Autophagy is an evolutionarily conserved intracellular degradation pathway that has emerged as an important regulator of plant immunity and a recurrent target of pathogen virulence strategies. In this review, we examine how Candidatus Liberibacter (CL) species and their hosts provide a useful informative system for understanding convergent pathogen manipulation of the ATG6-ATG8 autophagic hub in agricultural and model plants. We synthesize recent evidence showing that CL-effectors reprogram autophagy through mechanistically distinct but functionally convergent strategies, including interference with ATG6- and ATG8-associated processes and exploitation of host metabolic regulators linked to autophagic flux. By comparing these mechanisms with autophagy targeting strategies reported for other plant-associated pathogens, we highlight recurring vulnerability nodes within the host autophagic machinery and suggest that these nodes may represent promising targets for future resistance engineering. We further discuss how structure guided molecular design and programmable genome editing could, over time, inform the development of more precise and durable approaches to crop protection.

Autophagy restricts intracellular bacteria through xenophagy, yet many bacterial pathogens remodel this pathway to avoid degradation or support intracellular persistence. This review compares bacterial modulation of autophagy in mammalian cells and invertebrate vectors, with focusing on initiation, cargo recognition, autophagosome maturation, and autophagosome-lysosome fusion. In mammals, direct effector-host interactions have been defined for several pathogens. Legionella pneumophila RavZ effector removes lipidated ATG8/LC3 from autophagosome membranes. Salmonella typhimurium effectors interfere with AMPK-mTOR signaling, ATG16L1 recruitment, and Rab1A/TRAPPIII-dependent initiation. Shigella flexneri and Listeria monocytogenes mask bacterial surfaces to limit autophagic recognition. Mycobacterium tuberculosis, Anaplasma phagocytophilum, Staphylococcus aureus, and Coxiella burnetii exploit autophagy-related compartments while restricting degradative maturation. In invertebrate systems, especially psyllid vectors of Candidatus Liberibacter asiaticus and Candidatus Liberibacter solanacearum, current evidence indicates pathogen-associated changes in ATG gene expression, endoplasmic reticulum-associated vacuole formation, calcium and ROS signaling, lysosomal activity, and vitellogenin-linked regulation. However, these mechanisms are supported mainly by transcriptomic, microscopy-based, pharmacological, and protein-interaction evidence, and direct effector-mediated control of psyllid autophagy remains insufficiently demonstrated. We propose that bacterial control of autophagy follows conserved logic across host systems. This logic includes suppression of xenophagic recognition, remodeling of autophagosome biogenesis, and uncoupling of autophagosome formation from lysosomal dagradation. Defining which mechanisms are directly effector-driven and which are host-response signatures will be essential for translating autophagy biology into antimicrobial, vector-control, and plant disease-management strategies.

Cultivars (Waseem et al., 2023;Sahu et al., 2025). In this context, multi-omics technologies have emerged as transformative tools for dissecting the complex molecular networks that underpin plant stress perception, signaling, and adaptation.Over the past decade, genomics, transcriptomics, proteomics, metabolomics, ionomics, and phenomics have each contributed essential pieces of the salinity and drought tolerance puzzle (Waseem et al., 2025). The integration of these disciplines into a unified multi-omics approach represents a significant advancement, facilitating a systems-level understanding of stress responses that spans from alleles and regulatory modules to pathways, tissues, and entire plant phenotypes (Waseem et al., 2022). This Research Topic, "Multi-Omics Strategies for Salinity and Drought Stress Mitigation in Agriculture", serves as a critical reference point and inspiration for researchers aiming to harness integrative omics for climate-resilient agriculture. The six papers presented in this collection provide high-resolution insights across diverse plant species, revealing proline metabolism, ion homeostasis (e.g., HKT/SOS/NHX), transcriptional regulation (e.g., CPP, WRKY, NAC), and metabolic reprogramming as conserved tolerance pillars. By employing strategies ranging from Genome-Wide Association Studies (GWAS) and proteomics to immediate agronomic solutions like grafting, these works define precise molecular targets for improving both major and underepresented crops, including safflower, kiwifruit, okra, tomato, and Medicago.Finaly, the integration of these molecular insights with CRISPR editing and AI-driven modeling will accelrate the transition towards a more sustainable and stress-resilient agricultural future. We extend our sincere gratitude to all authors and reviewers for their contributions to this dynamic and rapidly evolving field.Ali et al. conducted a GWAS on 94 safflower (Carthamus tinctorius) accessions from 26 countries to explore the genetics of salt tolerance at seedling stage. They quantified multiple morphological and physiological traits related to salt injury and growth reduction and the GWAS detected 322 significant marker-trait associations across key traits such as biomass, root and shoot weights, leaf number, plant height, and root length. Gene annotation highlighted multiple candidate genes, including PLA1, APK4, GINT1, TPLATE, SPS2, DTX50, and RAF1, which are involved in secondary metabolite sulfation, chloroplast development, cell wall modification, sucrose biosynthesis, and calcium signaling. In silico expression analysis under salinity showed that several of these genes strongly upregulated (such as PLA1, SPS2, and DTX50) or downregulated, supporting their role in salt tolerance. Overall, the study delivered elite salt-tolerant genotypes (G-50, G-58, and G-94) and a set of biologically plausible candidate genes that merit functional validation for safflower improvement.Zheng et al. systematically identified 65 CPP transcription factor (TF) genes across six Theaceae species and grouped them into two subfamilies characterized by conserved CXC domains. The study showed that Class II genes are more structurally conserved, typically with 8 exons, while many Class I genes contained 10 exons, indicating evolutionary divergence. Whole-genome duplication was the primary driver of this family's expansion, and the gene promoters were found to be rich in stress-related regulatory elements. Expression and qRT-PCR data revealed that specific Class I genes (such as CsinCPP2, CcheCPP1, and ColeCPP12) were highly expressed in vegetative tissues like leaves, apical buds, and stems. Conversely, several Class II genes (including ColeCPP1, CsinCPP9, ColeCPP2, and CcheCPP8) were strongly induced by drought and salt stresses, highlighting them as key candidates for growth regulation and stress tolerance. Overall, the work clarifies evolutionary patterns and provided candidate CPP genes for functional studies and stress-resilience improvement in Theaceae.Yang et al. characterizes key proline metabolism genes in kiwifruit (Actinidia chinensis) and linked them to salt stress tolerance. The study identified two AcP5CS, one AcP5CR, one AcOAT, three AcPDH, and one AcP5CDH gene, and analyzed their evolution, structure, regulatory elements, chromosomal location, and expression under abiotic and hormonal treatments. Under salt stress, AcP5CS1, AcP5CR, and AcOAT were strongly upregulated, while AcP5CDH was repressed, a pattern confirmed by qRT-PCR. Overexpressing AcP5CS1 in Arabidopsis significantly improved salt tolerance, demonstrating its functional importance. The TF AcNAC30 was found to be highly correlated with AcP5CS1 expression and directly bound its promoter, indicating that AcNAC30 likely enhances proline accumulation under salt stress by activating proline biosynthesis genes. Overall, the work defines the proline metabolic gene network in kiwifruit and demonstrates its central role in abiotic stress resilience.Grafting is a widely used horticultural technique that joins the shoot of one plant (scion) to the root system of another (rootstock), often improving stress resilience. Mahapatra et al. showed that grafting drought-susceptible tomato (Solanum lysopersicum) scions onto drought-resistant rootstocks significantly improved drought tolerance. In the initial screening, two resistant genotypes use as rootstocks and susceptible genotypes as scion produced grafts (G1 and G4) that maintained higher relative water content, better chlorophyll fluorescence, and higher stomatal conductance under drought. Physiologically, these successful grafts alleviated drought damage by preserving photosynthetic pigments and reducing oxidative stress. Proteomic analysis indicated enhanced cellular stress responses, metabolism, and defense pathways in the grafted plants.Transcriptomic profiling revealed the upregulated expression of key stress-related genes, including DREB, WRKY,...

Metabolic diseases, such as obesity, type 2 diabetes (T2DM), and metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD), emerge from chronic nutrient overload that progressively disrupts cellular homeostasis and precipitates persistent inflammatory remodeling. Two stress-adaptive programs sit at the center of such pathological transition: autophagy, the homeostatic engine responsible for lysosomal recycling and organelle quality control, and cellular senescence, a tissue repair system that becomes deleterious when persistent, driving dysfunction through stable growth arrest and senescence-associated secretory phenotype (SASP)-associated inflammatory remodeling. Emerging evidence identifies lysine acetylation as a nutrient-sensitive molecular rheostat that orchestrates the reciprocal regulation of these two processes across metabolic tissues. Because acetylation dynamics are governed by the availability of acetyl-CoA and the NAD⁺-dependent deacetylation capacity of sirtuins, metabolic stress reshapes the enzymatic balance between acetyltransferases (KATs, e.g., p300/CBP) and deacetylases. This shift triggers a “double blow” to cellular health; the simultaneous suppression of autophagic flux and the epigenetic stabilization of senescent state. This review synthesizes mechanistic evidence showing how acetylation inhibits autophagy at multiple checkpoints, ranging from the activity of core autophagy proteins to lysosomal biogenesis, while concurrently reinforcing senescence through chromatin hyperacetylation and the activation of non-histone effectors such as NF-κB, p53 and FOXO proteins. We place particular emphasis on the mTORC1-p300-SIRT1 axis as the primary integration hub coupling nutrient status to this dual regulation. Finally, we discuss tissue-specific manifestations in the liver, adipose tissue, and other metabolic organs and highlight emerging therapeutic strategies, such as KAT inhibition/sirtuin activation, aimed at restoring the acetylation rheostat to improve autophagic competence while restraining senescence-driven metabolic decline.