Biology subjects

Li, C.

Publications and source records attributed to Li, C..

At least 127 records · Page 7Linked to original sources

bioRxiv2026

Analysis of persistence thresholds for a nonlocal PDE--ODE model of bacterial persister cells

Within many bacterial colonies, persister cells exist as a subpopulation that is tolerant to antibiotics and other stressors, yet not genetically distinct from the rest of the colony. A recent study has proposed epigenetic inheritance as a mechanism that leads to the presence of persister cells. We analyze a nonlocal PDE-ODE model introduced in that study to describe the epigenetic inheritance process and establish its mathematical well-posedness, including existence, uniqueness, and nonnegativity of solutions. We identify a sharp parameter threshold delineating extinction from persistence of the colony: below this threshold the washout equilibrium is globally asymptotically stable, while above it a unique positive equilibrium exists and the population is weakly persistent. Notably, this threshold is independent of the internal community structure.

microbiology↗

bioRxiv2026

Pan-cancer circular genomics identifies intratumoral Staphylococcus lugdunensis as a metabolic driver in bladder cancer

Intratumoral microbiota play key roles in cancer but are challenging to profile due to low biomass. We developed CIRCMIP, an enzymatic pipeline that eliminates linear DNA to enrich bacterial genomes, achieving 100-fold higher sensitivity than standard metagenomics. Applied to 312 pan-cancer specimens, CIRCMIP identified Staphylococcus lugdunensis as a signature bacterium enriched in early-stage bladder cancer (BLCA), where its presence predicts poor survival. Integrated modeling and lipidomics revealed that Staphylococcus lugdunensis colonization drives aberrant lipid metabolism with secretion of LPC14:0. Both Staphylococcus lugdunensis and LPC14:0 drive BLCA progression by promoting fatty acid uptake and {beta}-oxidation. Mechanistically, chemical proteomics revealed LPC14:0 as a direct PPAR{delta} ligand, binding via hydrogen bonds with Thr292/Thr289. This activation upregulates fatty acid transporters (CD36, FABP4) and metabolic enzymes (ACOX2), fueling malignant proliferation. Furthermore, CIRCMIP-derived biomarkers show robust diagnostic accuracy, establishing a new research paradigm and revealing the Staphylococcus lugdunensis-LPC14:0-PPAR{delta} axis as a therapeutic target in bladder cancer. HIGHLIGHTO_LICIRCMIP leverages DNA circularity to achieve 100-fold sensitivity in pan-cancer bacteriome profiling. C_LIO_LIStaphylococcus lugdunensis is a bacterial signature in early-stage bladder cancer that predicts poor patient survival. C_LIO_LIBacteria-derived LPC14:0 acts as a direct ligand for PPAR{delta} to drive host malignant metabolic reprogramming. C_LIO_LITargeting the Staphylococcus lugdunensis-LPC14:0-PPAR{delta} axis abrogates malignant progression in bladder cancer. C_LI

cancer biology↗

bioRxiv2026

A Brain-wide Neuronal Spiking and Behavior Dataset for Working Memory-Specific Activation and Reactivation in Mice

AbstractHow do millisecond-scale neural activities mediate multi-second behaviors such as working memory? This dataset provides brain-wide, high-spatiotemporal-resolution single-unit spiking activity recorded from 40 head-fixed mice performing an olfactory delayed paired-association (ODPA) task, encompassing 33,028 neurons across 62 anatomically defined brain regions. Utilizing this dataset enables the extraction of millisecond-scale within- and cross-region spike couplings enriched among memory-content-selective neurons. These couplings may be used to identify higher-order, hierarchically structured activity motifs. Because these multi-neuron patterns are captured both during active task performance and spontaneous inter-trial intervals, this dataset provides a resource for studying replay-related activity and for testing hypotheses about circuit-level processes associated with perceptual working memory. The dataset supports broad investigations into cross-regional spike organization, functional coupling, and temporal coding in working memory circuits.

neuroscience↗

bioRxiv2026

The influence of tension-compression switches on brain anisotropic modelling

Finite element (FE) head models are valuable tools for investigating brain injury mechanics, with their reliability critically dependent on accurate material modelling. White matter (WM) is often considered mechanically anisotropic due to its aligned axonal fiber architecture and is commonly represented using fiber-reinforced hyperelastic formulations such as the Gasser-Ogden-Holzapfel (GOH) model. A fundamental assumption of the GOH model is that fibers contribute only in tension and not in compression, requiring the use of tension-compression switches. However, inconsistencies were noted in the formulation of tension-compression switches with the influence on computational biomechanics unknown. To address this knowledge gap, three commonly used switching schemes - differing in both the switching parameter and the treatment of compressed fibers - were theoretically elaborated and numerical implementation within the GOH framework to simulate the mechanical anisotropy of WM in impact simulations. Results from the case-based and group-level analyses demonstrated that both the switching parameter and the treatment of compressed fibers affected WM deformation. Significant cross-scheme strain differences were noted in the first principal strain at the element level and fiber strain at the fiber level. These findings highlighted the mechanical role of tension-compression switch in the GOH-based brain modelling and advocated the adoption of fiber stretch itself as the switching parameter to discriminate the tensile and compressive fibers. The current study provides important guidance for the anisotropic constitutive models in brain tissue and calls for direct verification of the tension-compression switch hypothesis in axonal fibers.

biophysics↗

bioRxiv2026

Auxin promotes GPI-anchored protein-mediated trafficking of ABP1 to enable cell-surface auxin signaling

Rapid auxin responses are triggered by Auxin-Binding Protein 1 (ABP1) signaling; however, the coupling of hormone perception to signaling activation is unclear. ABP1, a cell surface auxin receptor, is localized to endoplasmic reticulum (ER), raising a fundamental question of where auxin is perceived and how signaling-competent receptors are mobilized to cell surface. Herein, we established a dark-induced auxin synthesis system in Arabidopsis hypocotyl; abp1 mutants showed pronounced elongation. Auxin dose-dependently stimulates LORELEI-like glycosyl-phosphatidylinositol-anchored protein 1 (GPI-AP, LLG1) interaction with ABP1, driving their outward trafficking from ER. However, this complex dissociated in acidic apoplast, facilitating H+-ATPase-mediated auxin signaling. Our findings reveal how intracellular auxin perception is converted into rapid cell-surface signaling, establishing a mechanistic framework for fast auxin responses and uncovering a GPI-AP-mediated trafficking mechanism for ER-retained receptors.

plant biology↗

bioRxiv2026

ARID1A deficiency unleashes centromeric RNA transcription to drive chromosomal instability and boosts PKMYT1 inhibitor efficacy via RNA sensing

Cancer gene-associated mutations and molecular hallmarks of chromosomal instability (CIN) are unexpectedly common in histologically normal cells and tissues. These emerging findings challenge the binary distinction between "normal" and "cancerous" cells and suggest that early tumorigenesis may commence against a background of widespread yet largely tolerated genomic instability. However, it remains largely unexplored how a cancer gene-associated mutation can initiate the development of CIN-like states in non-malignant cells and drive tumor evolution. ARID1A, a chromatin remodeling factor, was identified as the most frequently mutated gene in both gastric normal epithelium and tumors. This distinctive molecular convergence presents an opportunity to elucidate the mechanisms by which a cancer-associated gene facilitates the initiation of early CIN phenotypes and develop effective antitumor strategies. In the present study, using primary human gastric organoids, we employed optical genome mapping (OGM) and live-imaging technologies to demonstrate that ARID1A depletion induced a wide spectrum of structural variants (SVs), copy number variants (CNVs), and chromosomal segregation errors, characteristic features of CIN at a very early stage of gastric tumorigenesis. Mechanistically, ARID1A bound centromere repetitive satellite DNA (satDNA) sequences. Its SWI/SNF-associated chromatin remodeling activity was required for suppressing satDNA transcription and the production of -SatRNA, through restricting RNAPII elongation. Consequently, ARID1A depletion led to overexpression of -SatRNA, and a higher incidence of sister chromatid exchange (SCE), a sensitive indicator of CIN. Importantly, the elevated -SatRNA expression in ARID1A-deficient cells further established a dual therapeutic vulnerability for G2/M checkpoint blockade, such as PKMYT1 inhibitor (PKMYTi), by concurrently aggregating CIN-induced cell death and activating self-dsRNA sensing-mediated innate immune response. Notably, PKMYTi markedly promoted -SatRNA expression, aberrant release of these self-derived dsRNAs into the cytosol and a robust activation of the RIG/MDA5-MAVS-depenent type-I interferon response in ARID1A-depleted cells. As expected, PKMYTi potentiated the efficacy of immunotherapy in ARID1A-deficient gastric tumors. Together, our findings reveal that ARID1A deficiency unleashes centromeric -SatRNA transcription, which sets the molecular stage for tumor evolution and targeted therapy by coordinately inducing CIN and self-dsRNA-induced innate immune responses.

cancer biology↗

bioRxiv2026

MTB-KB: A Curated Knowledgebase of Mycobacterium tuberculosis Related Studies

Tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), has regained its position as the worlds leading killer among infectious diseases. Despite extensive research progress across epidemiology, diagnosis, drug development, treatment regimens, vaccines, drug resistance, virulence factors, and immune mechanisms, MTB-related knowledge remains fragmented across thousands of publications, limiting its effective use. To address this gap, we present MTB-KB, a literature-curated knowledgebase that systematically integrates high-impact findings from eight major sections of TB research. The current release contains 75,170 associations from 1,246 publications, covering 18,439 entities standardized using authoritative databases and WHO-endorsed classifications. A central feature is the interactive knowledge graph, which links cross-section associations to reveal and infer MTB-host interactions, treatment strategies, and vaccine development opportunities. MTB-KB also provides a user-friendly interface with browsing, advanced search, and statistical visualization. Overall, by consolidating dispersed MTB knowledge into a structured and accessible platform, MTB-KB provides a valuable resource for researchers, clinicians, and policymakers, supporting both basic and clinical TB research, enabling evidence-based TB prevention, diagnosis, and treatment, and contributing to global elimination efforts. MTB-KB is accessible at https://ngdc.cncb.ac.cn/mtbkb/.

bioinformatics↗

bioRxiv2026

Modification-aware AI enables terminal chemical modifications for peptide design and discovers potent antimicrobials

Antimicrobial resistance (AMR) is an escalating global health threat, intensifying the urgent need for novel antibiotics. Here, we introduce Termini, a generative machine learning (ML) framework that integrates peptide generation, classification, and regression modules to systematically identify potent antimicrobial peptides (AMPs). A key feature of this pipeline is its explicit design of both N- and C-terminal modifications, combined with predictive modeling across 15 bacterial species. We experimentally validated the framework against 11 pathogenic species, representing the broadest spectrum of testing reported to date in such a study. We synthesized and tested 120 peptides (including 60 unique amino acid sequences) with and without terminal modifications. Remarkably, 111 of these peptides (92.5%) demonstrated antimicrobial activity in vitro. Comparative analyses demonstrated that terminal modifications substantially enhanced antimicrobial potency. Furthermore, the lead candidates identified through in vitro screening exhibited robust anti-infective efficacy in subsequent in vivo experiments, confirming their therapeutic potential. Collectively, these results highlight the high hit rate, biological relevance, and translational promise of this integrative, modification-aware AI framework for next-generation antimicrobial peptide development.

microbiology↗

bioRxiv2026

Adaptive Integration of Heterogeneous Foundation Models to Find Histologically Predictable Genes in Breast Cancer

Foundation models for computational pathology have rapidly emerged as powerful tools for extracting rich biological and morphological representations from histopathology images. However, variations in model architecture, pre-training data, and optimization objectives often lead to task-dependent performance, rather than universal generalization. As a result, effective strategies for integrating their complementary strengths are essential to fully realize the potential of foundation models for robust histopathology analysis. Meanwhile, recent breakthroughs such as spatial transcriptomics provide an unprecedented opportunity to integrate genetic and histopathology information from the same patient sample, thereby maximizing both molecular and anatomical pathology insights. Specifically, each models embedding is first mapped to gene-level predictions via a dedicated prediction head, enabling model-specific feature utilization. A lightweight weighting network then adaptively aggregates these predictions to produce a unified and robust output at gene and spatial location levels. Across multiple spatial transcriptomics datasets, our approach consistently outperforms both individual foundation models and classical ensembling methods. Focusing on breast cancer, we observe substantial gains in prediction accuracy for clinically relevant PAM50 subtype markers and drug-target genes. Moreover, the proposed framework improves interpretability by revealing model-specific contributions and specialization at the gene level. Overall, our work presents an effective solution to integrating multiple foundation models for enhancing the genetic analyses of histopathology images.

bioinformatics↗

bioRxiv2026

PA-SfM: Tracker-free differentiable acoustic radiation for freehand 3D photoacoustic imaging

Three-dimensional photoacoustic imaging (3D PAI) has shown great potential in preclinical studies and clinical implementations, while it commonly has sparse sensor arrays, limiting both spatial sampling and the field of view (FOV). Freehand scanning could overcome these limitations through anatomy-adaptive scanning that extends spatial coverage and provides complementary views beyond the fixed array aperture, but its flexibility is conventionally constrained by the need for motor feedback or external pose tracking. Here we introduce PA-SfM, a tracker-free structure-from-motion (SfM) framework that recovers multiple poses directly from PA measurements with superior precision, enabling freehand 3D PAI without external pose measurements. PA-SfM integrates a differentiable acoustic radiation model with hierarchical optimization and rigid array constraints, it jointly estimates inter-view transformations and reconstructs 3D volumes. The performance of PA-SfM was demonstrated in numerical simulations, animal studies and human imaging experiments. Compared with motor encoder-based fusion of the mechanically scanned system, PA-SfM produced sharper and more continuous vascular reconstructions with an expanded FOV. In controlled quantitative validations, PA-SfM achieved high reconstruction fidelity, with PSNR values over 40 dB and SSIM values above 0.98 relative to ground truth or known pose reference reconstructions. These results demonstrate that PA-SfM enables robust freehand 3D PAI, with particular potential for clinical implementation of large-scale freehand imaging. The source code is publicly available at https://github.com/JaegerCQ/PA-SfM.

bioengineering↗

bioRxiv2026

A MinD-like ATPase couples flagellation and cell division in spirochetes

Spirochetes are evolutionarily distinct bacteria defined by their spiral morphology, unique means of motility, and periplasmic flagella (PFs). Because these filaments reside within the periplasm and are mechanically integrated with the cell body, their assembly must be precisely coordinated with cell growth and cytokinesis. However, the mechanism that couples flagellar biogenesis to cell division in spirochetes remains unclear. Using the Lyme disease spirochete Borrelia burgdorferi as a model, we identify FlhG (BB0269), a MinD-like ATPase, as a spatial regulator that links cell division to flagellar patterning. In wild-type cells, 7-11 long helical PFs originate from cell poles and assemble into ribbon-like bundles that wrap around the cell cylinder to drive motility. Deletion of flhG disrupts this ordered architecture, causing marked heterogeneity in flagellar number, defective ribbon assembly, aberrant septation, and severe motility impairment. Mechanistically, FlhG dynamically localizes to the poles and midcell during division, where it directs the positioning of FlhF, a signal recognition particle (SRP) -type GTPase controlling flagellar number and placement, and FliF, the MS-ring protein that nucleates flagellar assembly. Through this spatial regulation, FlhG coordinates flagellar assembly with cytokinetic progression. Together, these findings reveal a spatial regulatory mechanism coupling cell division to flagellation, providing insight into understanding how spirochetes coordinate their distinctive morphogenesis, flagellation and motility. SignificanceSpirochetes such as Borrelia burgdorferi, the causative agent of Lyme disease, rely on periplasmic flagella for motility and cell shape, yet how these structures are coordinated with cell division has remained unclear. We identify a MinD-like ATPase, FlhG, as a spatial regulator that couples flagellar assembly to cytokinesis. In contrast to its homologs in other bacteria, FlhG does not regulate flagellar protein levels but instead directs subcellular positioning of key assembly factors. By dynamically redistributing between the cell poles and division site, FlhG synchronizes flagellar patterning with septum formation. These findings uncover a previously unrecognized mechanism linking cell morphogenesis to the cell cycle and reveal how conserved ATPases can be repurposed to organize complex bacterial architectures.

microbiology↗

bioRxiv2026

Metabolic Engineering Boosts Strigolactone Production in Nicotiana benthamiana and Uncovers a Novel P450 Function

Strigolactones (SLs) are plant hormones regulating shoot branching and symbiotic interactions, but their trace-level abundance limits research and applications. Here, we optimized a Nicotiana benthamiana transient expression system for SL production by tuning agroinfiltration parameters and co-expressing rate-limiting carotenoid biosynthetic genes. Overexpression of Zea mays PSY1 or an Arabidopsis PSY-GGPS11 fusion increased carlactone production over 2-fold and enhanced downstream SL accumulation. Using this platform, we discovered that sorghum cytochrome P450 SbCYP728B35 catalyzes conversion of 5-deoxystrigol to sorgolactone, revealing a previously unknown function. These results establish metabolic engineering of precursor supply as an effective strategy for boosting SL production and demonstrate N. benthamiana as a robust system for pathway elucidation and biotechnological synthesis of bioactive strigolactones.

plant biology↗

bioRxiv2026

METTL14-dependent m6A modification restrains interferon signaling to prevent myocarditis and dilated Cardiomyopathy

The impact of inflammation on heart failure is increasingly recognized; but how cardiomyocyte restrains innate immune activation remains poorly defined, and nor does the role of N-methyladenosine (mA) modification in maintaining cardiac immune homeostasis. Here, we demonstrate that cardiomyocyte-specific deletion of the mA methyltransferase METTL14 triggers myocarditis, dilated cardiomyopathy, and premature lethality. Meanwhile, widespread hypomethylation and upregulation of innate immune and necroptosis-related transcripts in Mettl14-deficient hearts exemplified by IFN-1 and STAT1. Mechanistically, METTL14 deficiency promotes RIPK1 accumulation thereby priming cardiomyocytes for necroptosis and inflammatory cell death. Genetic ablation of IFN-I receptor Ifnar1 can largely rescue the processes and improve cardiac function and survival. Furthermore, METTL14 loss disrupts mitochondrial integrity and autophagy/mitophagy flux, suggesting mitochondrial dysfunction-driven innate immune activation upstream of IFN-I signaling. Collectively, these findings identify METTL14-mediated mA modification as a critical safeguard against cardiomyocyte-intrinsic IFN-I signaling and necroptosis and establish an epitranscriptomic-innate immune axis that drives inflammatory heart failure.

pathology↗

bioRxiv2026

Collective microfibril sliding underlies plant cell wall creep

Plant cell growth depends on slow, irreversible creep of the fibrous cell wall stretched by turgor, yet the mechanics of creep--and how it differs from elasto-plastic deformation--remains uncertain1-3. Using multiscale modeling, we show how wall creep emerges from elementary sliding of cellulose microfibrils along their contact interfaces. A dominant sliding mode involves localized dislocation-like defects that stochastically nucleate at laterally bonded microfibril contacts and then glide along the interface by surmounting discrete energy barriers. Embedding these sliding events into Monte Carlo simulations of stretched cellulose networks recapitulates whole-wall creep kinetics. Elevated stress lowers sliding energy barriers and triggers rapid irreversible deformation characteristic of plastic flow. Compared with elasto-plastic stretching, creep induces less microfibril reorientation but promotes bundling, thereby reducing subsequent yielding. These results clarify the microfibril rearrangements underlying cell wall creep and show how they redistribute stress to permit sustained wall expansion at steady turgor without compromising structural integrity.

biophysics↗

bioRxiv2026

Protein domain characterization reveals human MIC60 tolerates loss of helical bundle domain

The mitochondrial contact site and cristae organizing system (MICOS) is essential for cristae junction formation and inner mitochondrial membrane architecture. To define how MICOS integrity is established and maintained, we generated conditional deletion models of Immt (encoding MIC60), a core MICOS subunit, in tissue-specific settings and in cultured cells. Liver-specific deletion of Immt in mice induced profound defects in mitochondrial ultrastructure and function, establishing MIC60 as essential for mitochondrial integrity. Notably, despite the severity of the defects, we did not detect increased apoptosis in liver tissue or in cells. To directly link MIC60 structure to its function, we performed a systemic structure-function analysis of human MIC60 using domain-specific deletion mutants expressed in Immt-deleted cells. We identified that the transmembrane, coiled-coil, and mitofilin domains are required for MICOS assembly, mitochondrial morphology, and respiratory function. Unexpectedly, deletion of the predicted helical bundle (a region spanning 229 amino acids) substantially restored mitochondrial structure and function, nearly matching full-length MIC60. A mutation (K299E) associated with human disease within this domain similarly preserved most MIC60-dependent functions. Together, these results establish MIC60 as a non-redundant regulator of mitochondrial architecture while revealing that a large predicted structural domain is largely dispensable for MIC60s core functions, refining current models of MICOS organization and uncovering unexpected modularity within MIC60.

cell biology↗

bioRxiv2026

Cell type-resolved transcriptomic map of skeletal muscle in women with polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is associated with skeletal muscle insulin resistance, fibrosis, and lipotoxicity, yet the cellular origins remain unknown. Here, we present a comprehensive cellular atlas of skeletal muscle from hyperinsulinemic and hyperandrogenic women with PCOS and controls of similar age, weight, and BMI. Analysis of 72,247 nuclei from 19 biopsies revealed cell-type-specific dysregulation in PCOS, with fiber-type-specific metabolic impairment, converging with pro-fibrotic reprogramming of fibro-adipogenic progenitors (FAPs) and enhanced FAP-myofiber crosstalk, characterized by enhanced collagen and laminin signaling. Metformin intervention for 16-weeks selectively reversed PCOS-associated transcriptional dysregulation in FAPs, revealing heterogeneous cellular responses in skeletal muscle. In vitro, PCOS myotubes retained metabolic dysfunction, yet show normalized glucose responsiveness, indicating plasticity despite metabolic memory. Systemic hyperinsulinemia and hyperandrogenemia correlated with transcriptional signatures in muscle fibers and FAPs, linking endocrine imbalance to pro-fibrotic remodeling. These findings identify novel therapeutic targets beyond conventional insulin-sensitizing approaches. Highlights- First single-nuclei atlas of human skeletal muscle in women with PCOS - FAPs subpopulations display activated pro-fibrotic phenotype - Metformin selectively targets distinct cell populations - Hyperinsulinemia and hyperandrogenemia correlate with transcriptional signatures of skeletal muscle fibers and FAPs

physiology↗

bioRxiv2026

In vivo-compatible spatial multi-omics via hydrogen peroxide-independent APEX2 labeling

Proximity labeling (PL) technologies like APEX2 have transformed spatial multi-omics in live cells, but their long-standing dependence on hydrogen peroxide (H2O2) disrupts redox signaling and prevents use in live animals. Here we introduce H2O2-independent APEX2 (Hi-APEX), which uses a clickable tetrazine-phenol probe, requiring no enzyme engineering. We show that APEX2 directly catalyzes TP radical formation without H2O2 via a mechanism requiring the probes tetrazine group and a key histidine residue. We benchmarked Hi-APEX-based spatial multi-omics by mapping the mitochondrial matrix and dynamic secretomes. Hi-APEX significantly outperforms traditional APEX in capturing redox-sensitive processes such as stress response and ferroptosis, enabling discovering authentic stress granule components and protein interaction networks for mitochondria-localized GPx4. One mGPx4 interactor TRMT61B--known to regulate mitochondrial m{superscript 1}A modifications--promotes ferroptosis. Crucially, Hi-APEX achieves full in vivo compatibility, enabling direct PL in tumor xenografts and hippocampal neurons, thereby expanding PL-based spatial multi-omics from cellular systems to living organisms.

biochemistry↗

bioRxiv2026

Ubiquitination-mediated mitochondrial protein degradation ensures seedling emergence by regulating ER-mitochondrial interaction and mitophagy

Seedling emergence is a pivotal step of plant survival, requiring rapid hypocotyl elongation for soil penetration. This energy-demanding process necessitates active mitochondrial respiration, which inevitably induces oxidative damage. Therefore, plants evolved a quality control mechanism that selectively removes dysfunctional mitochondria through the mitophagy pathway. Here, we identified SPL2, a mitochondrial E3 ligase which is essential for hypocotyl elongation and seedling emergence through degrading mitochondrial outer membrane proteins, such as TRB1 and FIS1A. Intriguingly, these proteins also interact with an ER protein, VAP27-1, forming a complex at the ER-mitochondria contact sites, which is essential for mitophagy initiation. The spl2 mutant exhibits enhanced ER-mitochondrial tethering and mitophagy activation, whereas its overexpression has the opposite effects. The expression of SPL2 increases after light perception, in agreement with the reduced mitophagy. Collectively, our findings reveal novel mechanistic insights into seedling emergence, which are coordinated through protein ubiquitination, ER-mitochondrial interaction, and mitophagy.

plant biology↗