress molecules under oxidative stress and antibiotic exposure, thereby conferring virulence and survival during infection. The transcriptional regulator IscR responds to oxidative stress by upregulating pbp1a, which encodes an enzyme involved in peptidoglycan biosynthesis. Under oxidative stress, bacteria undergo a morphological shift from a rod to a coccoid form, reducing their surface area and thus decreasing their absorption of reactive oxygen species. Inactivation of either iscR or pbp1a results in an elongated morphology characterized by an elevated surface area, thereby reducing A. baumannii survival under oxidative stress. Furthermore, IscR-mediated morphological control is essential for survival under antibiotic treatment. Moreover, IscR-mediated morphology regulation is required for A. baumannii survival in macrophage and mouse models. These findings elucidate a strategy by which A. baumannii uses IscR to adapt to stress through morphological control, facilitating its survival during infections against both immune response and antibiotic therapy. IMPORTNACEAcinetobacter baumannii is a major cause of nosocomial infections. It poses a critical threat due to its extensive antibiotic resistance. This study reveals that the pathogen can change its cellular shape to survive immune system attacks and antibiotic treatment. This change represents a previously unknown survival strategy. A. baumannii transitions to a coccoid morphology under oxidative stress and antibiotic treatment. It does so by activating the peptidoglycan synthesis gene pbp1a through the IscR transcriptional regulator. This rapid morphological adaptation helps A. baumannii evade host defenses and resist antibiotic treatment by reducing uptake of stress molecules. Our findings advance understanding of how pathogens adapt to hostile environments and identify new therapeutic targets. By blocking this shape remodeling ability, it may be possible to render pathogenic bacteria more vulnerable to immune responses and antimicrobial treatments. This offers a promising strategy for combating this multidrug-resistant pathogen.

microbiology↗

bioRxiv2026

Cognitive load modulates cortical excitability in the human prefrontal cortex

The prefrontal cortex dynamically adjusts its excitability to meet changing cognitive demands, yet our understanding of how these rapid state changes unfold in real time remains limited. Existing evidence relies predominantly on correlational neuroimaging and invasive electrophysiology in clinical populations, neither of which affords causal measurement in healthy humans. Here, using concurrent single-pulse TMS-EEG during a parametric cognitive multi-source interference task (MSIT) in 27 healthy participants, we causally probed left prefrontal excitability across conditions spanning a range of cognitive interference levels. Prefrontal excitability scaled systematically with cognitive load, peaking at intermediate incongruency levels where trial-type uncertainty was greatest, and differentiating high-from low-conflict trials at the single-subject level. Critically, prefrontal excitability and midfrontal theta power showed parallel state dependency patterns, linking causal perturbation of prefrontal circuit responsiveness to an established oscillatory marker of cognitive control. The observed excitability modulation was selective to the left prefrontal cortex: stimulation of right dlPFC, pre-SMA, and vertex in a separate control cohort (N=5) produced no load-dependent effects. These results position prefrontal excitability as a real-time, regionally selective physiological readout of how the human prefrontal cortex adapts to cognitive demand. HighlightsO_LIWe evaluated the links between cognitive interference, prefrontal excitability, and intrinsic theta activity during a multi-source interference task C_LIO_LICognitive load, estimated based on behavioral performance, was greatest at at intermediate interference levels (33% congruent), where trial-type uncertainty was maximal C_LIO_LIPrefrontal excitability, measured via single-pulse TMS-evoked potentials, scaled with cognitive load C_LIO_LIEffects were observed at the single subject level and were specific to prefrontal stimulation C_LIO_LIPrefrontal excitability changes and midfrontal theta power showed parallel scaling with cognitive load, linking causal probing to established oscillatory markers C_LIO_LIThis noninvasive technique provides causal measurement of prefrontal engagement during cognitive processing C_LIO_LIThe methodology demonstrates potential for tracking brain state dynamics in both healthy cognition and neuropsychiatric disorders C_LI

neuroscience↗

bioRxiv2026

Soil-based disease bioassay for the study of rhizogenic Agrobacterium-tomato interactions

2.Hairy root disease (HRD), caused by rhizogenic Agrobacterium, is an economically important disease affecting hydroponic tomato (Solanum lycopersicum L.) production worldwide. HRD-affected plants show extensive root proliferation, resulting in decreased energy expenditure towards fruit production. Host plant susceptibility to rhizogenic Agrobacterium is typically evaluated through artificial wounding-based infection bioassays. However, under natural infection settings, rhizogenic Agrobacterium can induce disease symptoms without deliberate, artificial wounding. We developed a soil-based, non-wounding bioassay that closely mimics natural rhizosphere interactions and permits quantitative and qualitative assessment of HRD symptoms. The assay measured root dry weight, documented agravitropic root development typical of HRD and confirmed in planta T-DNA gene expression using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR). We used this bioassay to evaluate disease symptoms towards rhizogenic Agrobacterium in tomato cv. Moneymaker and the rootstocks Optifort, Maxifort, and Arnold. Optifort and Maxifort exhibited significantly higher root biomass than Arnold and Moneymaker, indicating more pronounced symptom development. The bioassay also differentiated virulence levels amongst various rhizogenic Agrobacterium strains isolated from HRD-affected plants. Together, these results show that our soil-based bioassay provides a robust and ecologically relevant platform for screening tomato genotypes and comparing virulence levels of rhizogenic Agrobacterium strains supporting resistance breeding and disease management efforts.

plant biology↗

bioRxiv2026

A dual-color miniature endoscope for calcium imaging in behaving mice

Calcium imaging with miniature endoscopes has become an essential tool in neuroscience, but conventional miniscopes typically record signals from only a single calcium indicator. Here, we present a dual-color miniature endoscope (miniscope) that enables simultaneous calcium imaging from two neuronal populations using spectrally distinct genetically encoded indicators. In freely moving mice, we used this system to record activity from striatal neurons of the direct (dSPN) and indirect (iSPN) pathways. We showed that dSPNs were activated earlier than iSPNs during contraversive movements, with dSPNs preferentially active during acceleration and iSPNs during deceleration. During ipsiversive turns, however, this temporal relationship was reversed. These findings indicate that dSPNs and iSPNs are not concurrently active, but instead exhibit complementary, direction-dependent dynamics that govern movement velocity. Our dual-color miniscope provides a compact, cost-effective platform for simultaneous two-population imaging, offering new opportunities to dissect coordinated activity across neural circuits in freely behaving animals.

neuroscience↗

bioRxiv2025

Cas9-enriched nanopore sequencing enables comprehensive and multiplexed detection of repeat expansions

Short tandem repeat (STR) expansion is a major genetic mechanism underlying numerous neurogenetic disorders. However, traditional PCR amplification and short-read next-generation sequencing (NGS)-based methods often fail to detect complex and large expansions including methylation information. Here, we modified an amplification-free nanopore Cas9-targeted sequencing (nCATS) platform and developed a dedicated analysis algorithm, STRiker, for the simultaneous assessment of all currently defined STR loci (56 sites) using a single test with genomic DNA from patient-derived blood cells. We ultimately identified pathogenic repeat expansions in 12 of 37 patients (32.4%) with cerebellar ataxia who remained genetically undiagnosed despite extensive prior genetic testing, in FGF14 (n=4), ATXN8OS, NOP56, RFC1 (n=2 each), and PRNP and NOTCH2NLC (n=1 each). Additionally, family-based cascade screening revealed six relatives with repeat expansions in five families. These results demonstrated a broader diversity of pathogenic repeat structures, particularly in FGF14, and illustrated that CpG methylation can mitigate the pathogenic effects of repeat expansions. This approach offers a powerful strategy for improving the diagnosis of STR-related neurogenetic diseases, for cerebellar ataxia and other STR-related diseases in the future. One Sentence SummaryImproved nanopore Cas9-targeted sequencing with STRiker enhances diagnosis of STR- related neurogenetic diseases and offers broader molecular insights.

bioengineering↗

bioRxiv2025

Prediction of zoonotic virus-host transmissibility using comparative airway organoids

AbstractThe emergence of new pandemic zoonotic diseases is accelerating. However, current approaches to control after outbreaks often allow the epidemic or pandemic spread of new zoonotic diseases, exemplified by the case of COVID-19. Prediction of zoonotic transmissibility will help minimize the outbreaks and socioeconomic damage. Here, we established highly efficient comparative airway organoids with minimal components from a panel of mammalian species for long-term culture and passaging and validated their utility to predict the transmissibility of zoonotic pathogens. Airway organoids from each species recapitulated the airway histology and contained the major cell types in the airway. They recapitulated the known susceptibility of their host species and tissues to diverse viruses. Transcriptomic analyses revealed that organoids from susceptible species induced genes of anti-viral immune responses only in common upon exposure to the same virus, although each species organoids displayed differential gene expression profiles. Also, organoids of the same species displayed differential transcriptomic responses against different viruses but induced anti-viral immune genes only in common. Our work provides a roadmap for comprehensive species- and tissue-level organoid panels for quick and reproducible uncharacterized pathogen surveillance to predict and prevent the next pandemic.

developmental biology↗

bioRxiv2025

The SAMM50 rs3761472 causes mitochondrial dysfunction and metabolic dysfunction-associated steatotic liver disease

Genome-wide association studies (GWAS) have identified the SAMM50 rs3761472 single nucleotide polymorphism (SNP) as a risk factor for metabolic dysfunction-associated steatotic liver disease (MASLD), although its in vivo functions remain unclear. SAMM50 encodes a mitochondrial outer membrane protein critical for maintaining mitochondrial structure. To investigate the biological effects of rs3761472, we generated Samm50-knock-in (KI) mice harboring a D110G substitution using CRISPR/Cas9. This variant impaired mitochondrial integrity by downregulating key regulators of mitochondrial architecture, dynamics, and quality control. This contributed to reduced ATP production and elevated oxidative stress, inflammation, and hepatocyte death. The mutation also induced insulin resistance and glucose intolerance. Samm50-KI mice fed a high-fat diet exhibited pronounced hepatic lipid accumulation and liver injury, highlighting its pathogenic role in MASLD progression. Our findings demonstrate that SAMM50 rs3761472 is a critical driver of mitochondrial dysfunction and MASLD susceptibility, supporting its potential as a therapeutic target and its relevance to precision medicine.

genetics↗

bioRxiv2025

Scalp EEG predicts intracranial brain activity in humans

Inferring deep brain activity from noninvasive scalp recordings remains a fundamental challenge in neuroscience. Here, we analyzed concurrent scalp and intracranial recordings from 1918 electrode contacts across 20 patients affected by drug-resistant epilepsy undergoing intracranial depth electrode monitoring for pre-surgical evaluation to establish predictive relationships between surface and deep brain signals. Using regularized and cross-validated linear regression within subjects, we demonstrate that scalp recordings can predict spontaneous intracranial activity, with accuracy varying by region, depth, and frequency. Low-frequency signals (<12 Hz) were most predictable, with our models explaining approximately 10% of intracranial signal variance across contacts. Prediction accuracy decreased with contact depth, particularly for high-frequency signals. Using Bayesian modeling with leave-one-patient-out cross-validation, we observed generalizable prediction of activity in mesial temporal, prefrontal, and orbitofrontal cortices, explaining 10-12% of low-frequency signal variance. This scalp-to-intracranial mapping derived from spontaneous activity was further validated by its correlation with scalp responses evoked by direct electrical stimulation. These findings support the development of improved inverse models of brain activity and potentially more accurate scalp-based markers of disease and treatment response.

neuroscience↗

bioRxiv2025

Combined inhibition of NAD synthesis and C-terminal binding protein cooperatively induce cell death and inhibit growth of High Grade Serous Ovarian Carcinoma

The transcriptional scaffolds C-terminal Binding Proteins (CtBP) 1 and 2 are overexpressed and act as oncogenic dependencies in multiple cancers but importantly encode a chemically targetable dehydrogenase domain. CtBP promotes survival of high grade serous ovarian carcinoma (HGSOC) cells by repressing expression of Death Receptors (DR) 4 and 5, which activate caspase 8-dependent apoptosis. We have previously developed a series of substrate competitive CtBP dehydrogenase inhibitors active in multiple cell and preclinical solid tumor models. In the current study, we validated CtBP 1 and 2 overexpression in a longitudinal series of primary and metastatic/recurrent HGSOC cases. Furthermore, our lead CtBP dehydrogenase inhibitor, JW-98 induced apoptosis and exhibited variable single agent IC50 values in HGSOC cell lines, but depletion of nicotinamide adenine dinucleotide (NAD) using the NAD synthesis inhibitor GMX1778 strikingly sensitized tumor cells to JW-98 treatment. Mechanistically, the JW-98/GMX-1778 combination effectively disrupted CtBP dimerization that requires stoichiometric levels of intracellular NAD and is required for oncogenic transcriptional activities. Highlighting the translational potential of this combination, combined JW-98/GMX1778 treatment of OVCAR3 HGSOC xenografts in immunodeficient mice abrogated tumor growth without observable toxicity. CtBP/NAD combined inhibition represents a novel therapeutic strategy that could improve outcomes in chemoresistant HGSOC.

cancer biology↗

bioRxiv2025

A high-quality genomic catalog of the human oral microbiome broadens its phylogeny and clinical insights

Understanding the taxonomic and functional diversity of the human oral microbiome requires comprehensive genomic catalogs. We present the human reference oral microbiome (HROM), with 72,641 high-quality genomes from 3,426 species, including 2,019 novel species, significantly improving metagenomic sequence read classification over existing catalogs. Notably, HROM unveils 1,137 novel candidate phyla radiation (CPR) species, establishing Patescibacteria as the most prevalent phylum in the oral microbiota, with oral Patescibacteria forming a distinct clade from environmental Patescibacteria. We also identify an oral CPR subclade associated with periodontitis, which complement Porphyromonas gingivalis in predicting the disease. Finally, comparing HROM with reference genomes of the human gut microbiome reveals significant taxonomic and functional divergence between the oral and gut microbiomes. We identify 42 ectopic oral species and demonstrate that their relative abundance in gut microbiota is predictive of intestinal, cardiovascular, and liver diseases, highlighting the clinical importance of the oral microbiota in systemic disorders.

microbiology↗

bioRxiv2025

Engineering of CRISPR-Cas PAM recognition using deep learning of vast evolutionary data

CRISPR-Cas enzymes must recognize a protospacer-adjacent motif (PAM) to edit a genomic site, significantly limiting the range of targetable sequences in a genome. Machine learning-based protein engineering provides a powerful solution to efficiently generate Cas protein variants tailored to recognize specific PAMs. Here, we present Protein2PAM, an evolution-informed deep learning model trained on a dataset of over 45,000 CRISPR-Cas PAMs. Protein2PAM rapidly and accurately predicts PAM specificity directly from Cas proteins across Type I, II, and V CRISPR-Cas systems. Using in silico deep mutational scanning, we demonstrate that the model can identify residues critical for PAM recognition in Cas9 without utilizing structural information. As a proof of concept for protein engineering, we employ Protein2PAM to computationally evolve Nme1Cas9, generating variants with broadened PAM recognition and up to a 50-fold increase in PAM cleavage rates compared to the wild-type under in vitro conditions. This work represents the first successful application of machine learning to achieve customization of Cas enzymes for alternate PAM recognition, paving the way for personalized genome editing.

synthetic biology↗

bioRxiv2024

Exclusive cataloging of near-complete genomes unveils novel functional insights into the human gut microbiome

Understanding the human gut microbiome requires comprehensive genomic catalogues, yet many lack geographic diversity and contain medium-quality metagenome-assembled genomes (MAGs) missing up to 50% of genomic regions, potentially distorting functional insights. Here, we describe an enhanced Human Reference Gut Microbiome (HRGM2) resource, a catalogue of near-complete MAGs ([≥]90% completeness, [≤]5% contamination) and isolate genomes. HRGM2 comprises 155,211 non-redundant near-complete genomes from 4,824 prokaryotic species across 41 countries, representing a 66% increase in genome count and a 50% boost in species diversity compared to the Unified Human Gastrointestinal Genome catalogue. It enabled improved DNA-based species profiling, resolution of strain heterogeneity, and survey of human gut resistome. The exclusive use of these genomes improved metabolic capacity assessment enabling high-confidence, automated genome-scale metabolic models (GEMs) of the entire microbiota, revealing disease-associated microbial metabolic interactions. This resource will facilitate reliable functional insights into gut microbiomes.

microbiology↗

bioRxiv2024

Effect of the daily exposure of 1.7 GHz LTE electromagnetic field in early fetal brain development using a human brain organoid model of the cerebral cortex

Wireless communication technologys ubiquity means constant exposure to radiofrequency electromagnetic fields (RF-EMF). While concerns exist about RF-EMFs effects on fetal brain development, studying this in pregnant women poses ethical and safety challenges. Our study examined 1.7 GHz LTE RF-EMFs impact on early human fetal brain development using brain organoids derived from human induced pluripotent stem cells (hiPSCs). Previous research showed that 100-day-old human cerebral cortical brain organoids correspond to 19-24 weeks post-conception of fetal brain development. We exposed organoids to 1.7 GHz LTE RF-EMF at 8 W/kg specific absorption rate (SAR) for 5 hours daily up to 100 days. We monitored size, developmental morphology, and developmental stage markers using immunofluorescence microscopy and qPCR analysis. Comparing RF-EMF-exposed organoids with controls showed no significant differences in size, development, or expression of key markers: SOX2 and PAX6 (pluripotent cell markers), NEUN (mature neuronal marker), MAP2 (dendrite marker), and SYN1 (synapse marker). Results suggest that daily exposure to 1.7 GHz LTE RF-EMF at 8 W/kg SAR may not significantly affect early human fetal brain development.

developmental biology↗

bioRxiv2024

In vivo Treatment of a Severe Vascular Disease via a Bespoke CRISPR-Cas9 Base Editor

Genetic vascular disorders are prevalent diseases that have diverse etiologies and few treatment options. Pathogenic missense mutations in the alpha actin isotype 2 gene (ACTA2) primarily affect smooth muscle cell (SMC) function and cause multisystemic smooth muscle dysfunction syndrome (MSMDS), a genetic vasculopathy that is associated with stroke, aortic dissection, and death in childhood. Here, we explored genome editing to correct the most common MSMDS-causative mutation ACTA2 R179H. In a first-in-kind approach, we performed mutation-specific protein engineering to develop a bespoke CRISPR-Cas9 enzyme with enhanced on-target activity against the R179H sequence. To directly correct the R179H mutation, we screened dozens of configurations of base editors (comprised of Cas9 enzymes, deaminases, and gRNAs) to develop a highly precise corrective A-to-G edit with minimal deleterious bystander editing that is otherwise prevalent when using wild-type SpCas9 base editors. We then created a murine model of MSMDS that exhibits phenotypes consistent with human patients, including vasculopathy and premature death, to explore the in vivo therapeutic potential of this base editing strategy. Delivery of the customized base editor via an engineered SMC-tropic adeno-associated virus (AAV-PR) vector substantially prolonged survival and rescued systemic phenotypes across the lifespan of MSMDS mice, including in the vasculature, aorta, and brain. Together, our optimization of a customized base editor highlights how bespoke CRISPR-Cas enzymes can enhance on-target correction while minimizing bystander edits, culminating in a precise editing approach that may enable a long-lasting treatment for patients with MSMDS.

bioengineering↗

bioRxiv2024

Structure determinants of DANGEROUS MIX 3, an alpha/beta hydrolase, for triggering NLR-mediated genetic incompatibility in plants

Genetic incompatibility occurs when a mismatched pair of plant immune components mounts autoimmune responses in hybrids. Highly diversified NLR receptors are main culprits of the genetic conflict, recognizing host proteins from different origin as immune trigger. Here, we report the molecular mechanism underlying a DANGEROUS MIX (DM) autoimmunity, comprising DM2h/RPP1 NLR and its incompatible partner DM3, an alpha/beta hydrolase. Cryo-electron microscopy reveals the oligomeric nature of two natural DM3 variants in a trimer of dimer configuration. The polymorphism triggering autoimmunity is located at the dimer interface, resulting in drastic structural differences such that dimerizing helix and loop reinforcing the interface is lost and disordered. Structure-function analysis shows that integrity of the dimer interface, but neither maintenance of hexamer nor its enzymatic activity, is the key factor contributing to autoimmunity. Our finding pinpoints checkpoints embedded in the oligomeric configuration of a host enzyme that controls the switching mechanism of NLR activity.

plant biology↗