Biology subjects

Liu, Y.

Publications and source records attributed to Liu, Y..

At least 559 records · Page 31Linked to original sources

bioRxiv2025

Restoration of Spermatogenesis is Dependent on Activation of a SPRY4-ERK Checkpoint Following Germline Stem Cell Damage

Mammalian spermatogonial stem cells (SSCs) sustain male fertility through continuous self-renewal and differentiation, leading to the production of haploid spermatozoa throughout adulthood. However, SSCs are vulnerable to genotoxic drugs, and patients receiving chemotherapy face a high risk of germline instability and infertility. The molecular mechanisms and cellular pathways that choreograph SSC recovery after chemotherapeutic insult remain unknown. Previously, we identified SPRY4 as an ERK-dependent negative feedback regulator of growth factor signaling that is critical for preservation of stem cell activity in cultured mouse SSCs. Here, we demonstrate that following alkylating agent busulfan (BU)-induced injury in adult mice, germline-specific Spry4 gene deletion (Spry4G-KO) reduces stem cell regeneration with an enhanced genotoxic stress response and differentiation with rapidly enhanced nuclear ERK1/2 activity in undifferentiated (Aundiff) spermatogonia (including SSCs). Genes essential for stem cell maintenance, including Id1 and Cxcl12, were dysregulated by loss of Spry4. Furthermore, the MEK1/2 inhibitor PD0325901, but not mTORC1 inhibitor Rapamycin, was sufficient to promote spermatogonial proliferation in Spry4G-KO testis 10 days post-BU treatment. Notably, the restoration of both spermatogonia pool and fertility was delayed in adult Spry4G-KO males long-term after injury. In summary, germline-specific deletion of Spry4 results in hyper-activation of the MAPK/ERK pathway in Aundiff spermatogonia, reducing spermatogonial genome integrity, unleashing excessive spermatogenesis after germline damage, and ultimately impairing germline regeneration in adult males. Our study indicates an essential role for SPRY4-ERK signaling as a molecular checkpoint in securing SSC recovery upon chemotherapy drug-induced germline damage, revealing how stem cells normally withstand environmental stress.

cell biology↗

bioRxiv2025

A Population-scale Single-cell Spatial Transcriptomic Atlas of the Human Cortex

The genetic and spatial determinants of cell type diversity in human cerebral cortices remain poorly defined. Here, we present a population-level single-cell spatial transcriptomic atlas of human cortices from 71 donors across the lifespan. We identified 906 layer-specific genes showing conserved and divergent laminar expression patterns between humans and other species. Spatial analysis revealed neuronal vulnerability and glial activation during aging, together with a decline in the proportion of superficial SST neurons and their interactions with other cells. Disease-associated genes exhibited high cell-type and layer-specific expression, implicating the pathogenic role of spatially specific gene expression. Spatial cis-eQTL analysis identified regulatory variants linked to genes related to diseases like Tourette syndrome. Cross-species comparison demonstrated glial expansion in the human cortex, accompanied by enhanced neuron-glia communication via the neuregulin signaling. Together, we provide a comprehensive single-cell atlas of the human cortex that is essential for understanding aging, evolution, and disease pathogenesis.

neuroscience↗

bioRxiv2025

DEEPReditor-CMG: A deep-learning-based predictive RNA editor for crop mitochondria genomes

C-to-U RNA editing is a pervasive phenomenon in crop mitochondria, playing a pivotal role in the processing of functional proteins encoded by mitochondrial genes and serving as a crucial regulatory mechanism for nuclear control over mitochondrial gene expression. However, identifying editing sites across the mitochondrial genome with high precision remains a formidable challenge. To address this challenge and uncover the potential regulatory patterns of C-to-U RNA editing, this study compiled a comprehensive dataset of mitochondrial genome sequences from 13 crops, including Arabidopsis thaliana, Lactuca sativa var. Capitata, Oryza sativa Japonica, and Zea mays, among others, annotated with editing sites from NCBI. Utilizing TensorFlow 2.0, we constructed a rigorous hyperparameter optimization framework, which facilitated the development of the DEEPReditor-CMG model, demonstrating superior predictive capabilities. Based on the DEEPReditor-CMG model and three interspecies relationship indices, we discovered that species with closer phylogenetic relationships exhibit more similar C-to-U RNA editing mechanisms, providing valuable insights into the evolutionary conservation of RNA editing mechanisms. We further developed executable programs for predicting C-to-U RNA editing sites in crop mitochondrial genomes, leveraging the conserved nature of the crop RNA editing machinery to maximize prediction reliability and uncover new editing sites with great potential. This research not only deepens our understanding of C-to-U RNA editing and post-transcriptional regulatory mechanisms in crop mitochondria but also paves a novel avenue for investigating RNA editing mechanisms. Experimental data, computational code, and applications are publicly accessible at https://github.com/Qinsidong/DEEPReditor-CMG. HighlightsHigh-precision prediction model for C-to-U RNA editing in crops--DEEPReditor-CMG Three interspecies relationship indices describing C to U RNA editing Prediction tools based on the conservation of crop RNA editing mechanisms Open-sourced experimental data, computational code, and applications

bioinformatics↗

bioRxiv2025

Distinct Filament Conformation for Receptor-Bound Amyloid-β from Alzheimers Disease Brain

Alzheimers disease is triggered by amyloid-{beta}, with symptoms linked to synapse loss. Oligomeric amyloid-{beta}, rather than monomeric or fibrillar amyloid-{beta}, has been proposed to be the proximate mechanistic cause, but the relevant molecular characteristics have remained unclear. Here, we define a distinct receptor-bound amyloid-{beta} pool in Alzheimers brain by release with a receptor antagonist and purification to homogeneity. Receptor-bound amyloid-{beta} is ten times more abundant than free unbound amyloid-{beta}. The amyloid-{beta} associated with receptor is composed of 65 nm long filaments with prion protein binding at its tips. There is no evidence for an oligomeric A{beta} state interacting with human brain receptors. Cryo-electron microscopy shows two symmetric S-shaped monomers per filament rung. The tilt between rung monomers, twist along the filament axis, amino terminal conformation and amyloid seeding properties distinguish this structure from plaque-associated amyloid-{beta} filaments of the same brain. High tip:length ratio is critical for prion protein receptor interaction and synaptic damage. Characterizing receptor-bound amyloid-{beta} filament provides insight into neuronal dysfunction separate from plaque aggregation.

neuroscience↗

bioRxiv2025

Viral tRNA-like structure hijacks host ribosomes for poly(A)-independent translation

Positive-sense RNA viruses often use 3' tRNA-like structures (TLSs) instead of poly(A) tails to capture the host translation machinery. While TLSs resemble canonical tRNAs and engage host factors, their ability to directly recruit ribosomes has remained unresolved. Here, we present cryo-electron microscopy snapshots of the histidine-accepting TLS (TLSHis) from tobacco mosaic virus bound to the 60S subunit, the 80S ribosome, and the 80S-tRNAiMet initiation complex. Across these states, TLSHis is consistently anchored to the L1 stalk of 60S, even under cycloheximide treatment, yet remains dynamic on the 40S subunit. Structural analysis shows that TLSHis transitions from the E-site to an adjacent Z-site to accommodate initiator tRNA. Functional assays show that TLSHis preferentially associates with ribosomal subunits over polysomes and can substitute for a poly(A) tail to promote robust cap-dependent translation. Together, these findings reveal how a viral tRNA mimic hijacks host ribosomes to promote poly(A)-independent translation.

molecular biology↗

bioRxiv2025

A hierarchical nickel organic framework confers high conductivity over long distances in cable bacteria

Multi-cellular cable bacteria have evolved a unique machinery that efficiently transports electrons across centimetre-scale distances. Currents flow through a parallel network of periplasmic fibres, which display an extraordinary conductivity for a biological material. However, the conduction mechanism remains elusive as the molecular structure of the fibres has not been resolved. Here, we demonstrate that each fibre embeds a bundle of intertwined nanoribbons, which are built from Nickel Bis(Dithiolene) (NiBiD) repeat units that are formed by linking nickel centres with ethenetetrathiolate ligands. The planar and conjugated NiBiD complexes are aligned and stacked to form an elongated supramolecular coordination network, thus explaining the observed organo-metal electronic properties of the fibres. Our results hence demonstrate that biology is capable of producing extensive metal organic frameworks. These structures enable highly conductive one-dimensional conduits, ensuring efficient charge transport over macroscale distances, thus providing a novel design principle for bio-based, sustainable organo-electronic materials.

molecular biology↗

bioRxiv2025

Agro-STARR-seq enables in planta genome-wide enhancer discovery and AI-empowerd enhancer design

Comprehensive enhancer screening is essential for dissecting gene regulatory networks. However, methods for such screening remain limited in plants. We present Agro-STARR-seq, an in planta enhancer screening platform using Agrobacterium-mediated delivery of STARR-seq libraries into Nicotiana benthamiana leaves. In the Arabidopsis genome, we identified 14,715 sequences with enhancer activity, of which 91.59% were located outside of open chromatin regions. This largest in planta enhancer dataset to date enabled AI-assisted design of highly active synthetic enhancers. For the large N. benthamiana genome, we pre-processed the genomic DNA with an Assay for Transposase Accessible Chromatin (ATAC) procedure before the Agro-STARR-seq protocol,and found that only one-third of open chromatin exhibited enhancer activity, 76.00% of which showed no canonical H3K27ac histone marks. Footprinting analysis further enables systematic linkage of transcription factor (TF) binding to enhancer function. Overall, Agro-STARR-seq provides a novel platform for dissecting and engineering plant enhancers.

genomics↗

bioRxiv2025

The role of medicinal Cu2+ salts in expanding the multi-pathway application of tigecycline against drug-resistant bacteria

Tetracyclines are highly susceptible to photolysis, causing pollution in water, land and other ecosystems, as well as posing threats to human health. In this study, we found that only tigecycline and minocycline reduce the antibacterial activity in light, and this inferiority has severely hindered their scope of clinical use. By strategically regulating the photolysis pathway, we identified chalcanthite, which primarily contains Cu2+. By conducting antibiotic susceptibility test and electron microscopy analysis, Cu2+ salts (including copper sulfate, copper chloride, and copper gluconate) were confirmed to restore the antibacterial activity of tigecycline under light exposure against all tested bacterial strains. Spectroscopic characterization combined with quantum chemical calculations elucidated the molecular mechanism by which Cu2+ selectively modulates the photolytic degradation pathway of tigecycline and structural determinants (dimethylamino groups on the D ring). Multi-omics technologies revealed the mechanism underlying the Cu2+-mediated (non-antibacterial) inhibition of bacterial ferric citrate transporter. Animal infection models were developed using diverse drug-resistant pathogens to validate the in vivo therapeutic efficacy of copper gluconate-tigecycline combination therapy under photic conditions. These findings revealed effective adjuvants that facilitate the development of topical tigecycline formulations, and the establishment of a scientific foundation for synthesizing photostable tetracycline-based antibiotics through structural optimization.

biochemistry↗

bioRxiv2025

Aberrant Neural Entrainment to Word-Level Speech Patterns in Fragile X Syndrome: Evidence for a Statistical Learning Deficit

Fragile X syndrome (FXS), the most common inherited cause of intellectual disability and autism spectrum disorder, causes significant language and cognitive impairments. Statistical learning refers to the ability to extract patterns from sensory input through mere exposure and plays a central role in language acquisition. Surprisingly, statistical learning in FXS has not been explored. Given that children with FXS typically follow a delayed developmental trajectory for language, we hypothesized that they would show impaired statistical learning. To test this hypothesis, we used an EEG measure of neural entrainment to index statistical learning of hidden trisyllabic words within a continuous speech stream in children with FXS (n = 17) and in typically developing controls (n = 31). Children with FXS showed significantly reduced neural entrainment to words compared to controls, particularly in the superior temporal gyrus and transverse temporal gyrus (primary auditory cortex), providing evidence of statistical learning impairment. Notably, syllable-level entrainment was preserved or even enhanced in FXS, indicating that word-level deficits cannot be attributed to general auditory processing impairments. In addition, while typically developing controls showed an increase in word-level entrainment over the course of learning, children with FXS failed to show a similar increase over time. Taken together, this pattern of results demonstrates that children with FXS can process rapid, lower-order acoustic structure but struggle to integrate these syllables into longer, chunk-like word representations. Overall, these findings suggest that statistical learning is impaired in FXS, and also suggest neural entrainment to statistical structure as a potential therapeutic target.

neuroscience↗

bioRxiv2025

Ultra-mild bisulfite outperforms EM-seq for 5-methylcytosine detection with low input DNA

We present Ultra-Mild Bisulfite Sequencing (UMBS-seq), a method for 5-methylcytosine (5mC) detection that minimizes DNA degradation and background noise. UMBS-seq outperforms conventional bisulfite and enzymatic methyl-sequencing (EM-seq) methods in library yield, complexity, and conversion efficiency when applied to low-input DNA samples. In particular, its effectiveness with low-input cell-free DNA (cfDNA) and hybridization-based target capture highlight its potential for clinical applications, including 5mC biomarker detection and early disease diagnosis.

genomics↗

bioRxiv2025

Deterministic co-encapsulation of microparticles in droplets via synchronized merging for single-cell genomics

Droplet encapsulation of microparticles such as hydrogel beads and cells is fundamental to high-throughput bioanalytical assays, including single-cell genomics. However, co-encapsulation of multiple particles at defined ratios remains a technical challenge. Here, we present a simple and robust strategy for deterministic co-encapsulation, combining particle-triggered droplet generation with synchronized droplet merging. Close-packed hydrogel particles initiate droplet formation, and the resulting droplets are synchronized and merged within a microfluidic channel, enabling efficient encapsulation of microparticles at user-defined ratios. We systematically characterized the process and demonstrated reliable co-loading of 55 {micro}m and 80 {micro}m hydrogel particles at 1:1 and 2:1 ratios. Using this platform, we developed a single-cell 16S rRNA gene sequencing workflow by co-encapsulating hydrogel capsules containing amplified microbial genomes with barcode beads. Applied to a 1:1 mixture of Escherichia coli and Bacillus subtilis, the method enabled accurate, high-throughput single-cell taxonomic profiling. This co-encapsulation approach offers broad applicability for single-cell genomics, digital assays, and interaction-based studies requiring precise particle pairing.

microbiology↗

bioRxiv2025

A Unifying Mechanism for Shared Splicing Aberrations in Splicing Factor Mutant Cancers

Cancer-associated splicing factor (SF) mutations in SF3B1, U2AF1, and SRSF2 induce distinct changes in alternative splicing (AS). Yet these mutations are strikingly mutually exclusive, pointing to a convergent downstream mechanism. We hypothesized this would be reflected in the AS transcriptome. By analyzing transcriptomes of 395 patients with clonal myeloid disorders and 64 healthy donors, we found most AS alterations to be mutation-specific. However, a robust subset, enriched in the retained intron (RI) program, was shared across mutants. These RI events were bidirectional but highly concordant, and mirrored the effects of SRSF1 loss. SF-mutant states induced hypophosphorylation of RS domains in SRSF1, reducing its function. This arose from an altered AMPK-AKT balance impairing the AKT-SRPK1-SRSF1 axis. A common upstream trigger was activation of DNA damage response (DDR) by transcriptional R-loops, which increased AMPK signaling and reduced AKT activity. Pharmacologic DDR activation recapitulated reduced AKT/SRPK1 activity and SRSF1 hypophosphorylation, while relieving DDR restored SRSF1 phosphorylation and corrected RI defects. Thus, beyond cis-acting, mutation-specific changes, SF-mutant cancers share a trans-acting, stress-driven AS signature wherein DDR signaling rewires SRSF1 activity impacting AS. Our results link replication stress, kinase signaling, and RNA processing across genetically diverse clonal states, highlighting potential therapeutic approaches at these nodes. HighlightsO_LIWhile most splicing changes differ by splicing factor (SF) mutation, certain retained introns are common across subtypes. C_LIO_LIChanges in RI are bidirectional, concordant across mutant groups, and mirrors SRSF1 loss. C_LIO_LISF mutations activate DDR, triggering an AMPK/AKT imbalance that culminates in SRSF1 hypophosphorylation. C_LIO_LIRelieving R-loop induced DDR restores SRSF1 phosphorylation and reverses RI. C_LI

cancer biology↗

bioRxiv2025

PTH-Induced Behavioral and Metabolic Alterations in Mouse Models of Hyperparathyroidism

Parathyroid hormone (PTH) is a critical endocrine regulator of calcium homeostasis and bone remodeling and is widely employed in clinical settings through synthetic analogs for the treatment of osteoporosis. Although traditionally considered a peripheral regulator, emerging evidence indicates that PTH also exerts effects through the central nervous system (CNS). This study investigated the neuropsychiatric impact of elevated PTH and explored potential CNS involvement using multiple murine models of hyperparathyroidism (HPT). Distinct behavioral phenotypes were observed across models, indicating that psychiatric symptoms vary depending on disease etiology and progression. The effects of hPTH(1-34), a clinically approved PTH analog, were further assessed in male and female mice. Under pharmacological concentrations, hPTH(1-34) enhanced locomotor activity in males but induced mild anxiety-like behavior in females. These behavioral changes in females were independent of the estrus cycle and were amplified by ovariectomy. Metabolic analysis indicates PTH affects the basic metabolism by inhibiting the respiratory exchange ratio, promotes the energy expenditure and locomotion without affecting the food consumption in a 48hr range. To further investigate the molecular effect of PTH in the brain, a PTH1R-Cre mouse line was generated to map PTH receptor-1 (PTH1R) expression. Widespread expression of PTH1R was detected across the brain, including in both neuronal and non-neuronal cell populations. These findings suggest that PTH may influence behavior through interactions with PTH1R-expressing cells in brain vasculature and circumventricular regions. However, further studies are warranted to define the specific brain nuclei and cell types involved in PTH-driven modulation of neurobehavioral function.

neuroscience↗

bioRxiv2025

In Vivo Metabolic Tagging and Targeting of Circulating Red Blood Cells

Engineering red blood cells (RBCs) has been widely explored for drug delivery, imaging, vaccination, and other applications. However, effective strategies to directly engineer RBCs in vivo still do not exist. Here, for the first time, we report successful metabolic glycan labeling of RBCs in vivo. We demonstrate that systemically administered azido-sugars can metabolically label circulating RBCs with azido groups in the form of glycoproteins and glycolipids, with contributions from the labeling of both mature RBCs in the bloodstream and RBC precursor cells in the bone marrow. The RBC labeling efficiency can be improved by optimizing the choice and dose and dosing frequency of azido-sugars. The surface azido tags on RBCs can persist for >42 days in mice (nearly the lifespan of mouse RBCs), in sharp contrast to azido tags on leukocytes in the blood and cells in healthy tissues that decay to undetectable levels within 3 days. This in vivo RBC labeling technology does not induce any noticeable toxicity to RBCs, leukocytes, and healthy tissues. We further demonstrate that azido-labeled RBCs can covalently capture dibenzocyclooctyne-bearing cargos in vivo via click chemistry, prolonging the blood circulation of cargos from typical hours to >35 days. In a few examples, we show that the unprecedented RBC tagging and targeting technology can improve the fluorescence imaging of blood vessels and tumor tissues, enable long-term magnetic resonance imaging of brain vasculatures with one dose of gadolinium agent, and enhance the pharmacokinetics of drugs such as insulin.

bioengineering↗

bioRxiv2025

Nanochirality-programmed Type-I photosensitizer enables deep-tumor photodynamic therapy by reducing extracellular-matrix adhesion

Tumor hypoxia and poor penetration of therapeutics across tumor-microenvironment barriers remain major obstacles to effective cancer therapy, including photodynamic therapy (PDT). Here we introduce a nanochirality-programmed assembly (L-Chi-GAIN) in which nanochirality drives site-selective assembly that activates oxygen-independent Type-I reactive oxygen species (ROS) generation and reduces hyaluronan-mediated matrix adhesion, thereby permitting deep intratumoral therapy. Glycosylation imparts structural chirality to graphene quantum dots (GQDs), directing site-selective assembly of indocyanine green (ICG) that turns on photoinduced electron transfer (PET), producing a 64-fold increase in ROS relative to free ICG. Nanochirality also modulates assembly-extracellular matrix (ECM) interactions. L-GQDs show a less favorable hyaluronan binding free energy ({Delta}Gbind), thus accelerating interstitial transport and resulting in [~]21-fold deeper tumor penetration by L-Chi-GAIN than conventional nanocarriers. Under near-infrared irradiation, L-Chi-GAIN elicits strong oxidative stress and triggers Gasdermin-D (GSDMD)-dependent pyroptosis, leading to significant suppression of tumor growth. This work offers a nanochirality-guided design strategy for PDT in deep tumors by coupling site-selective assembly with stereoselective navigation of the ECM.

bioengineering↗

bioRxiv2025

Hepatic ceramide synthesis links systemic inflammation to organelle dysfunction in cancer

Paraneoplastic syndromes arise when tumor-derived cytokines reprogram distant organs. Although mediators such as Interleukin-6 have been implicated, how these signals impair host organ function remains incompletely defined. Here, we identify a cytokine-lipid axis that drives hepatic autophagy dysfunction. Specifically, in Drosophila, the gut tumor-derived interleukin-like cytokine Upd3 induces the expression of the triglyceride lipase CG5SCC, which we named "cancer-associated lipid mobilizer (calm)", and the ceramide synthase schlank in the fat body. This upregulation rewires fat body lipid metabolism, resulting in an autophagic-flux blockade. Genetic reduction of either CG5SCC or schlank restores organelle homeostasis and mitigates paraneoplastic phenotypes. This mechanism is conserved in mammals: in mice, IL-6 upregulates the lipoprotein lipase Lpl and ceramide synthases which in turn trigger a hepatic autophagy-flux blockade; in humans, hepatic LPL and ceramide synthases expression correlates with poorer survival in hepatocellular carcinoma. Our findings position hepatic lipid metabolism rewiring, especially ceramide synthesis as a critical, conserved node coupling systemic inflammation to organelle dysfunction, and suggest this pathway as a possible therapeutic entry point for cancer-associated liver disorders.

genetics↗

bioRxiv2025

Loss of tight junction protein claudin 18 uncovers alveolar epithelial stem cell plasticity and emergence of non-fibrogenic transitional progenitors

Persistence of senescent alveolar transitional progenitors following lung injury is implicated in the pathogenesis of fibrosis. We identified transitional cells in uninjured Cldn18 knockout (KO) mouse lungs distinct from previously reported damage-associated transitional progenitors (DATPs) with a less fibrogenic transcriptomic profile. Cldn18 KO mice are protected from bleomycin-induced fibrosis, with early restoration of cellular homeostasis. Lineage tracing implicates accelerated differentiation as a mechanism for protection from fibrosis, leading us to name these cells regeneration-associated transitional progenitors (RATPs). Multiome confirms that RATPs and DATPs are epigenetically distinct, with RATPs comprised of RATP2s and RATP1s based on epigenomic proximity to AT2s and AT1s, respectively, and suggests dynamic regulatory remodeling during AT2-to-AT1 differentiation, with NKX2.1 and AP-1 active in early transitions and TEAD factors in later stages. These results reveal an unexpected role for Cldn18 in regulation of AEC plasticity, while identification of RATPs challenges the notion that persistence of transitional alveolar cells is invariably pathologic.

cell biology↗

bioRxiv2025

Tryptophan-Driven Metabolomic Shift in Acidobacteriaceae Reveals Phytohormones and Antifungal Metabolites

Acidobacteriota is one of the most abundant phyla in soils and has recently attracted attention for its potential role in promoting phytosanitary benefits. The metabolomic capabilities of this phylum remain poorly characterised, with few experimentally confirmed metabolites described. To address these gaps, we combined metabolomic profiling with comparative genomic analysis to explore the functional potential of novel strains within the Acidobacteriaceae family. Genome mining across the phylum for plant-growth-promoting traits revealed the presence and taxon-specific enrichment of genes related to phytohormone production, as well as other genes associated with plant-beneficial microorganisms. When tryptophan was added to the cultivation medium, it triggered a strong metabolic response in the strains, resulting in measurable changes in the production levels of phytohormones such as indole-3-acetic acid and indole-3-pyruvate. Building on these findings, we examined the metabolic reprogramming caused by tryptophan supplementation, which suppressed the growth of phytopathogenic fungi, leading to the identification of malassezindoles and pityriacitrins as active agents. This was confirmed by isolating and elucidating the structure of pityriacitrin B and one of its methyl esters through NMR studies. Overall, these findings shed light on the previously unexplored metabolic potential of the Acidobacteriota phylum, emphasising its ecological importance for phytosanitary applications. ImportanceDespite their ubiquity and genomic diversity, the functional metabolism of members of the Acidobacteriota has largely remained uncharacterised. This study links genomic predictions to experimentally verified metabolomic outputs of Acidobacteriaceae, demonstrating tryptophan-responsive metabolic shifts translating to phytohormones and metabolites suppressing fungal growth. Our work underscores the emerging role of Acidobacteriota as important contributors to soil ecosystem functioning and plant-microbe interactions.

microbiology↗