Biology subjects

Wang, C.

Publications and source records attributed to Wang, C..

At least 73 records · Page 4Linked to original sources

bioRxiv2026

RNA m6A demethylase ALKBH4 governs whitefly development

N6-methyladenosine (m6A) modification is the most predominant and ubiquitous internal modification of RNA in eukaryotes, serving as a key post-transcriptional regulator of gene expression that is dynamically modulated by methyltransferases (writers) and demethylases (erasers). However, while the functions of m6A methylases have been partially elucidated in insects, the identity of m6A erasers in arthropods and their chemical catalytic mechanisms, as well as biological functions, remains largely enigmatic. Here, we uncovered 2499 putative methylase genes and 1148 putative demethylase genes in 266 insect genomes, and demonstrated that ALKBH4 functions as an m6A demethylase in the whitefly, Bemisia tabaci, catalyzing the oxidative reversal of mRNA m6A modifications both in vitro and in vivo. Furthermore, we established that ALKBH4, in coordination with other core components of the m6A pathway, fulfills an essential function in regulating the transcript stability of Imaginal Disk Growth Factor 1 (IDGF1) during whitefly development. Collectively, our findings expand the evolutionary scope of the eukaryotic m6A modification system, and reveal a conserved yet insect-specific epitranscriptomic regulatory mechanism governing fundamental physiological processes and adaptive phenotypes. Significance statementThe addition of a methyl group to the N6-position of adenosine (m6A) is a highly abundant chemical modification of RNA. However, the functional role of m6A in insects and the key enzymes that regulate its levels remains poorly understood. In this study, we explored putative methylase genes and demethylase genes in hundreds insect genomes, and identified an m6A RNA demethylase, ALKBH4, in the whitefly, Bemisia tabaci. We demonstrate that ALKBH4 oxidatively reverses mRNA methylation in vivo and in vitro, in combination with other components of the m6A pathway, plays an important role in whitefly development. These findings provide new insight into m6A methylation system of insect.

zoology↗

bioRxiv2026

Continuous attractor circuits for decision making with Laplace-domain neural representations

Decision formation is commonly described as the accumulation of noisy evidence in a low-dimensional decision variable, but it remains unclear how this latent computation is implemented by heterogeneous neural responses. Here, we propose that ramping and sequentially firing neurons form complementary population codes for the same decision variable. Inspired by Laplace-domain neural representations of time, exponential receptive fields in a ramping population give rise to a translatable edge-like activity profile; localized receptive fields in a sequential population give rise to an aligned bump-like profile. We construct a continuous attractor neural network that dynamically maintains these complementary representations while implementing evidence accumulation along a shared latent manifold. At the behavioral level, simulations show that the circuit closely reproduces the single-trial trajectories, choice probabilities, and reaction-time statistics of a standard diffusion decision model while generating heterogeneous ramping and sequential neural responses. Our framework connects latent behavioral dynamics, population geometry, and recurrent circuit mechanisms. More broadly, it provides a circuit-level realization of computation in the Laplace domain that may support the representation and updating of continuous cognitive variables across decision making, timing, memory, and spatial cognition.

neuroscience↗

bioRxiv2026

A functional genomics screen of human B-cell differentiation reveals convergent mechanisms of inherited childhood leukemia predisposition

B-cell acute lymphoblastic leukemia (B-ALL) is the most common childhood cancer, yet the mechanisms by which inherited risk variants predispose to leukemia development remain poorly understood. A major challenge to studying these mechanisms has been the lack of model systems that faithfully capture the transient developmental states in which predisposition alleles are thought to act. Here, we establish a human B-cell differentiation platform from hematopoietic stem/progenitor cells that enables CRISPR-based engineering, recapitulates early B-cell lymphopoiesis, and enriches for rare developmental intermediates. By applying systematic perturbations with multiplexed single-cell transcriptomic profiling to mimic the effects of mutations in nine familial B-ALL predisposition genes, we decipher mechanisms by which B-cell development can be altered by such inherited variation to predispose to B-ALL. Through these studies, we identify convergent delays in B-cell differentiation at progenitor stages characterized by high-level RAG1/2 recombination activity. We propose that these delays at progenitor stages increase the likelihood that cells can undergo illegitimate RAG-mediated recombination to promote transformation, a finding consistent with similar rates of illegitimate RAG-associated genomic alterations in those with B-ALL associated with familial predisposition variants compared to sporadic cases.

cancer biology↗

bioRxiv2026

Paternal Metabolic Reversal Remodels Sperm RNA Profiles and Ameliorates Intergenerational Metabolic Disorder in Mice

Paternal obesity increases metabolic risk in offspring, but whether this risk can be reduced by restoring paternal health before conception remains unresolved. We developed a within-sire induction-and-reversal model in outbred CD1 mice in which high-fat diet (HFD)-exposed males generated offspring before and after transition to an ingredient-matched control diet with voluntary exercise. HFD caused obesity, glucose intolerance, insulin resistance, and extensive remodeling of sperm mRNA, lncRNA, and sncRNA profiles, together with transcriptomic changes in metabolic tissues. Diet and exercise reversal normalized paternal metabolic indices and broadly restored tissue RNA profiles, although sperm retained a limited transcriptional memory of prior HFD exposure. Offspring sired before reversal developed sex-dependent metabolic dysfunction despite control-diet rearing, whereas offspring sired after reversal showed substantial improvement. These findings show that paternal metabolic risk is modifiable before conception and that this reversibility is linked to remodeling of sperm RNA. (140 words) HighlightsO_LIPaternal HFD-Ex induces obesity, glucose intolerance and insulin resistance in CD1 males C_LIO_LISperm shows much stronger RNA response than four metabolic organs profiled C_LIO_LIDiet and exercise reversal restores metabolism and RNA profiles in sperm and four metabolic organs analyzed C_LIO_LIOffspring metabolic risk is reduced when sires conceive after reversal through diet and exercise intervention C_LI eTOC BlurbChen, Magalhaes, et al. show that paternal metabolic recovery before conception remodels sperm RNA and reduces transmission of HFD-associated metabolic risk to offspring in a within-sire mouse model.

genetics↗

bioRxiv2026

Beyond point estimates: quantifying predictive uncertainty reveals hidden dimensions of biological age acceleration and improves risk interpretation

Biological age estimates are increasingly used to study aging, disease risk, and mortality, yet their predictive uncertainty is rarely quantified. Consequently, conventional age-gap measures can treat deviations as equally informative even when the underlying biological age predictions differ substantially in reliability. We developed a framework for uncertainty-aware biological aging that generates calibrated prediction intervals and individualized probabilities of accelerated or decelerated aging alongside point estimates. We applied this framework to the UK Biobank Pharma Proteomics Project, evaluating three composite and eleven organ-specific biological age clocks. Predictive uncertainty varied substantially both within and across clocks, revealing that apparently extreme age gaps can differ markedly in the strength of evidence supporting accelerated or decelerated aging. In particular, low-accuracy clocks, including many organ-specific clocks, provided little evidence for confidently accelerated or decelerated aging. Beyond biological age gaps, prediction-interval width was independently associated with disease risk and mortality, particularly for composite, brain, and immune clocks, suggesting that predictive uncertainty captures an additional dimension of biological aging that may reflect increased molecular heterogeneity and dysregulation associated with aging and disease. We replicated these findings in Biobank Japan and an independent clinical cohort from Stanford. By incorporating individual-specific predictive uncertainty, our framework provides a more informative characterization of biological aging and enables improved individual-level risk stratification for disease prevention and longitudinal monitoring.

bioinformatics↗

bioRxiv2026

Decorin-mediated Extracellular Matrix Stabilization Maintains Cartilage Integrity During Aging

Aging is a primary risk factor for osteoarthritis (OA), yet the mechanisms that preserve extracellular matrix integrity in long-lived connective tissues remain poorly defined. The function of articular cartilage depends on maintaining extracellular matrix integrity over a lifetime of mechanical use. Here we identify failure of matrix stabilization as an initiating mechanism of age-associated OA. Cartilage-specific deletion of decorin in mature mice disrupted the superficial collagen II fibrillar network, reduced aggrecan retention, and impaired poroelastic fluid pressurization by 9 months of age, preceding substantial transcriptional changes in resident chondrocytes. With advancing age, these matrix defects culminated in cartilage erosion, fibrotic remodeling, and spontaneous OA by 18 months. Mechanistically, decorin attenuated force-induced collagen II fibril realignment and reinforced the superficial fibrillar network, preserving matrix architecture under sustained physiological loading. These findings establish decorin-mediated extracellular matrix stabilization as a critical determinant of cartilage longevity and support a matrix-first model of age-associated degeneration.

biophysics↗

bioRxiv2026

Single-cell lineage tracing of human neuromesoderm organoids reveals TBX6-mediated posterior mesoderm fate diversification

Neuromesodermal progenitors (NMPs) drive vertebrate posterior axis elongation, but the lineage hierarchy of human NMP derivatives remains poorly defined. Here, we integrated a CRISPR/Cas9-based single-cell lineage tracing system with paired multiomics profiling--including scRNA-seq and scATAC-seq--in human pluripotent stem cell-derived neuromesodermal organoids (NMOs) to reconstruct high-resolution lineage relationships spanning 50 days of differentiation. Our data analysis reveal that intermediate mesoderm (IM) and paraxial mesoderm (PM) originate from a shared presomitic mesoderm (PSM) progenitor downstream of NMPs, whereas lateral plate mesoderm (LPM) segregates early from committed mesodermal progenitors. Notably, TBX6 ablation disrupts both IM and somite development, demonstrating that TBX6 functions as an upstream regulator of these two lineages. Mechanistically, TBX6 loss arrests PSM at the progenitor stage and abolishes activation of development programs required for IM maturation. We further delineate neural crest differentiation pathways from NMPs, identifying pre-bifurcation molecular signatures that predict neural crest fate. This work provides a clonal-resolution lineage map of human NMP differentiation and advances our understanding of human posterior trunk development and the etiology of TBX6-associated congenital disorders affecting both the spine and the kidney.

developmental biology↗

bioRxiv2026

scSAID: A Comprehensive Cross-Species Single-Cell Skin Atlas Reveals Species-Specific Responses to Psoriasis

Single-cell RNA sequencing has rapidly expanded the scale of skin transcriptomic data, yet these datasets remain fragmented across studies spanning different species, diseases and experimental manipulations. An up-to-date, comprehensive, and queryable single-cell cross-species repository for skin is still lacking. Here, we present scSAID (skin-scsaid.com), a single-cell database with an interactive web portal offering a broad suite of in-depth analyses for human and mouse skin. It integrates more than 1.2 million high-quality cells collected from 252 samples, establishing a unified reference for cell-type annotation, cross-species comparison and pathological studies. Using psoriasis as a case study, we demonstrate how scSAID can be used to evaluate how faithfully mouse models reproduce human pathology. Systematic comparison with the imiquimod-induced mouse model revealed numerous species-specific molecular signatures of psoriasis, including human-specific NFKB1 activation and STAT1 involvement, indicating that the current mouse model captures only limited aspects of the disease. We further introduce psoSpotter, a disease-biomarker-selection algorithm that, coupled with in silico perturbation using scSAID data, uncovers PPIA as a novel psoriasis drug target, illustrating the potential of scSAID for identifying therapeutic approaches. Overall, scSAID delivers a large-scale, cross-species skin single-cell resource and analysis platform, opening new opportunities for the discovery of disease-relevant targets in skin diseases.

bioinformatics↗

bioRxiv2026

Tailoring Precise Genomic Integration Toward Isolate-to-Industry Strain Development for Scalable High-Titer Production of Polyhydroxyalkanoate

Halophilic chassis has emerged as a promising biomanufacturing platform for industrial polyhydroxyalkanoate (PHA) production. However, challenges still remain in improving the production capacity, scalability and robustness, thereby lowering cost to meet market demands. Here, a high-performing halophilic strain Halomonas LY03 was isolated with over 38% glucose- to-PHA conversion rate and broad non-grain substrate utilization capability. Multidimensional tools, including algorithm-guided high-expression neutral integration site (HENIS) screening toolkit designated SiteSeek, stop codon (TAA)-dependent enhancement of gene expression and recombinase-mediated large-fragment (> 9 kb) genomic integration, were then developed to enable precise, efficient and interference-free genomic integrative expression. Using these tools, various chromosomally engineered strains were rapidly constructed to achieve high-level production of poly-3-hydroxybutyrate (PHB, 151 g L-{superscript 1}) and poly(3-hydroxybutyrate-co-4-hydroxybutyrate) (P34HB, 139 g L-{superscript 1}) under high cell-density fermentation (up to 186 g L-1 cell dry weight) in a 5-L bioreactor. Scalability was demonstrated at 2-m3 and 20-m3 industry-scale fermentations, yielding up to 134 g L-{superscript 1} PHB and 127 g L-{superscript 1} P34HB (6.1 mol% 4HB). Building on the proven robustness, a two-stage continuous fermentation (TCF) process was developed using a twin-bioreactor system at 5-L and 20-m3 scales, where stable and sustained PHA production lasted over 260 h and 160 h, respectively. Techno-economic analysis revealed a substantial cost-reduction space of 48% compared with conventional fed-batch process. This study demonstrates a successful paradigm for engineering a newly isolated strain toward robust, high-titer and cost-competitive PHA production across lab-to-industry scales.

synthetic biology↗

bioRxiv2026

seqsizzle: decoding complex barcode and adapter architectures in long-read sequencing data

Visualizing and troubleshooting long-read sequencing data is a common task when analyzing novel protocols, but identifying several primer sequences from reads exceeding 2 kb with fuzzy matching is challenging for the human eye. Here, we present seqsizzle, a cross-platform terminal user interface (TUI) based tool for convenient visualization of long-read sequencing data directly from the command-line, applicable to all sequencing technologies that produce FASTQ or FASTA output. seqsizzle allows primer sequences to be matched with user-specified fuzzy matching thresholds and highlighted with configurable colors. Additional styling can be applied to distinguish mismatches and quality scores, allowing convenient quality control of long-read sequencing data. To further aid troubleshooting, seqsizzle includes a built-in $k$-mer enrichment analysis, enabling the detection of unknown primer sequences or unexpected artifacts, which can then be reviewed via manual inspection. seqsizzle is implemented in Rust and is available open-source from https://github.com/ChangqingW/SeqSizzle.

bioinformatics↗

bioRxiv2026

Tear Proteomics Reveals RAGE and NLRP3 Inflammasome Pathway Activation in Lacrimal Glands of a Sjögren's Disease Mouse Model

PurposeTo characterize tear proteome changes in male non-obese diabetic (NOD) mice with Sjogrens disease (SjD)-like autoimmune dacryoadenitis and determine whether identified tear proteins are associated with lacrimal gland (LG) pathogenesis. MethodsTears were collected from 14-week-old male NOD mice and age-matched male BALB/c controls and analyzed by tandem mass tag (TMT)-based liquid chromatography tandem mass spectrometry (LC-MS/MS). Differentially expressed proteins (DEPs) were defined using adjusted P < 0.05 and absolute fold change > 1.5. Functional enrichment analysis was performed using Enrichr. Selected upregulated DEPs were further examined in tear and LG samples from independent mouse cohorts using Western blotting, immunofluorescence, and RT-qPCR. ResultsA total of 142 proteins were quantified across all tear samples. Hierarchical clustering and principal component analysis (PCA) separated NOD from BALB/c tear proteomes. A total of 41 proteins were differentially expressed in NOD mouse tears (33 increased, 8 decreased). Increased tear proteins were enriched in immune and inflammatory responses, secretory compartments, RAGE receptor binding, glutathione metabolism, oxidative stress, and redox regulation. S100A8/A9, GSTO1-1, Gal-3, and pIgR/secretory component (SC) were increased in both NOD mouse tears and LG. In NOD LG, increased S100A8/A9 was accompanied by elevated RAGE, whereas increased GSTO1-1 was associated with increased NLRP3, cleaved caspase-1, cleaved gasdermin, cleaved IL-1{beta}, and increased Il1b, Il18, and Il18r gene expression. ConclusionsMale NOD mouse tears contain disease-related proteins reflecting pathological inflammatory and epithelial changes in the LG including increased RAGE signaling, NLRP3 inflammasome activation, and altered epithelial transcytosis.

immunology↗

bioRxiv2026

Palliative Irradiation Affects Temporal Degradation of Rodent Vertebral Bone Mechanics, Architecture, and Composition

BackgroundPalliative radiation therapy (RT) for metastatic spine disease significantly increases the risk of vertebral fractures. However, the temporal mechanisms underlying radiation-induced vertebral bone fragility remain poorly understood. ObjectiveTo evaluate the longitudinal effects of a single high-dose irradiation, simulating palliative RT, on vertebral bone mechanical, architectural, and compositional properties in a healthy, skeletally mature rat model. MethodsThirty-one male Sprague Dawley rats received a single 15 Gy lumbar spine irradiation (IR). L4 vertebrae were assessed across all groups (irradiation: 7, 14, and 28 days post-IR, controls: at 0 and 28 days post-IR) for compressive strength and stiffness, micro-CT-derived bone composition and trabecular indices, serum bone turnover markers (NTX and BAP) and advanced glycation endproducts (AGEs). ResultsIrradiation induced progressive deterioration of vertebral bone mechanical properties, with strength decreasing up to 44% and stiffness up to 38% by 28 days post-IR, compared to 0- day controls. Trabecular bone exhibited reduced BMD, BV/TV, and Tb.N with increased Tb.Sp, a shift toward a more rod-like structure. Early post-IR changes suggested disrupted bone remodeling, characterized by elevated NTX and AGEs, but decreased BAP. Multivariable regression demonstrated that Tb.Th and AGEs were independent predictors of stiffness, collectively explaining 61% of its variance. DiscussionHigh-dose irradiation induces sustained temporal degradation of vertebral mechanical properties driven by both trabecular architectural deterioration and alterations in bone matrix quality. Measures of bone composition and non-enzymatic bone turnover suggest this early damage was driven by disruption of bone cellular homeostasis, favoring increased resorption over formation. These findings support that radiation impairs both structural integrity and pre-yield mechanical behavior, providing mechanistic insight into the elevated fracture risk observed clinically after irradiation for metastatic spine disease. Lay summaryThis study used a rat model to mimic palliative radiation therapy for cancer that has spread to the spine and evaluated the changes in bone quality up to 28 days post-therapy. We found that irradiation progressively weakened the structural integrity and composition of the bones in the spine and disrupted the normal balance of bone breakdown and repair, leading to greater bone loss and fragility. Our findings provide insight into the increased risk of fractures observed in patients receiving radiation therapy to the spine and may support efforts to better protect bone health during treatment.

bioengineering↗

bioRxiv2026

De novo design of ligand binding and sensing with a physics based generative approach

The de novo design of ligand-binding proteins has tremendous potential to revolutionize biosensor technology, yet converting these designs into functional sensors remains a major challenge due to the need for ligand-induced conformational changes or modulation of protein-protein interactions. Here, we introduce a physics-based generative approach for the de novo creation of proteins that bind small molecules and metal ions. Our method achieves customizable ligand-binding pocket formation in parallel with simulated protein folding, allowing for precise architectural control of the protein-ligand complex and facilitating the development of biosensors based on either ligand-triggered protein reassociation via split-protein reassembly or ligand-induced protein folding. We demonstrate the versatility of our computational method through successful designs targeting five small molecules, including the very small neurotransmitters serotonin and dopamine, and two metal ions. Biophysical characterization confirmed correct ligand binding, and crystal structures closely matched computational models. We demonstrated the biosensor engineering potential of these designs by constructing serotonin and dopamine sensors using a split protein strategy and explored several approaches to enhance sensor activity. Additionally, we developed a zinc sensor through a zinc-induced protein folding mechanism. Overall, our physics-based generative approach provides a robust framework for the de novo design of ligand-binding proteins, opening new avenues for the development of ligand-responsive biosensors.

bioinformatics↗

bioRxiv2026

A unique compact genomic island co-localizing iron and anammox genes in Candidatus Brocadia sinica, but not in other species

microbiology↗

bioRxiv2026

OLD sentinel: an abortive tRNase surveys phage replication and DNA defects in RecBCD-compromised cells

OLD, an abortive immunity protein from prophage P2, consists of an ABC ATPase sensor and a TOPRIM nuclease effector -- a core architecture shared by a large protein family, including components of antiphage systems Gabija, PARIS, Septu, and Lamassu. OLD was originally identified for its lethality in recB-deficient cells and inhibition of bacteriophage {lambda} infection, but the mechanisms governing its activation have remained elusive. Here, we present the cryo-EM structure of an inactive OLD tetramer and show that destabilization into dimeric form opens the TOPRIM catalytic site, stimulating tRNA cleavage. This activity arrests translation, a phenotype rescued by phage-encoded tRNAs. We demonstrate that OLD activation is not strictly RecBCD-dependent: OLD binds aberrant DNA structures in recB-deficient cells, but activation during infection requires recognition of single-stranded DNA hairpins at the phage replication origin. Collectively, our findings reveal how host and phage DNA processing factors create a complex landscape controlling OLD-mediated immunity.

molecular biology↗

bioRxiv2026

A Comprehensive DNA Methylome BodyMap across 12 Organs/Tissues from Spaceflight Mice

Spaceflight imposes unique physiological stresses on mammals, including microgravity and cosmic radiation, which drive complex molecular adaptations. However, the systemic and temporal dynamics of space-induced epigenetic regulation remain poorly understood. We constructed a comprehensive DNA methylome BodyMap across 12 organs or tissues from mice exposed to long-duration spaceflight across three time points using Reduced Representation Bisulfite Sequencing (RRBS). We also performed RNA-seq for five organs and integrated with DNA methylome. We mapped the methylome and transcriptome landscapes and found that spaceflight induces limited but highly tissue-specific differentially methylated CpGs (DMCs). Most spaceflight-induced methylation changes were reverted toward baseline within one to six months of post-flight. Functional enrichment analysis of DMCs highlighted metabolic and mitochondrial dysregulation commonly across organs, while developmental responses in immune, reproductive, and structural tissues were tissue-specific. Transcriptome data revealed that spaceflight suppressed immune and increased inflammatory responses at the multi-organ level, triggering a phenomenon resembling aging. Our study provides a comprehensive DNA methylome BodyMap across 12 organs/tissues in spaceflight mice, elucidating the tissue specificity of epigenetic changes. These insights are essential for developing biomarkers and countermeasures to safeguard astronaut health during extended missions.

genomics↗

bioRxiv2026

Stereoselective Covalent Targeting of BTK(C481S) and Kinases with β-Lactone Electrophiles

The cysteine to serine mutation at residue 481 of Brutons tyrosine kinase (BTK) is the most common mechanism of clinical resistance against ibrutinib for the treatment of mantle cell lymphoma and chronic lymphocytic leukemia. We report small molecule ligands containing chiral {beta}-lactone electrophiles to address this challenge. The asymmetric warhead enabled stereoselective covalent modification of wild-type and ibrutinib-resistant mutant BTK(C481S) through distinct sites of reactivity. Building on these findings, we developed kinase-directed {beta}-lactone probes and demonstrated that individual enantiomers preferentially engage distinct subsets of the kinome. These studies establish {beta}-lactones as stereochemically encodable covalent warheads whose stereochemistry can serve as a selectivity filter in covalent drug discovery. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=83 SRC="FIGDIR/small/736436v1_ufig1.gif" ALT="Figure 1"> View larger version (15K): org.highwire.dtl.DTLVardef@1b407c6org.highwire.dtl.DTLVardef@6a79ddorg.highwire.dtl.DTLVardef@66a59dorg.highwire.dtl.DTLVardef@102ecc7_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2026

Horizontal gene transfer drives DNRA capacity in wastewater treatment systems

Anammox bacteria require large amounts of iron for hydrazine synthase (HZS) and hydrazine oxidoreductase (HZO). By analyzing 8 anammox genomes across four genera, we found that only Candidatus Brocadia sinica harbors a compact genomic island (<10 kb) where hzs co-localizes with iron uptake (TonB, FeoAB) and Fe-S cluster assembly (NifU/NifS) genes. All other species show dispersed architectures (>100 kb separation). In the dispersed species Ca. Kuenenia stuttgartiensis, transcriptomic data revealed a 300- to 1500-fold excess of hzs over iron genes, indicating severe expression uncoupling. Thus, physical co-localization of iron support genes with anammox core enzymes is rare but exists in one Brocadia lineage, potentially enabling better co-regulation. These findings provide a genomic basis for predicting iron responsiveness across anammox species in engineered systems. Significance StatementOnly Candidatus Brocadia sinica harbors a compact <10 kb iron-nitrogen genomic island. All other anammox species show dispersed iron-nitrogen architectures (>100 kb separation). Dispersed species exhibit 3001500-fold expression mismatch between hzs and iron genes. Physical co-localization may enable co-regulation of iron supply with anammox metabolism. Genomic architecture predicts lineage-specific iron responsiveness in anammox engineering.

microbiology↗