Biology subjects

Zhao, Y.

Publications and source records attributed to Zhao, Y..

At least 181 records · Page 10Linked to original sources

bioRxiv2026

CTLA-4 inhibitors drive colitis through metabolic reprogramming-mediated Treg/Th17 imbalance

Immune checkpoint inhibitors (ICIs), especially CTLA-4 inhibitors (CTLA-4), exhibit a high incidence of colitis as an immune-related adverse event (irAE) during cancer treatment, severely limiting patient benefit. Clinically, both treatment interruption and existing intervention drugs for ICI-mediated colitis may compromise antitumor efficacy. However, there is inadequate research on the pathogenesis of ICI-mediated colitis, with findings often conflicting. Here, we first established multiple clinically relevant animal models, including an immuno-humanized ICI-mediated colitis model. Through time-series transcriptomics, we discovered that CTLA-4-induced colonic toxicity exhibits characteristics ranging from early metabolic reprogramming represented by glycolysis to later immune disorders represented by Th17 responses. By targeting colonic CTLA-4+ T cells, CTLA-4 blocked CD80/CD86-CTLA-4 interaction, thereby activating the PI3K-AKT-mTOR pathway. Subsequently, mTOR mediated metabolic reprogramming in T cells, shifting them from Treg-biased oxidative phosphorylation to Th17-biased glycolysis. The colonic toxicity of CTLA-4 has also been demonstrated to depend on the PI3K-AKT-mTOR pathway, glycolysis, and Th17 responses. Notably, metformin significantly relieved ICI-mediated colitis by inhibiting mTOR without impeding antitumor efficacy. Collectively, these findings highlighted the metabolic-immune axis in the colonic toxicity of ICI and provided a clinically superior intervention strategy.

pharmacology and toxicology↗

bioRxiv2026

Microhomology-mediated end joining acts directly on replication forks to repair single-ended double strand breaks

Replication stress, intrinsic to oncogenesis, often leads to fork breakage and double-strand break (DSB) formation. Conventionally, break-induced replication (BIR) is considered the primary mechanism for repairing replication-associated single-ended DSBs (seDSBs). Here, we demonstrate that microhomology-mediated end joining (MMEJ) acts directly to repair seDSBs at broken replication forks (fork-MMEJ), preferentially on the leading strands, and functions cooperatively with BIR. We also showed that while fork-MMEJ is promoted by Pol{theta}, it operates independently of MRE11/CtIP-mediated end resection, relies on RPA, and produces asymmetric deletion patterns, which is distinct from canonical MMEJ (cMMEJ) defined at replication-independent double-ended DSBs (deDSBs). ATR, activated as end resection proceeds, serves as a pivotal switch to suppress fork-MMEJ while promoting BIR. Combined inactivation of ATR and Pol{theta} synergistically kills cancer cells under high replication stress with minimal toxicity to normal cells. Together, our study provides fundamental insights into the MMEJ mechanism and offers new strategies for cancer treatment.

molecular biology↗

bioRxiv2026

Integration of early-stage cryopreservation and cell cycle modulation into a flexible kidney organoid differentiation system

Kidney organoids derived from human pluripotent stem cells (hPSCs) represent a promising platform for modeling nephrogenesis and renal diseases. However, conventional differentiation protocols are continuous and time-sensitive, limiting their scalability and reproducibility. Here, we developed a method to pause and resume organoid formation through cryopreservation at an early differentiation stage using a chemically defined formulation that maintains high post-thaw viability and differentiation potential. We further found that synchronizing hPSCs in the G1 phase with PD-0332991 enhanced post-thaw organoid formation and transcriptional fidelity, while G2 phase enrichment with Ro-3306 promoted the development of SLC12A3-positive distal convoluted tubules. The post-thaw organoids exhibited well-organized nephron architecture and function comparable to uninterrupted cultured controls. This platform proved effective for modeling BK polyomavirus (BKV) infection, drug-induced nephrotoxicity, and renal fibrosis. Together, our cryopreservation and cell cycle synchronization strategy provides a flexible, practical framework to advance organoid-based research and translation.

developmental biology↗

bioRxiv2026

Context-aware Multi-Property Antibody Predictor: a Novel Framework Integrating Text and Protein Language Models

Recent advances in Machine Learning have transformed antibody development through in-silico models, accelerating therapeutic candidate identification. However, challenges persist: rapid adaptation of property predictors to laboratory-specific assays with incomplete datasets; batch effects introducing systematic bias; assay costs necessitating efficient unseen property prediction. We introduce a novel multi-modal architecture featuring specialized tokenization and embedding projection that integrates text and protein language models (pLM) and a learning strategy to enable in-context learning for multi-property prediction without learning shortcuts. Our framework enables prompting without dictionary merging across modalities, creating a compact model capable of in-context learning for multi-property prediction. The orchestrating model avoids pLM-to-text projection while enabling inference-time adaptation without retraining. Using 876,898 antibodies with batch effect simulation, our architecture achieved Spearmans {rho}>0.8 across multiple developability properties, significantly outperforming fine-tuned multimodal-LLMs and showed the ability of leveraging correlation between properties for prediction. This approach has the potential to address critical antibody development challenges.

bioinformatics↗

bioRxiv2026

Mechanistic insights into chromatin modulation by the orphan remodeler ATRX

Alpha-thalassemia/mental retardation syndrome X-linked protein (ATRX) is an ATP-dependent chromatin remodeler that performs diverse functions, including spacing nucleosomes, facilitating the deposition of histone variant H3.3, and preventing replication stress. The mechanism by which ATRX modulates chromatin is unknown. Here, our cryo-EM structure revealed that ATRX recognizes and modulates the nucleosome through its C-terminal regions by embracing and unwrapping [~]18 base-pair nucleosomal DNA near the entry/exit sites in the presence of ADP*BeF3. Strikingly, the DNA minor groove between SHL6 and SHL7 is profoundly deformed by a "pin-like" structure in ATRX, which uniquely intercalates the aromatic side chain of a phenylalanine into the base stackings. Biochemical assays revealed the crucial role of this phenylalanine in sliding the nucleosome without affecting the ATPase activity. Such a "pin-like" structure mimics a "foot-step" on the DNA ladder, which differentiates ATRX from other remodelers. To translocate the DNA on the nucleosome, two more features, including a disordered insertion that contacts the histone surface and a positively charged loop bridging the cross-gyre interactions, serve as essential anchors for the nucleosome modulation by ATRX. Together, we propose a "climbing" model for how ATRX mobilizes the DNA upon ATP hydrolysis.

biochemistry↗

bioRxiv2026

A plug-and-play ROI imaging module and deep-learning denoising framework extend three-photon microscopy to 1.7 mm depth

Three-photon microscopy (3PM) has extended optical imaging beyond the reach of two-photon microscopy (2PM), but its practical depth remains far below theoretical predictions because of low photon efficiency and severe noise contamination. Here we present an integrated hardware and software solution that addresses these limitations. We developed a plug-and-play region-of-interest (ROI) imaging module that selectively excites neuron-occupied regions to improve power efficiency and reduce photothermal stress. The module incorporates frame-partitioned accumulative (FPA) imaging for high signal-to-noise ratio (SNR) structural acquisition, automated neuron segmentation, and motion-robust registration for stable recordings. Complementing this, OptiCal is a cascaded deep-learning framework that removes mixed noise including periodic, motion-induced, and random components. Together, these innovations enable high-fidelity imaging to 1.7 mm depth, extending the practical limit of 3PM by about 400 {micro}m while maintaining low excitation power. Our results reveal reliable calcium activity and behavior-correlated dynamics in deep medial prefrontal cortex of awake mice.

neuroscience↗

bioRxiv2025

Kilohertz-rate two-photon voltage imaging of population dynamics in vivo

Understanding how neural circuits compute requires capturing voltage dynamics across large neuronal populations with millisecond resolution in vivo. However, two-photon voltage imaging remains fundamentally limited by a trade-off among imaging speed, field of view, and excitation efficiency. We introduce HS2PM, a hybrid scanning two-photon microscope that overcomes this bottleneck, enabling kilohertz-rate imaging over a 650 x 524 m2 field of view at single-cell resolution while preserving the photon efficiency of single-point excitation. HS2PM stably records deep-layer membrane potentials from over 160 neurons simultaneously, with minimal photobleaching and phototoxicity. It resolves both spikes and subthreshold voltage dynamics in vivo, revealing how these jointly shape sensory adaptation and population coding. Beyond voltage imaging, HS2PM supports high-speed fluorescence lifetime and vascular flow imaging, establishing a multimodal platform for dissecting fast circuit dynamics with precision previously inaccessible to optical methods.

neuroscience↗

bioRxiv2025

In situ cryo-ET reveals restricted docking of intraflagellar transport at the base of the trypanosome flagellum

Cilia and flagella are conserved organelles essential for sensory and motility functions and are assembled and maintained by bidirectional intraflagellar transport (IFT) along the axoneme. In Trypanosoma brucei, IFT is concentrated at the flagellar base near the transition zone and is restricted to four microtubule doublets (MTDs) as it traverses from the transition zone to the axoneme before reaching the extra-axonemal structure, the paraflagellar rod (PFR), associated region. To gain an insight on its initial working model before IFT restriction occurs, we revealed the in situ architecture of the IFT complex during the initial and complete landing to the transition zone using cryo-focused ion beam (cryo-FIB) milling and cryo-electron tomography (cryo-ET). IFT proteins assemble into polymeric trains upon landing. However, in the proximal portion of the flagellum, subtomogram averaging revealed that each single train is associated with individual MTDs at variable A- or B-tubule positions. By using miniaturized and enucleated T. brucei zoids that preserve the full circular arrangement of MTDs without milling, we revealed an alternating but spatially restricted IFT train pattern during the landing process, resembling the anterograde train scaffold known in Chlamydomonas. Magnify expansion microscopy further confirmed this restricted distribution of IFT proteins at the basal pool. Depletion of the IFT component IFT46 protein reduced the number of simultaneously docked trains without altering the restricted landing spatial pattern. These findings reveal a previously unrecognized spatial regulation governing IFT train initiation at the flagellar base, which could operate independently of IFT-B structural integrity, bridging the gap between the IFT architecture and doublet-spatial docking prior to anterograde transport.

cell biology↗

bioRxiv2025

15-Hydroxyeicosatetraenoic Acid and GPR39 Together Orchestrate Coronary Autoregulation: A Comprehensive Metabolomic Analysis

BackgroundCoronary autoregulation is the ability of the normal heart to maintain constant coronary blood flow (CBF) over a wide range of coronary driving pressures (CDP). Despite being vital for survival, the mechanism of coronary autoregulation is unknown. We hypothesized that GPR39, present in vascular smooth muscle cells, together with its endogenous agonist 15- hydroxyeicosatetraenoic acid (15-HETE) orchestrate coronary autoregulation. MethodsWe created coronary stenoses of varying degrees in open-chest, anesthetized dogs where we measured CBF and CDP. In a subset of animals, coronary venous blood was sampled for eicosanoid, adenosine, endothelin-1, polyunsaturated fatty acids, and prostaglandins levels. Stenoses were recreated during intravenous administration of VC108, a specific GPR39 antagonist and systemic, pulmonary, and coronary hemodynamics measured. ResultsGPR39 was identified in coronary arterioles by immunohistochemistry and in heart tissue by western blot. In-vivo, 15-HETE correlated the best (r2=0.4851, p=0.0144) with CDP over the autoregulatory range using a linear mixed-effects model. Prior to administration of VC108, CBF did not change within the autoregulatory range. VC108 had no effect on systemic and pulmonary hemodynamics but increased CBF (p=0.02 versus vehicle) by decreasing coronary microvascular resistance (p=0.01 versus vehicle), indicating that GPR39 participates in control of normal coronary vascular tone. With VC108, coronary autoregulation was abolished and CBF became CDP dependent (r2=0.9562, p=0.0039). ConclusionGPR39 and its endogenous agonist 15-HETE together orchestrate coronary autoregulation when CDP is reduced. These novel findings provide a mechanism for coronary autoregulation and could direct pharmacological treatment of various coronary syndromes in humans. Clinical Perspectives What is new?The new finding from this study is that the vasoconstrictor, 15- hydroxyeicosatetraenoic acid (15-HETE), acting via the G-protein coupled receptor 39 (GPR39) participates in coronary arteriolar tone, and when perfusion pressure falls because of coronary stenosis, 15-HETE levels decrease causing vasodilation to maintain resting coronary blood flow. What are the Clinical implicationsThis mechanism, termed coronary autoregulation, causes patients with coronary artery disease to remain asymptomatic at rest until coronary stenosis is very severe. Pharmacological inhibition of GPR39 causes selective coronary vasodilation and could be used to treat coronary artery disease.

physiology↗

bioRxiv2025

A Hybridization-Based Novel DNA Storage Technology with Rapid Read Performance

The development of traditional silicon-based microelectronic storage media has increasingly lagged behind the rapidly growing demands of contemporary data storage. DNA storage, with its ultra-high information density and long-term preservation advantages, has rapidly become a research hotspot for next-generation storage technologies. However, current mainstream DNA storage methods based on synthesis and sequencing suffer from slow read/write speeds, hindering practical applications. To address this limitation, we propose an innovative hybridization-based DNA storage scheme. Through principle validation experiments, short-text read/write and error-correction tests, and high-density multi-format file storage experiments, we verify the feasibility of this approach. The proposed method exhibits high parallelism, rapid read speeds, and robust encryption capabilities, demonstrating promising application prospects in scenarios such as confidential data storage.

synthetic biology↗

bioRxiv2025

Density-based longitudinal neuron tracking in high-density electrophysiological recordings

Tracking single neurons across days in high-density extracellular recordings is essential for establishing neural mechanisms of learning, memory, and post-injury recovery. However, in weeks-long recordings, identifying cross-day matches among thousands of units is confounded by changes in spike waveforms, unit turnover, and representational drift in neural responses. We introduce DANT (Density-based Across-day Neuron Tracking), an unsupervised framework that jointly estimates probe motion and neuron identity by alternating between density-based clustering in feature space and probe-motion correction inferred from provisional matches. Estimated drift is used to re-register spike waveforms across sessions, after which clustering is recomputed; this iterative loop continues until the set of matches stabilizes. In parallel, DANT learns a decision boundary from match and non-match assignments derived from the clustering results, enabling it to reject low-similarity candidate pairs. Applied to weeks-long Neuropixels recordings from the cortex and striatum in freely moving rats during stable behavior and task switching, DANT substantially increases match yield and reduces false negatives while maintaining a low false-positive rate relative to existing approaches. Together, these results indicate that DANT provides a general, unsupervised solution for longitudinal tracking in chronic, high-density recordings. The bigger pictureModern high-density probes such as Neuropixels record hundreds of units per session. When chronically implanted, many of these units can be stably recorded over extended periods, opening the door to tracking how large neural populations change over days to weeks, a question central to learning, memory, internal states, and recovery from brain injury. Yet, small shifts in probe position, changes in spike waveforms, and drifts in firing properties mean that linking units across sessions is challenging. DANT (Density-based Across-day Neuron Tracking) addresses this problem by providing an unsupervised framework that combines density-based clustering and iterative motion correction to identify cross-day matches with minimal subjective decisions. Applied to chronic Neuropixels recordings from freely moving, task-performing rats, DANT recovers longer and more complete chains of putative same neurons than existing approaches, while keeping the false-positive rate low. By making cross-day tracking more sensitive, scalable, and reproducible, DANT enables a wider range of neuroscience studies to examine the longitudinal behavior of single neurons and neural populations.

neuroscience↗

bioRxiv2025

A Federated and Privacy-Preserving Framework for Large-Scale Genome-Wide Association Studies with Mixed-Effects Models

Genome-wide association studies (GWAS) increasingly rely on large-scale data integration to achieve the statistical power necessary to detect variants with weak effects. However, genomic data are typically siloed across institutions, and privacy constraints often preclude centralized analysis. While federated learning (FL) offers a viable alternative by enabling cross-site computation without sharing individual-level data, applying mixed models, which are essential for correcting population structure, in a distributed setting remains a challenge in terms of statistical accuracy and computational scalability. Here, we present a federated mixed-model framework for GWAS that achieves high fidelity to centralized analyses while maintaining efficiency at biobank scale. Building on mixed-model theory and distributed optimization, we introduce algorithms for continuous (FedLMM) and binary (FedGLMM) traits that perform parameter estimation and association testing through site-local computation and aggregation of intermediate statistics. Comprehensive simulations spanning varied sample sizes and genomic densities demonstrate that our methods closely mirror centralized benchmarks (fastGWA and fastGWA-GLMM). Effect-size estimates exhibit near-perfect correlation, and over 99% of significant loci are recovered with well-controlled type I error rates. Empirical analyses on [~]100,000 UK Biobank participants further confirm that the framework delivers consistent inference while sustaining high computational performance. This work establishes a practical, open-source, and statistically reliable federated solution for large-scale GWAS, resolving the tension between data privacy and the need for statistical power in modern genomics.

genomics↗

bioRxiv2025

Multicolored, Sonosensitizer-optimized Organic Mechanoluminescent Nanoparticles for Functional Sono-optogenetics

Light enables precise visualization and control of cellular processes, but its utility in deep tissues is fundamentally limited by poor optical penetration, particularly in the deep brain. Ultrasound-triggered mechanoluminescence offers a non-invasive strategy for remote light delivery, yet existing organic systems remain monochromatic and low-intensity, largely due to an incomplete understanding of ultrasound-induced emission. Here, we report a multicolor mechanoluminescence platform that couples reactive oxygen species-responsive chemiluminescent donors with fluorescent acceptors via Forster resonance energy transfer, generating tunable emission from blue (459 nm) to red (592 nm). Systematic screening potentially reveals that electronic energy gap-dependent reactive oxygen species generation serves as a predictive design principle for high-performance mechanoluminescent materials. The emitted spectrum and intensity are sufficient to activate ChR2 and ChRmine and inhibit eOPN3, enabling bidirectional, fiber-free neuromodulation under focused ultrasound. By integrating spatially precise ultrasound with programmable photon output, this platform establishes a non-invasive strategy for deep-tissue neural monitoring and provides a foundation for applications in bioimaging, gene editing, and precision therapeutics.

bioengineering↗

bioRxiv2025

Multi-Timescale Neural Adaptation Failure as a Mechanistic Signature of Major Depression

Major depression (MD) is usually characterized in terms of momentary abnormalities, such as negative bias or emotional blunting, derived from paradigms that measure only the first response to a stimulus. Yet depressive experience in daily life is repetitive and cumulative. Here we test the hypothesis that a failure of neural adaptation across repetitions is a core feature of MD. Using a repeated negative-stimulus paradigm, we quantified adaptation at micro (within-trial) and macro (across-session) scales via electroencephalography in 28 MD patients and 34 healthy controls, measuring both conventional event-related potentials and large-scale traveling-wave propagation. MD patients exhibited pervasive maladaptation: neural rigidity at the micro scale (absent repetition suppression) and progressive regulatory depletion at the macro scale (escalating emotional reactivity with declining cognitive control). Across analyses, adaptation-based metrics revealed larger group differences than single-shot indices, and classifiers built on adaptation features--especially traveling-wave dynamics--outperformed single-shot models (task AUC = 0.83 vs 0.78) and generalized to two independent datasets (up to AUC = 0.91). These findings challenge conventional symptom-based characterizations of MD, establishing adaptation failure--not initial reactivity--as the mechanistically primary pathological signature. This reframing provides a unified mechanistic explanation for rumination and cognitive inflexibility while offering a standardized, low-cost biomarker requiring minimal electrodes ([≤]8 channels), enabling large-scale screening in resource-limited settings.

neuroscience↗

bioRxiv2025

In depth characterisation of the tumour microenvironment reveals HHV-8 dependent immune regulation in HIV-associated and classic Kaposi Sarcoma.

BackgroundKaposis sarcoma (KS) is the most common malignancy occurring in people living with HIV (PLWH). The clinical course of KS in PLWH established on combined anti-retroviral therapy (cART) resembles that of classic KS. However, no studies have so far been conducted to compare clinical and immunologic characteristics of these subtypes. ObjectivesTo compare the clinical and biological characteristics of HIV-associated KS in patients with well-controlled viral infection (N=21) and non-HIV associated KS (N=19). MethodsClinical data were prospectively collected from patients treated at the National Centre for HIV malignancies at Chelsea & Westminster Hospital. Archival tumour samples were retrieved to perform targeted transcriptomic analysis using the Nanostring nCounter platform. The results were validated by multiplex immune-fluorescence. ResultsMedian progression free survival (mPFS) was comparable between groups. The tumour microenvironment (TME) of non-HIV associated KS was characterized by upregulation of pathways associated with adaptive and innate immunity and angiogenesis. Transcripts relating to glycolysis and endothelial to mesenchymal transition were upregulated in the TME of HIV-associated cases. Furthermore, the TME of HIV-associated cases was associated with lower infiltration of CD4 activated cell. In both cohorts, we found the expression of HHV-8 genes to positively correlate with activated CD4, CD8, NK and immune checkpoints gene expression. ConclusionsIn conclusion, we showed that the TME of KS in the presence of well-controlled HIV infection is characterized by a lower degree of inflammation and more pronounced epithelial to mesenchymal transition. We also identified intra-tumoral HHV-8 gene expression as a driver of TME composition.

immunology↗

bioRxiv2025

Mining of natural diversity enables efficient and expressible peptide asparaginyl ligases

Peptide asparaginyl ligases (PALs) are powerful tools for protein engineering but are limited by natural rarity and poor expression. We mined 23 cyclotide-rich Viola species, uncovering 29 new PALs that expanded the known repertoire to 47. A dual-objective screen identified VdiPAL1 as the best-performed natural PAL, with twice efficiency of wt-VyPAL2 and 12 mg L-1 soluble expression in E. coli. A broad P2 specificity including Trp/Ile/Leu/Phe/Tyr/Met was discovered across diverse PALs, which enables sequential click-compatible liposome dual-functionalization. 1.8L[A] crystal structure of VdiPAL1 reveals a pre-organized near-attack conformation (NAC), supported by constant-pH MD simulations linking pH-dependent reactivity to NAC geometry. Our homology- and structure-based design yielded VyOpt1, a quintuple mutant of VyPAL2 with over 24-fold improved expression via enhanced cap-domain foldability in a single design-test cycle. This work expands the PAL family and demonstrates a transferable cap-domain-based engineering strategy, highlighting natural diversity as a powerful driver of enzyme discovery and optimization. TOC summaryMining of cyclotide-rich Viola genus expanded the total number of natural peptide asparaginyl ligases (PALs) to 47, including the discovery of highly expressible VdiPAL1. Its high-resolution structure provided new insights for mechanism, and its sequence guided us to a generalized PAL engineering strategy, leading to 24-fold increment in VyPAL2 expression.

biochemistry↗

bioRxiv2025

Stereoselective Degradation of Diacylglycerol Kinases Potentiate T cell Activation and Tumor Cell Cytotoxicity

Stereoselective recognition is a powerful means to differentiate selective versus non-specific activity of small molecules in complex biological systems. Here, we disclose stereochemically defined, sulfonyl-triazole inhibitors of the lipid enzyme diacylglycerol kinase-alpha (DGK), a key metabolic checkpoint for T cell effector function. Acute treatment with the covalent DGK inhibitor AHL-7160 recruited endogenous DGK to the plasma membrane in a stereoselective and isozyme-specific manner. The membrane translocation activity of AHL-7160 correlated with blockade of cellular phosphatidic acid production and potentiation of primary T cell-mediated killing of a glioblastoma cell line. Quantitative chemoproteomics revealed Y669 and K411 as sites of AHL-7160 modification on endogenous DGK in cells. Extended treatments resulted in proteasome-dependent and proteome-wide selective degradation of DGK in T cells. Collectively, these findings establish covalent DGK ligands as potent molecular glues with translational potential in immunotherapy.

biochemistry↗

bioRxiv2025

Structural Basis of Human Kinetochore-Microtubule Coupling by the Ndc80 and Ska Complexes

Faithful chromosome segregation depends on kinetochore-microtubule attachments that must be load-bearing, dynamic, and tightly regulated. In human cells, the Ska and Ndc80 complexes (SkaC and Ndc80C) cooperate to sustain these attachments, but how they are organized on microtubules and coupled to end dynamics remains unclear. Here, our cryo-EM structure shows that Ndc80C and SkaC form a coupled assembly across neighboring protofilaments. A phosphorylation-sensitive SKA3 tether binds a defined kink in the Ndc80 coiled-coil, positioning SKA1 beside Ndc80C. These two complexes jointly sandwich the -tubulin tail and sense its polyglutamylation state. SkaC recognizes the extended microtubule lattice and, through the SKA3 tether, confers this selectivity onto Ndc80C, enabling Ndc80C tip tracking while strengthening microtubule stabilization. Together, our findings define the structural basis of Ndc80C-SkaC cooperation and uncover a phosphorylation-regulated, polyglutamylation-sensitive, and lattice-state-dependent mechanism for robust and regulated KT-MT coupling during chromosome segregation in mitosis.

biophysics↗