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Lysine lactylation (Kla) is a lactate-derived post-translational modification that has emerged as a critical metabolic-epigenetic regulator linking cellular metabolic states to innate immune signaling. The cGAS-STING pathway, a central cytosolic DNA-sensing mechanism essential for antiviral defense, antitumor immunity, and inflammatory regulation, is profoundly influenced by the metabolic milieu. However, the precise role of lactylation in modulating this pathway remains to be systematically synthesized. This review aims to comprehensively analyze the molecular mechanisms by which lysine lactylation regulates the cGAS-STING signaling axis, and to discuss the pathophysiological implications and therapeutic potential of targeting this modification in diseases ranging from autoimmunity and neuroinflammation to cancer. A comprehensive review of the relevant literature was conducted to summarize the biochemical basis of lactylation (including writers, erasers, and readers) and to systematically examine emerging evidence demonstrating direct and indirect regulation of cGAS-STING components by lactylation. Studies involving site-specific modifications, disease models, and therapeutic interventions were collated and analyzed. Lactylation directly targets core pathway components-cGAS at residues such as K21, K131, K156, K162, K275, and K409, and STING-altering their stability, enzymatic activity, DNA-binding capacity, phase separation, and downstream signaling outputs. Depending on context, lactylation exerts dual effects: it stabilizes cGAS and amplifies type I interferon responses in autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis) and hypoxic-ischemic encephalopathy, but promotes cGAS degradation or suppresses STING activity in cancer (lung adenocarcinoma, glioblastoma) and neuropathic pain, thereby facilitating immune evasion or pain sensitization. Indirectly, lactylation modulates cytosolic DNA ligand availability by influencing mitochondrial DNA release (via HMGB1, VDAC1, Arg1, DRP1) or DNA repair (via KU70). The discovery of specific lactyltransferases (AARS1/2, p300) and delactylases (SIRT1-3, HDAC1-3) establishes lactylation as a dynamic, enzymatically controlled process. Lactylation functions as a pivotal metabolic-immune checkpoint that fine-tunes cGAS-STING signaling in a cell-type- and disease-specific manner. Targeting the lactylation regulatory axis-by inhibiting pathogenic lactylation to restore anti-tumor immunity or enhancing it to dampen deleterious inflammation-offers a novel immunometabolic therapeutic strategy for autoimmune disorders, chronic infections, neurodegeneration, and cancer.

This study explores the experiences of formula-feeding mothers in Israel as they navigate their maternal identity within a hegemonic infant-feeding discourse that promotes exclusive breastfeeding. While extensive research has focused on the benefits of breastfeeding, limited qualitative attention has been given to the lived experiences of formula-feeding mothers. Drawing on Adrienne Rich's concept of institutionalized motherhood, this study positions the lack of formula-related support as a disciplinary mechanism targeting mothers who deviate from institutional norms. Based on in-depth semi-structured interviews of 31 educated, middle-class Jewish mothers who primarily or exclusively formula fed, we offer a theoretical contribution by illuminating how institutionalized motherhood constructs 'good mothering' through prescribed maternal foodwork (i.e., breastfeeding), thereby perpetuating the stigmatization of formula feeding. The formula warning label is examined as a manifestation of institutionalized motherhood that, according to participants' accounts, undermines the legitimacy of formula feeding and casts doubt on mothers' competence and reasoning for using it. Empirically, the study contributes to the limited qualitative literature on formula-feeding mothers' experiences. Positioned as marginalized, at times ideologically deviant autonomous agents, the women offer critical insights into the inequities of support systems, the persistence of social stigma, and the role of shame and judgment in shaping maternal identity through feeding practices. Four key findings emerged: (a) the label perpetuates the perception of formula as harmful; (b) it triggers feelings of inadequacy and self-doubt; (c) it erases the diversity of reasons behind formula use; and (d) it reinforces hierarchical feeding norms. This study contributes to matricentric feminism by exposing how rigid hierarchical feeding prescriptions shape maternal identity through shame and regulation. Findings point to the importance of developing a more supportive, inclusive discourse that acknowledges maternal agency and diverse infant-feeding experiences.

Culinary Medicine (CM) is positioned by physician leaders as an innovative, interdisciplinary model addressing the long-neglected role of food and nutrition in clinical healthcare. Yet its institutional rise recenters medical authority and erases the feminized and racialized expertise that had led dietary care for over 100 years. This article critiques CM as a case study in epistemic erasure and medical dominance, examining how professional and institutional hierarchies shape which knowledge is recognized as legitimate. Drawing on frameworks of racial capitalism, epistemic injustice, and feminist standpoint theory, this article finds that CM devalues and marginalizes dietetics and ignores community-based models of nutritionally tailored meals, despite decades of success. By framing CM as novel, the origins, knowledge, and expertise informing culinary-focused dietary care is recoded through male- and physician-dominated institutions. CM's implementation often reproduces structural biases, including racialized gatekeeping through biometric eligibility and the dismissal of cultural foodways. While CM holds potential for addressing diet-related health disparities, it must confront the exclusionary logics it reproduces to truly achieve health equity. CM must center the expertise of those historically excluded, particularly women, communities of color, and community-based practitioners, to build equitable, interprofessional models that prioritize professional humility and structural transformation over institutional prestige to improve population health.

This study aims to synthesize qualitative evidence on the lived experiences and perceived support needs of suicide-bereaved family members, including extended relatives. A qualitative systematic review and quote-based thematic meta-synthesis was conducted. Searches were undertaken in PubMed, Scopus, and Web of Science. Eligible studies were primary qualitative research published in English involving family members bereaved by suicide. Methodological quality was appraised using the JBI Critical Appraisal Checklist for Qualitative Research, and confidence in each synthesized finding was assessed using GRADE-CERQual. Verbatim participant quotations extracted from findings/results sections were analyzed using Braun and Clarke's thematic analysis, guided by Doka's disenfranchised grief as a sensitizing framework, with inductive coding for data not captured by the lens. Twenty-seven studies were included. Six cross-cutting themes described suicide bereavement as layered disenfranchisement: (1) stigma and anticipatory judgment prompting secrecy and withdrawal; (2) relational erasure through silence and loss of permission to name the deceased; (3) institutional non-recognition and lack of navigable postvention pathways; (4) moral injury and persistent culpability; (5) embodied, trauma-like distress and enduring existential suffering; and (6) legitimacy repair through peer support, compassionate witnessing, continuing bonds, and meaning-making. Synthesized support needs converged on stigma-competent and culturally safe care, permission-based communication, proactive coordinated pathways, trauma-informed long-term follow-up with attention to suicide risk, and accessible, tailored peer support. Suicide bereavement among family members is frequently shaped by social, relational, and institutional disenfranchisement, with important implications for designing proactive, culturally safe, and longitudinal postvention that addresses both symptom burden and social-ecological barriers. Silence erases the deceased and removes permission to name and remember.System non-recognition excludes families and leaves no clear postvention pathway.Stigma and system gaps amplify guilt, sustaining moral injury and isolation.

Protein lysine lactylation (Kla) is a newly identified post-translational modification (PTM), in which lactyl groups are transferred to specific lysine residues in proteins. As a crucial intermediary between cellular metabolism and epigenetic regulation, Kla immensely increases the functional diversity of the proteome. This intriguing modification extends beyond histones to non-histone proteins, signaling molecules, enzymes, and substrates. In addition to enzymatic L-lactylation utilizing lactate as a lactyl donor and involving enzymes including writers (lactyltransferases), readers (lactylation-binding enzymes), erasers (delactylases), and lactyl-coenzyme A (lactyl-CoA) synthases, non-enzymatic D-lactylation derived from the glyoxalase II substrate S-D-lactoylglutathione (SLG) has also been identified. Emerging evidence underscores the molecular significance of Kla, including gene transcriptional activation, protein stability, enzyme activity, protein‒protein interactions, protein subcellular translocation, crosstalk with other PTMs, RNA modification, epigenetic instability, and phase separation, in orchestrating diverse biological processes. Functionally, Kla plays a fundamental role in physiology, such as somatic cell reprogramming, as well as embryonic, neural, and cochlear development, by regulating gene expression, cell cycle progression, and signal transduction. Conversely, dysregulated Kla renders extensive impacts on the pathogenesis of various diseases, including cancer, neuropsychiatric disorders, cardiovascular and ophthalmic diseases, and immunoinflammatory and metabolic dysregulation, through modulating immune homeostasis, metabolic adaptation, and epigenetic remodeling. This review systematically elucidates the molecular regulatory mechanisms and biological significance of Kla while comprehensively summarizing its involvement in both physiology and pathology. Furthermore, we emphasize the translational potential of Kla as a diagnostic or prognostic biomarker and therapeutic target, offering novel insights for future research and development of innovative therapeutic strategies.

The truncated constitutive active form of protein kinase C (PKC) called protein kinase M (PKM) plays a role in long-term memory maintenance in vertebrate and invertebrate models. Previously we have shown that the Aplysia Kidney/Brain protein (KIBRA) stabilizes the atypical PKM Apl III, but not the classical PKM Apl I in Aplysia neurons. Expression of Aplysia KIBRA with changes in the proposed atypical PKM binding site does not stabilize PKM Apl III and erases forms of plasticity supported by PKM Apl III. Here, we have examined biomolecular fluorescence complementation (BIFC) between KIBRA variants and PKM Apl III in Aplysia neurons. These KIBRA variants include: the KIBRA with changes in the proposed atypical binding site noted above; a splicing variant that stabilizes PKM Apl I, but not PKM Apl III; and several mutations identified in mammalian WW and C2 domain containing protein 3 (WWC3, a member of the chordate-specific expansion of the KIBRA family) associated with cancer or neurodevelopmental disorders. Surprisingly, we find that some KIBRA variants show BIFC with PKM Apl III but do not stabilize PKM Apl III. We used models of protein-protein interactions (AlphaFold 3) to gain insights into the discrepancy between BIFC and stabilization of PKMs by KIBRA and KIBRA variants and suggest a model where stabilization is linked to stable inhibition of PKMs by KIBRA.

The discourse surrounding surrogacy portrays pregnancy as a temporary process, depicting surrogates as neutral "carriers" whose involvement concludes at birth. This narrative minimizes gestation's biological significance despite evidence of its lasting effects on both women and children. We interviewed 47 retired Israeli surrogates using thematic analysis to examine how they navigate biological experiences. Surrogates employ frameworks that dismiss gestational bio-ties and emphasize genetic kinship, empowering their act of giving by rendering gestation inconsequential. This framework benefits surrogates, intended parents, and the industry by allowing narratives that overlook certain bio-ties. Two instances challenge this: bodies "talking back" through biological disruptions and intended mothers confronting surrogates about lasting bio-imprints on their babies. These challenges produce "embodied dissonance"-biology clashing with social expectations-and lead to "collaborative biologies," forcing recognition of connections the dominant framework erases. This study addresses bio-ties in surrogacy, paving the way for new frameworks reflecting human reproduction's complexities.

N6-methyladenosine (m6A) is one of the most important RNA modifications and is widely distributed across mRNAs and non-coding RNAs. Its deposition, removal, and recognition are dynamically regulated by a set of proteins, including methyltransferases (writers), demethylases (erasers), and binding proteins (readers). Through these regulators, m6A modifications influence key aspects of RNA metabolism, including stability, splicing, nuclear export, and translation efficiency, dynamically regulating cell fate. Protein lactylation is a reversible post-translational modification occurring on lysine residues of both histones and non-histones, with lactate or lactyl-CoA serving as the substrate. Lactylation modulates protein properties, including structure, function, and activity, thereby influencing gene expression. RNA m6A modifications and protein lactylation significantly regulate the biological behaviors of tumors, including proliferation, invasion, metastasis, metabolic reprogramming, immune evasion and treatment resistance. In recent years, their crosstalk has garnered increasing attention. On one hand, m6A regulatory proteins can be regulated by lactylation, either directly or via histone lactylation-mediated epigenetic regulation. On the other hand, m6A modifications may promote protein lactylation by regulating glycolysis and lactate production. This bidirectional interaction forms a regulatory loop that influences tumor progression. This review summarizes the emerging role of the crosstalk between RNA m6A modification and protein lactylation in tumor progression.

Robust electrochemical modulation and environmental stability remain difficult to co-optimize with performance in organic semiconductors. Using a poly (propylenedioxythiophene) (ProDOT)-based polymer as an amorphous model conductor, we show that carbene-enabled and selective formation of covalent linkages between side-chains enhances thermo-chemical robustness while optimizing device performance. While pristine films of ProDOT degrade at ∼130 °C and dissolve in common solvents, cross-linked films retain physicochemical properties, redox activity, and stability (>2000 cycles) under such conditions. Upon cross-linking, mixed conduction follows a nonmonotonic, volcano-like profile, peaking at ∼6 wt % diazirine used as the cross-linker, where transconductance (gm) is enhanced by ∼35-fold and remains stable under external stress when integrated in organic electrochemical transistors (OECTs). Implementation of cross-linked films in electrochemical random access memory (ECRAM) devices demonstrates a performance profile that uniquely combines analog metrics that are comparable to state-of-the-art─large dynamic range (>30×), robust write/erase endurance (>120,000 pulses), high linearity, and training accuracy (>90%)─with thermo-chemical robustness under harsh conditions, which has been a longstanding bottleneck for the applicability of organic semiconductors in scalable manufacturing. This side-chain-based cross-linking is a versatile strategy to impart robustness and enable facile postsynthetic tuning of mixed conduction, especially for amorphous semiconducting polymers, unlocking their practical use in next-generation iono-electronic and computing hardware.

Lactate accumulation is strongly associated with poor neurological outcomes in traumatic brain injury (TBI), creating a "lactate paradox" given its role as an energy substrate in the early stages of trauma. Imbalanced reactive oxygen species (ROS) act as cell injury factors throughout the pathological progression of TBI. This study aims to elucidate the key mechanisms connecting dysregulated lactate metabolism and cellular damage. We discovered that the high-lactate environment induced by TBI drives lysine lactylation of the mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2), inhibiting its enzymatic activity and leading to mitochondrial ROS (mtROS) accumulation. Mechanistically, aminoacyl-tRNA synthetase 2 (AARS2) and NAD+-dependent deacetylase sirtuin 3 (SIRT3) coordinate SOD2 lactylation through "resident sensor-writer" and "dynamic patrol-eraser" modes, respectively. Proteomic analysis revealed that SOD2 lactylation triggers a reprogramming of its interaction network, shifting its interactome away from proteins involved in energy metabolism and toward those associated with proteostasis. In a mouse model of TBI, activating SIRT3 reversed SOD2 lactylation, restored its enzymatic function, and reduced neuronal apoptosis in the injured area. This study clarifies how AARS2/SIRT3-regulated SOD2 lactylation influences neuronal fate, providing potential targets for treating secondary injury in TBI.

Many plant species can propagate asexually or be regenerated in vitro; but asexual offspring are more likely to maintain environmentally induced epigenetic marks, for instance, inheritance of the prolonged cold-induced 'vernalized state' in overwintering plants through asexual reproduction. Here we demonstrate that 'vernalized state' is reprogrammed during Arabidopsis asexual propagation through somatic embryogenesis. This overturns a long-standing idea, that the vernalized state could not be reset through asexual reproduction, and provides a strategy to erase parental effects on offspring during asexual reproduction.

Mechanical stress is the most important factor affecting the progression of osteoarthritis (OA), but the mechanism linking mechanical stress to transcriptional repression remains elusive. Here, the study finds that mechanical stress induced epigenetic changes that can serve as therapeutic targets for osteoarthritis. By using Piezo1 conditional knockout (Col2a1CreERT; Piezo1flox/flox) mice, it was found that Piezo1 activation by excessive mechanical stress can trigger chromatin remodeling via cytoskeletal force transmission, promoting the histone demethylase Kdm5c-mediated epigenetic silencing. Kdm5c in turn erases H3K4me3 marks from promoters of cartilage-anabolic genes Col2a1 and Runx3, silencing their expression. Genetic ablation of Kdm5c rescues mechanical stress-induced cartilage degradation. Through drug repurposing, the study identifies telmisartan as a direct Kdm5c inhibitor that blocks this pathway and demonstrates disease-modifying efficacy in mouse OA models and human cartilage explants. These results establish the Piezo1-Kdm5c axis as a fundamental driver of OA and position telmisartan as a mechano-epigenetic therapy with immediate translational potential.

Tumor metastasis is the primary cause of cancer-related mortality. This complex process is orchestrated by the tumor microenvironment (TME) and metabolic reprogramming. Protein lactylation, a newly recognized post-translational modification derived from lactate metabolism, is emerging as a critical regulator of tumor progression and metastasis. This review aims to provide an overview of the current understanding of lactylation within the metastatic process and to offer an updated perspective on its regulatory role in tumor metastasis and its promise as a new therapeutic avenue. The review focuses on both the enzymatic and non-enzymatic mechanisms of lactylation and delineates the enzymatic machinery, including writers, erasers, and readers, that dynamically regulate this modification. It emphasizes how lactylation influences critical stages of metastasis, such as the epithelial-mesenchymal transition (EMT) and invasion, cancer stemness maintenance, immune evasion and TME remodeling, angiogenesis and vascular dissemination, and survival during colonization. Beyond these stage-specific roles, this review discusses how lactylation operates within a broader post-translational modification (PTM) network through crosstalk with acetylation, ubiquitination, and RNA methylation to amplify oncogenic signaling. Finally, the review evaluates emerging therapeutic strategies targeting lactate metabolism, the lactylation machinery, and site‑specific modifications, and addresses persistent challenges including context‑dependent functions, limited causal validation, and technical hurdles in isomer‑specific detection.

Achieving aggregation-induced emission (AIE) in polymers via in situ, real-time generation of chemically explicit emissive motifs, while simultaneously enabling programmable 4D (time-/sequence-dependent) luminescence, remains challenging. Herein, we report a facile platform that converts nonemissive polymer precursors into AIE-active materials through photo-triggered radical reactions that dynamically construct thiocarbonyl (C = S) motifs in polymer backbones. Two kinetically programmable modules are established by molecular design: Switch 1 affords a metastable C = S motif with reversible write-read-erase behavior, and can further evolve into a stabilized thiobenzophenone-like state under prolonged irradiation; Switch 2 yields a more stable C = S motif featuring delayed-write and write-fix characteristics. Spectroscopic evidence supports the radical pathway and reversible/stable C = S formation. By substituent engineering of diphenylmethane-derived cores and sulfur-containing groups, the emission is rationally tuned across the full visible range, supported by quantum-chemical simulations correlating color with frontier-orbital gaps. Leveraging orthogonal control of activation and erasure kinetics via photoinitiators and oxygen-free atmospheres, we demonstrate two modes of 4D fluorescence encryption with time-gated decryption and time-window decoding. This work shifts AIE polymer design from "preinstalled AIEgens" to writable covalent emissive motifs, providing a scalable strategy for smart luminescent coatings and advanced information-security materials.

Radiation detection technology is critical in medical diagnosis, high-energy physics experiments, nuclear environmental monitoring, and radiation safety protection. Its technological iteration stems from innovations in high-performance radiation detection materials. Traditional materials often have narrow dose-response intervals, insufficient high-precision measurement capability, low spatial resolution, and poor stability, failing to meet high-precision detection requirements. Ag-doped phosphate glass (Ag-PG), based on radio-photoluminescence (RPL), effectively addresses these limitations with its comprehensive advantages: high radiation sensitivity, a wide linear dose-response range, submicron spatial resolution for radiation imaging, write-erase-rewrite capability, and visualized dose monitoring potential, and it also boasts significant fundamental research value and engineering application prospects. Specifically, while existing RPL reviews mainly provide a comprehensive analysis from the perspective of RPL and present typical RPL material systems, this paper systematically analyzes the structural characteristics of the Ag-PG matrix and the coordination configuration and site occupation of Ag ions. It clarifies RPL luminescence properties, dose-response mechanisms, and the evolution of luminescence centers, while reviewing advancements in applications such as radiation dose detection and high-resolution X-ray imaging. By summarizing the current research status, technical advantages and existing challenges of Ag-PG, this study provides theoretical references and conceptual insights to promote breakthroughs in its fundamental research and practical applications in high-precision radiation dose detection, advanced medical imaging, micro-nano-scale radiation detection, and nuclear industry non-destructive testing.

Gout is increasingly recognized as a systemic metabolic disorder driven by the "gut-joint axis" rather than a purely localized joint disease. However, the exact mechanisms by which intestinal dysfunction causes persistent joint inflammation remain unclear. This review proposes a novel "Two-Hit" theoretical framework mediated by bacterial outer membrane vesicles (OMVs) and N6-methyladenosine (m6A) epigenetic modifications. We hypothesize that the high uric acid environment in the gut exerts a metabolic stress on specific bacteria, driving the release of highly pathogenic OMVs. Following intestinal barrier damage, these OMVs, working synergistically with intestinal-derived lipopolysaccharide (LPS), act as cross-organ messengers to deliver a "two-hit" strike to the joint. First, they prime synovial macrophages (SMs) by upregulating m6A methylation (via the methyltransferase-like 3 enzyme, METTL3), creating a pro-inflammatory epigenetic memory. Second, they induce metabolic reprogramming, characterized by enhanced glycolysis and local acidification in synovial fibroblasts, which physically forces the crystallization of uric acid. Based on this theoretical model, we evaluate emerging therapeutic strategies. These include stabilizing bacterial membranes to block OMV release, using biomimetic nanotechnology to intercept circulating vesicles, and targeting m6A enzymes to erase inflammatory memory. Ultimately, this hypothesis suggests a potential framework to conceptually shift gout management from symptom relief toward source-to-epigenetic precision interventions, while highlighting the necessary directions for future experimental validation.

The AlkB homolog (ALKBH) family of Fe(II)/α-ketoglutarate-dependent dioxygenases mediates nucleic acid demethylation, thereby governing RNA metabolism and genomic stability. Despite their pivotal roles in epitranscriptomic regulation across vertebrates, the evolutionary dynamics and functional significance of ALKBH proteins in bivalve mollusks remain largely unexplored. Here, we present a comprehensive phylogenomic analysis of 210 ALKBH genes identified across 35 bivalve species. Our analyses reveal a distinct evolutionary trajectory characterized by the lineage-specific loss of ALKBH4 and the restricted distribution of ALKBH5 to the Mytilidae family, contrasting sharply with vertebrate repertoires. Using the noble scallop (Chlamys nobilis) and Pacific oyster (Crassostrea gigas) as model systems, we demonstrate that ALKBH genes exhibit conserved spatiotemporal expression patterns, with pronounced enrichment in gonadal tissues and during metamorphic transitions, implicating these enzymes in gametogenesis and larval development. Furthermore, comparative thermal stress experiments reveal divergent transcriptional plasticity: the subtropical scallop C. nobilis mounts rapid, transient induction of ALKBH1/2/6 under heat shock, whereas the eurythermal oyster C. gigas maintains sustained ALKBH3 expression, potentially underpinning its superior thermal tolerance. Conversely, cold stress elicits bimodal regulation in C. nobilis, with ALKBH1/2 upregulation contrasting with ALKBH6/7/8 suppression. These findings illuminate the functional diversification of bivalve ALKBH genes and their potential utility as molecular biomarkers for assessing developmental competence and thermal resilience in shellfish aquaculture.

We show that a single Hodgkin-Huxley (HH) neuron with Pyragas-type delayed feedback control (DFC) can store multiple symbols as stable periodic orbits, where the specific orbit is selected by tuning the DFC gain K and time delay τ. Sweeping the (K,τ) parameter plane at fixed bias current Ibias = 10.0 μA/cm2 reveals 207 orbit types across 12 topological categories, with inter-spike interval (ISI) means from 5.9 to 56.9 ms. We establish: (i) a write protocol that reliably locks orbits with 13.9 ms median settling time; (ii) a novel Pattern-Oriented Limit-cycle Decoder (POLD) that reads orbits at 100% accuracy from only five observed ISIs (1200 trials across 12 orbits; Wilson 95% CI: 99.7-100%); (iii) a complete single-symbol write-read-erase (W-R-E) cycle with 100% read accuracy, 92% erase verification, and no decay over hold durations up to 50 s; and (iv) a fully validated 12-symbol memory capacity with a read-discriminable upper bound of 67 symbols (11.2× over rate coding; write viability confirmed only for the conservative 12-symbol subset). Reliable orbit addressing needs delay precision of ±2%, which constitutes a write-precision specification and not a fundamental capacity limit. These findings show that parametric delayed feedback is a viable mechanism for limit-cycle-based information storage in conductance-based spiking neurons. The biological interpretation is analogical, not direct: the ±2% delay-precision requirement exceeds what has been demonstrated for biological autaptic variability, and the orbit-coded memory framing is best understood as a computational proof-of-principle aimed at neuromorphic engineering, not as a claim about biological working memory.

m6A is an important RNA modification involved in post-transcriptional regulation in plants. However, putative m6A writers and erasers in G. biloba remain poorly characterized. In this study, a total of 17 candidate m6A regulatory genes, including 8 writers and 9 erasers, were identified through genome-wide analysis. Phylogenetic and structural analyses indicated that these proteins are generally conserved, with some members showing potential functional divergence. Promoter analysis revealed abundant hormone- and stress-responsive cis-elements, and expression profiling showed tissue-specific patterns and dynamic responses to ABA, MeJA, and NaCl treatments, with erasers exhibiting greater transcriptional responsiveness than writers. In addition, protein interaction network and phase separation predictions suggested potential roles in RNA methylation-related processes. These results provide a foundation for further functional studies of m6A regulation in G. biloba.