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Han, S.

Publications and source records attributed to Han, S..

At least 109 records · Page 6Linked to original sources
bioRxiv2024

Sex differences in central amygdala glutamate responses to calcitonin gene-related peptide

Women are disproportionately affected by chronic pain compared to men. While societal and environmental factors contribute to this disparity, sex-based biological differences in the processing of pain are also believed to play significant roles. The central lateral nucleus of the amygdala (CeLC) is a key region for the emotional-affective dimension of pain, and a prime target for exploring sex differences in pain processing since a recent study demonstrated sex differences in CGRP actions in this region. Inputs to CeLC from the parabrachial nucleus (PB) play a causal role in aversive processing, and release both glutamate and calcitonin gene-related peptide (CGRP). CGRP is thought to play a crucial role in chronic pain by potentiating glutamatergic signaling in CeLC. However, it is not known if this CGRP-mediated synaptic plasticity occurs similarly in males and females. Here, we tested the hypothesis that female CeLC neurons experience greater potentiation of glutamatergic signaling than males following endogenous CGRP exposure. Using trains of optical stimuli to evoke transient CGRP release from PB terminals in CeLC, we find that subsequent glutamatergic responses are preferentially potentiated in CeLC neurons from female mice. This potentiation was CGRP-dependent and involved a postsynaptic mechanism. This sex difference in CGRP sensitivity may explain sex differences in affective pain processing. Significance statementThe central lateral nucleus of the amygdala (CeLC) receives a dense projection from parabrachial nucleus (PB) neurons that corelease calcitonin gene-related peptide (CGRP) and glutamate following aversive stimuli. This PBCGRP[->]CeLC projection plays a causal role in chronic pain. We show that endogenous CGRP release potentiates glutamate signaling in female, but not male, CeLC neurons. In the context of previous work in male CeLC, this suggests that that females are more sensitive to even transient CGRP release events. Understanding how this sex difference in CGRP sensitivity arises could enhance strategies for treating chronic pain in both women and men.

neuroscience↗
bioRxiv2024

Encoding opposing valences through frequency-dependent transmitter switching in single peptidergic neurons

Peptidergic neurons often co-express fast transmitters and neuropeptides in separate vesicles with distinct release properties. However, the release dynamics of each transmitter in various contexts have not been fully understood in behaving animals. Here, we demonstrate that calcitonin gene-related peptide (CGRP) neurons in the external lateral subdivision of the parabrachial nucleus (CGRPPBel) encode opposing valence via differential release, rather than corelease, of glutamate and neuropeptides, according to firing rate. Glutamate is released preferentially at lower firing rates with minimal release at higher firing rates, whereas neuropeptides are released at higher firing rates, resulting in frequency-dependent switching of transmitters. Aversive stimuli evoke high frequency responses with accompanying neuropeptide release to encode negative valence, whereas appetitive stimuli evoke low frequency responses with glutamate release to encode positive valence. Our study reveals a previously unknown capability of single CGRPPBel neurons to bidirectionally encode valence via frequency-dependent differential release of transmitters in vivo.

neuroscience↗
bioRxiv2024

Inhibition and Updating Share Common Resources: Evidence from Drift Diffusion Model

Inhibition and updating are fundamental cognitive functions in humans, yet the nature of their relationship--whether shared or distinct--remains ambiguous. This study investigates the relationship between inhibition and updating within a unified task framework using a novel paradigm that integrates the N-back task with the congruent/incongruent Stroop task, creating conditions that require either updating alone or both inhibition and updating. Employing Signal Detection Theory (SDT) and the hierarchical drift diffusion model (HDDM), the results provided overall extremely strong Bayesian evidence that participants exhibited longer response times and lower accuracy in conditions requiring both inhibition and updating, compared to those requiring only updating. SDT analysis revealed a decline in discriminability, while HDDM analysis showed slower drift rates, longer non-decision times and a lower decision threshold in inhibition-demanding conditions. Even after controlling for the congruency sequence effect and current stimulus attributes, the results remained robust, showing a larger inhibition effect size compared to the traditional Stroop task. These findings suggest that inhibition consumes cognitive resources, impairing updating performance, and implying that both functions may rely on shared cognitive resources. Overall, the results elucidate the relationship between these fundamental executive functions, supporting the notion that inhibition and updating share cognitive resources.

neuroscience↗
bioRxiv2024

Repulsion of CA3 / dentate gyrus representations is driven by distinct internal beliefs in the face of ambiguous sensory input

Recent human neuroimaging studies of episodic memory have revealed a counterintuitive phenomenon in the hippocampus: when events are highly similar, corresponding hippocampal activity patterns are sometimes less correlated than activity patterns associated with unrelated events. This phenomenon--repulsion--is not accounted for by most theories of the hippocampus, and the conditions that trigger repulsion remain poorly understood. Here, we used a spatial route-learning task and high-resolution fMRI in humans to test whether hippocampal repulsion is fundamentally driven by internal beliefs about the environment. By precisely measuring participants internal beliefs and actively manipulating them, we show that repulsion selectively occurred in hippocampal subfields CA3 and dentate gyrus when visual input was ambiguous--or even identical--but internal beliefs were distinct. These findings firmly establish conditions that elicit repulsion and have broad relevance to theories of hippocampal function and to the fields of human episodic memory and rodent spatial navigation.

neuroscience↗
bioRxiv2024

Arginine methylation coordinates with phosphorylation to regulate NADP+ synthesis

NADK is the sole cytosolic enzyme responsible for synthesizing NADP+ from NAD+ within cells. The homeostasis of NAD+/NADP+ is controlled by NADK, usually dysregulated in various cancers, yet the precise underlying regulatory mechanisms remain largely unknown. In this study, we discover that PRMT6 methylates NADK at R39, R41, and R45, resulting in the suppression of NADK kinase activity and NADP+ synthesis. Mutations of these sites promote cancer cell proliferation and tumor growth. PRMT6-mediated methylation of NADK coordinates with Akt-mediated phosphorylation to regulate NADK, which stimulates its activity to increase NADP+ production through relief of an autoinhibitory function inherent to its amino terminus. PRMT6 also inhibits NADK activity in a phosphorylation-independent manner. Furthermore, NADK methylation is upregulated by RB1/E2F pathway in high-fat diet mice. Downregulation of NADK methylation in HCC enhances NADP+ production to promote cancer development. Our findings illuminate the molecular regulatory mechanisms governing NAD+/NADP+ homeostasis, suggesting that the PRMT6-NADK axis emerges as a direct player in high energy state. Furthermore, our research suggests potential therapeutic targets through chemical and genetic interventions. SignificancePrevious studies revealed that phosphorylation of NADK activates its activity in response to nutrient or other signaling pathways. Here, we discovered that PRMT6 methylates NADK at residues R39, R41, and R45, leading to the suppression of NADK kinase activity and NADP+ synthesis. This PRMT6-mediated methylation works in conjunction with Akt-mediated phosphorylation to regulate NADK. Additionally, we found that NADK methylation is upregulated by the RB1/E2F pathway in mice on a high-fat diet. In hepatocellular carcinoma (HCC), the downregulation of NADK methylation enhances NADP+ production, thereby promoting cancer development. Our findings provide a significant breakthrough in understanding the regulation of NADK and its response to environmental factors.

cancer biology↗
bioRxiv2024

Analyzing Biodiversity in Protected vs. Unprotected Tide Pools

This study assessed the efficacy of marine protected areas (MPAs) by comparing tide pool biodiversity in Half Moon Bay, California between a protected site (Fitzgerald Marine Reserve) and an unprotected site (Mavericks Beach). Samples were collected through random quadrat surveys. ImageJ and RStudio were used to analyze data through three methods utilizing the Simpsons Diversity Index along with three metrics. The unprotected Mavericks Beach displayed greater biodiversity through two metrics while the third did not find significant difference in biodiversity between sites. 30 unique species were present at each site with 43 species between both. These mixed findings prevent us from drawing definitive conclusions on the effectiveness of Half Moon Bays tide pool MPAs but suggest the MPA is less biodiverse. Potential explanations include the Intermediate Disturbance Hypothesis, lack of sample size, or that the MPA is not effective in maintaining biodiversity.

ecology↗
bioRxiv2024

Coordinated multi-level adaptations across neocortical areas during task learning

The coordinated changes of neural activity during learning, from single neurons to populations of neurons and their interactions across brain areas, remain poorly understood. To reveal specific learning-related changes, we applied multi-area two-photon calcium imaging in mouse neocortex during training of a sensory discrimination task. We uncovered coordinated adaptations in primary somatosensory area S1 and the anterior (A) and rostrolateral (RL) areas of posterior parietal cortex (PPC). At the single-neuron level, task-learning was marked by increased number and stabilized responses of task neurons. At the population level, responses exhibited increased dimensionality and reduced trial-to-trial variability, paralleled by enhanced encoding of task information. The PPC areas, especially area A, became gradually engaged, opening additional within-area subspaces and inter-area subspaces with S1. Task encoding subspaces gradually aligned with these interaction subspaces. Behavioral errors correlated with reduced neuronal responses, decreased encoding accuracy, and misaligned subspaces. Thus, multi-level adaptations within and across cortical areas contribute to learning-related refinement of sensory processing and decision-making.

neuroscience↗
bioRxiv2024

Pythia: Non-random DNA repair allows predictable CRISPR/Cas9 integration and gene editing

CRISPR-based genome engineering holds enormous promise for basic science and therapeutic applications. Integrating and editing DNA sequences is still challenging in many cellular contexts, largely due to insufficient control of the repair process. We find that repair at the genome-cargo interface is predictable by deep-learning models and adheres to sequence context specific rules. Based on in silico predictions, we devised a strategy of triplet base-pair repeat repair arms that correspond to microhomologies at double-strand breaks (trimologies), which facilitated integration of large cargo (>2 kb) and protected the targeted locus and transgene from excessive damage. Successful integrations occurred in >30 loci in human cells and in in vivo models. Germline transmissible transgene integration in Xenopus, and endogenous tagging of tubulin in adult mice brains demonstrated integration during early embryonic cleavage and in non-dividing differentiated cells. Further, optimal repair arms for single- or double nucleotide edits were predictable, and facilitated small edits in vitro and in vivo using oligonucleotide templates. We provide a design-tool (Pythia, pythia-editing.org) to optimize custom integration, tagging or editing strategies. Pythia will facilitate genomic integration and editing for experimental and therapeutic purposes for a wider range of target cell types and applications.

molecular biology↗
bioRxiv2024

The Pattern and Staging of Brain Atrophy in Spinocerebellar Ataxia Type 2 (SCA2): MRI Volumetrics from ENIGMA-Ataxia

ObjectiveSpinocerebellar ataxia type 2 (SCA2) is a rare, inherited neurodegenerative disease characterised by progressive deterioration in both motor coordination and cognitive function. Atrophy of the cerebellum, brainstem, and spinal cord are core features of SCA2, however the evolution and pattern of whole-brain atrophy in SCA2 remain unclear. We undertook a multi-site, structural magnetic resonance imaging (MRI) study to comprehensively characterize the neurodegeneration profile of SCA2. MethodsVoxel-based morphometry analyses of 110 participants with SCA2 and 128 controls were undertaken to assess groupwise differences in whole-brain volume. Correlations with clinical severity and genotype, and cross-sectional profiling of atrophy patterns at different disease stages, were also performed. ResultsAtrophy in SCA2 relative to controls was greatest (Cohens d>2.5) in the cerebellar white matter (WM), middle cerebellar peduncle, pons, and corticospinal tract. Very large effects (d>1.5) were also evident in the superior cerebellar, inferior cerebellar, and cerebral peduncles. In cerebellar grey matter (GM), large effects (d>0.8) mapped to areas related to both motor coordination and cognitive tasks. Strong correlations (|r|>0.4) between volume and disease severity largely mirrored these groupwise outcomes. Stratification by disease severity showed a degeneration pattern beginning in cerebellar and pontine WM in pre-clinical subjects; spreading to the cerebellar GM and cerebro-cerebellar/corticospinal WM tracts; then finally involving the thalamus, striatum, and cortex in severe stages. InterpretationThe magnitude and pattern of brain atrophy evolves over the course of SCA2, with widespread, non-uniform involvement across the brainstem, cerebellar tracts, and cerebellar cortex; and late involvement of the cerebral cortex and striatum.

neuroscience↗
bioRxiv2024

In Vivo Optical Clearing of Mammalian Brain

Established methods for imaging the living mammalian brain have, to date, taken the brains optical properties as fixed; we here demonstrate that it is possible to modify the optical properties of the brain itself to significantly enhance at-depth imaging while preserving native physiology. Using a small amount of any of several biocompatible materials to raise the refractive index of solutions superfusing the brain prior to imaging, we could increase several-fold the signals from the deepest cells normally visible and, under both one-photon and two-photon imaging, visualize cells previously too dim to see. The enhancement was observed for both anatomical and functional fluorescent reporters across a broad range of emission wavelengths. Importantly, visual tuning properties of cortical neurons in awake mice, and electrophysiological properties of neurons assessed ex vivo, were not altered by this procedure.

bioengineering↗
bioRxiv2024

Phosphoryl group wires stabilize pathological tau fibrils as revealed by multiple quantum spin counting NMR

Hyperphosphorylation of the protein tau is one of the biomarkers of neurodegenerative diseases in the category of tauopathies. However, the molecular level, mechanistic, role of this common post- translational modification (PTM) in enhancing or reducing the aggregation propensity of tau is unclear, especially considering that combinatorial phosphorylation of multiple sites can have complex, non-additive, effects on tau protein aggregation. Since tau proteins stack in register and parallel to elongate into pathological fibrils, phosphoryl groups from adjacent tau strands with 4.8 [A] separation must find an energetically favorable spatial arrangement. At first glance, this appears to be an unfavorable configuration due to the proximity of negative charges between phosphate groups from adjacent neighboring tau fibrils. However, this study tests a counterhypothesis that phosphoryl groups within the fibril core-forming segments favorably assemble into highly ordered, hydrogen-bonded, one-dimensionally extended wires under biologically relevant conditions. We selected two phosphorylation sites associated with neurodegeneration, serine 305 (S305p) and tyrosine 310 (Y310p), on a model tau peptide jR2R3-P301L (tau295-313) spanning the R2/R3 splice junction of tau, that readily aggregate into a fibril with characteristics of a seed-competent mini prion. Using multiple quantum spin counting (MQ-SC) by 31P solid-state NMR of phosphorylated jR2R3-P301L tau peptide fibrils, enhanced by dynamic nuclear polarization, we find that at least six phosphorous spins must neatly arrange in 1D within fibrils or in 2D within a protofibril to yield the experimentally observed MQ-coherence orders of four. We found that S305p stabilizes the tau fibrils and leads to more seeding-competent fibrils compared to jR2R3 P301L or Y310p. This study introduces a new concept that phosphorylation of residues within a core forming tau segment can mechanically facilitate fibril registry and stability due a hitherto unrecognized role of phosphoryl groups to form highly ordered, extended, 1D wires that stabilize pathological tau fibrils. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=168 SRC="FIGDIR/small/606685v1_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@eb7176org.highwire.dtl.DTLVardef@1661a3forg.highwire.dtl.DTLVardef@4548dforg.highwire.dtl.DTLVardef@b353b2_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗
bioRxiv2024

S-RNase Evolution in Self-Incompatibility: Phylogenomic Insights into Synteny with S-Like Genes

S-RNases are essential in the gametophytic self-incompatibility (GSI) system of many flowering plants, where they act as stylar-S determinants. Despite their significance, the syntenic genomic origin and evolutionary trajectory of S-RNase genes in eudicots have remained largely unclear. Here, we performed large-scale phylogenetic and microsynteny network analyses of RNase T2 genes across 130 angiosperm genomes, encompassing 35 orders and 56 families. Based on the connections observed in the synteny network, particularly the persisting synteny block in none-SI Cucurbitaceae species, we infer that well-characterized S-RNase genes (Class III-A RNase genes) were duplicated and evolved from Class I S-like RNase genes, possibly as a result of the gamma triplication event shared by core eudicots. Additionally, we identified frequent lineage-specific gene transpositions of S-RNase genes across diverse angiosperm lineages, including Rosaceae, Solanaceae, and Rutaceae families, accompanied by a significant increase in transposable element (TE) activity near these genes. Our findings delineate the precise genomic origin and evolutionary path of eudicot S-RNase genes, enhancing our understanding of the evolution of the S-RNase-based GSI system.

evolutionary biology↗
bioRxiv2024

Glycolytic flux controls retinal progenitor cell differentiation via regulating Wnt signaling

Metabolic pathways are remodeled in response to energy and other homeostatic demands and are dynamically regulated during embryonic development, suggesting a role in guiding cellular differentiation. Here, we show that glycolytic flux is required and sufficient to bias multipotent retinal progenitor cells (RPCs) to acquire a rod photoreceptor fate in the murine retina. In RPC-specific Phosphatase and tensin homolog conditional knock-out (Pten-cKO) and RPC-specific conditional gain-of-function of dominant active PFKB3 (cytoPFKB3) mice, glycolytic gene expression and activity are elevated, correlating with precocious rod photoreceptor differentiation and outer segment maturation. Conversely, glycolytic inhibition in retinal explants suppresses RPC proliferation and photoreceptor differentiation, achieved either with 2-deoxy-d-glucose, a competitive inhibitor of glucose metabolism, by lowering media pH, which disables PKM2, a rate-limiting enzyme, or by inhibiting lactate/H+ symporters, which lowers intracellular pH. Mechanistically, we show that Wnt signaling, the top-upregulated pathway in Pten-cKO retinas, is a glycolysis-dependent pathway. Pharmacological and genetic perturbation of Wnt signaling by knocking-out Ctnnb1, encoding {beta}-catenin, phenocopies glycolytic inhibition, suppressing RPC proliferation, photoreceptor differentiation and outer segment maturation. Thus, developmental rewiring of glycolytic flux modulates Wnt signaling to drive rod photoreceptor differentiation and maturation, an instructive role that may be exploited therapeutically for cell replacement strategies. IMPACT STATEMENTTransgenic and pharmacological approaches reveal developmental elevations in glycolytic flux have an instructive role in promoting rod photoreceptor differentiation and maturation via activation of Wnt signaling.

developmental biology↗
bioRxiv2024

Pre-cancerous Niche Remodelling Dictates Nascent Tumour Survival

Interactions between mutant cells and their environment play a key role in determining cancer susceptibility. However, our understanding of how the pre-cancer microenvironment contributes to early tumorigenesis remains limited. Here, we show that newly emerging tumours at their most incipient stages shape their microenvironment in a critical process that determines their survival. Analysis of nascent squamous tumours in the upper gastrointestinal tract of the mouse reveals that the stress response of early tumour cells instructs the underlying mesenchyme to form a supportive "pre-cancer niche", which dictates the long-term outcome of epithelial lesions. Stimulated fibroblasts beneath emerging tumours activate a wound healing response that triggers a dramatic remodelling of the underlying extracellular matrix, resulting in the formation of a fibronectin-rich stromal scaffold that promotes tumour growth. Functional heterotypic 3D culture assays and in vivo grafting experiments, combining carcinogen-free healthy epithelium and tumour-derived stroma, demonstrate that the pre-cancerous niche alone is sufficient to confer tumour properties to healthy epithelial cells. We propose a model where both mutations and the stromal response to genetic stress defines the likelihood of early tumours to survive and progress towards more advanced disease stages.

cancer biology↗
bioRxiv2024

The m6A reader IGF2BP3 promotes gastric cancer progression via increasing the expression of FBXO32 protein

N6-methyladenosine (m6A) represents the most prevalent chemical modification on eukaryotic mRNA, with an accumulating body of literature indicating its pivotal significance in the pathogenesis of human cancers. Nevertheless, the precise molecular interplay between the m6A reader protein IGF2BP3 and gastric cancer remains to be thoroughly delineated. Our study uncovered that the expression of IGF2BP3 in gastric cancer tissues is markedly elevated in comparison to adjacent normal tissues, and this upregulation is tightly correlated with the incidence of lymph node metastasis, more advanced TNM stages, and deeper invasion depth of tumor in patients. In vitro experiments demonstrated that IGF2BP3 potentiates the proliferative, migratory, and invasive capacities of gastric cancer cells, while concurrently inhibiting apoptosis and augmenting the intracellular levels of aerobic glycolysis. In vivo experiments revealed that IGF2BP3 contributes to the growth of gastric cancer. Mechanistically, IGF2BP3 can increase the expression of FBXO32 protein by recognizing and binding to the m6A binding site on FBXO32 mRNA and further activate the downstream cGMP-PKG signaling pathway, thereby modulating various biological functions of gastric cancer cells and ultimately promoting the progression of gastric cancer. In summary, our findings suggest that IGF2BP3 upregulates the expression of FBXO32 protein in an m6A dependent manner and subsequently activates the cGMP-PKG signaling pathway, ultimately leading to the onset and progression of gastric cancer. Consequently, the targeting of the IGF2BP3/FBXO32/cGMP-PKG axis emerges as a promising therapeutic modality for the treatment of gastric cancer.

cancer biology↗
bioRxiv2024

Deep genetic substructure within bonobos

Establishing the genetic and geographic structure of populations is fundamental both to understand their evolutionary past and preserve their future, especially for endangered species. Nevertheless, the patterns of genetic population structure are unknown for most endangered species, including some of our closest living relatives. This is the case of bonobos (Pan paniscus) which together with chimpanzees (Pan troglodytes) are humans closest living relatives. Chimpanzees live across equatorial Africa and are classified into four subspecies (Groves, 2001), with some genetic population substructure even within subspecies. Conversely, bonobos live exclusively in the Democratic Republic of Congo and are considered a homogeneous group with low genetic diversity (Fischer et al. 2011) despite some population structure inferred from mtDNA. Nevertheless, mtDNA aside, their genetic structure remains unknown, hampering our understanding of the species and conservation efforts. Placing bonobos genetics in space is however challenging because, being endangered, only non-invasive sampling is possible for wild individuals. Here, we jointly analyse the exomes and mtDNA from 20 wild-born bonobos, the whole-genomes of 10 captive bonobos and the mtDNA of 61 wild individuals. We identify three genetically distinct bonobo groups of inferred Central, Western and Far-Western geographic origin within the bonobo range. We estimate the split time between the central and western populations to [~]145,000 years ago, and genetic differentiation to be in the order of that of the closest chimpanzee subspecies. We identify putative signatures of differential genetic adaptation among populations for genes associated with homeostasis, metabolism and the nervous system. Furthermore, our estimated long-term Ne for Far-West ([~]3,000) is among the lowest estimated for any great ape lineage. Our results highlight the need of attention to bonobo substructure, both in terms of research and conservation. Highlights- We identified three genetically distinct populations of bonobos, inferred as having Central, Western and Far-Western geographic origin within the species range. The estimated split time is [~]145,000 years ago for the Central and Western populations, and [~]60,000 years ago for the two Western populations. - The genetic differentiation between the Central and Far-Western bonobo populations is in the order of that between Central and Eastern chimpanzee subspecies, while the genetic differentiation among Western bonobo populations is similar to that among human groups. - Once substructure is accounted for, we infer a long-term effective population size (Ne) of only [~]3,000 for Far-Western bonobos, genetic isolation and inbreeding.

evolutionary biology↗
bioRxiv2024

m6A methylation dynamically participates in the immune response against Vibrio anguillarum in half-smooth tongue sole (Cynoglossus semilaevis)

N6-methyladenosine (m6A) is the most prevalent RNA modification and a multifaceted regulator capable of affecting various aspects of mRNA metabolism, thereby playing important roles in numerous physiological processes. However, it is still unknown whether, when, and to what extent m6A modulation are implicated in the immune response of an economically important aquaculture fish, half-smooth tongue sole (Cynoglossus semilaevis). Herein, we systematically profiled and characterized the m6A epitranscriptome and transcriptome in C. semilaevis after the infection of Vibrio anguillarum, a serious threat to the aquaculture industry. We demonstrated that m6A could be modulated as early as 4-hour post infection (hpi), and the overall intensity of m6A methylation was enhanced following infection. Both conservative and novel motifs were uncovered from the m6A modification sites. Furthermore, differentially m6A methylated genes (DMGs) and differentially expressed genes (DEGs) were identified, and functional enrichment revealed multiple immune-related pathways, especially the FoxO signaling pathway which showed significance in every comparison. Joint analysis highlighted the remarkedly dynamic role of m6A on gene expression, i.e. early on, m6A mainly prioritized the down-regulation of specific genes, and later, it switched gears to promote expression of another set of genes. Moreover, key immune-related genes, including pdp1, rgs5l, and plk2b, were identified. To our limited knowledge, this is the first study comprehensively characterizing the global m6A atlas in aquaculture fish species. The presented results provide new insights into the dynamics of m6A modifications in the transcriptome of the half-smooth tongue sole following bacterial infection. Further studies are warranted to elucidate the functional significance of these changes and to understand how they affect specific biological processes.

molecular biology↗