The plant plasma membrane serves as the primary interface for perceiving extracellular signals, a function largely mediated by plasma membrane receptors (PMRs). In wheat (Triticum aestivum), the functional characterization of these receptors is impeded by the species’ large, hexaploid genome, which results in extensive gene duplication and functional redundancy. This review synthesizes current knowledge on wheat PMRs, covering their diversity, classification, and signaling mechanisms, with a particular emphasis on their central role in plant immunity. We highlight the remarkable structural and functional diversification of PMR families, which range in size from 10 members, as seen in the case of wheat leaf rust kinase (WLRK), to over 3424 members in the receptor-like kinase (RLK) family. Furthermore, we reviewed the role of PMRs in being critical for detecting a wide array of biotic stimuli, including pathogen-associated molecular patterns (PAMPs), herbivore-associated molecular patterns (HAMPs), and symbiotic signals. Upon perception, PMRs initiate downstream signaling cascades that orchestrate defense responses, including transcriptional reprogramming, cell wall reinforcement, and metabolic changes. The review also examines the complex cross-talk between immune receptors and other signaling pathways, such as those mediated by brassinosteroid and jasmonic acid receptors, which underpin the delicate balance between growth and defense. Finally, we bridge these fundamental insights to applications in crop improvement, delineating strategies like marker-assisted selection, gene stacking, and receptor engineering to enhance disease resistance. After identifying key obstacles such as genetic redundancy and pleiotropic effects, we propose future research directions that leverage multi-omics, systems biology, and synthetic biology to fully unlock the potential of wheat PMRs for sustainable agriculture.

Wheat (Triticum aestivum), a key global crop, faces rising drought stress that limits root growth and water uptake. Root meristem growth factors (RGFs) are small peptides that regulate root stem cell maintenance, meristem activity, and lateral root formation in model plants, yet the RGF gene family remains unexplored in wheat. Here, we performed a comprehensive genome-wide analysis of the TaRGF gene family, identifying 15 genes distributed across the A, B, and D subgenomes and classified into five homeologous groups (TaRGF1–TaRGF5), predominantly located on chromosomes 2 and 6. All TaRGFs contained a characteristic RGF motif, with dibasic cleavage sites and Asp–Tyr motifs indicating conserved maturation mechanisms. Based on the phylogenetic analysis, the TaRGF5 homeologs showed the highest similarity to Arabidopsis thaliana RGF5. Tested RNA-seq data revealed predominantly root-enriched expression for all TaRGF genes, with TaRGF5 exhibiting the most root-preferential and downregulation under drought stress. Quantitative real-time PCR (qRT-PCR) confirmed that drought stress suppressed the expression of TaRGF5A, TaRGF5B, and TaRGF5D in roots of wheat cultivar Sids-13 across all time points, unlike the higher accumulation seen in controls. Promoter analysis predicted a unique BES1 transcription factor binding site exclusively in TaRGF5B, linking brassinosteroid signaling to peptide-mediated root regulation. Structural modeling and molecular docking predicted an interaction between wheat TaRGF5 homeologs and root growth factor-insensitive receptor kinase (TaRGI3), characterized by conserved sulfotyrosine-mediated binding and favorable interaction energetics. Based on this characterization of the wheat RGF gene family, particularly the potential role of TaRGF5 in root development and drought-adaptation signaling, we propose targeting this gene for functional analysis to improve wheat resilience under water-limited conditions.

Background/Objectives: Although statins are still the main treatment for dyslipidemia, differences in patient responses, residual cardiovascular risk, and treatment side effects highlight the need for additional methods. Curcumin has attracted considerable interest because of its reported cardioprotective and lipid- and glucose-modulating effects, as well as its ability to influence cellular stress and survival pathways, highlighting its potential relevance to cardiovascular and metabolic disease. This study investigated the effects of atorvastatin (ATO), curcuminoid extract (CUR), and their combination on lipid and glucose metabolism and cell fate in hepatocellular carcinoma-derived cell lines. Methods: Huh-7 cells were treated for 48 h with ATO (10 μM), CUR (20 μM), or their combination (MIX). MTT assays characterized concentration-dependent cytotoxicity and informed concentration selection, and CellTiter-Glo assessed cell viability. ApoB expression and secretion were evaluated by Western blot and ELISA. Lipid accumulation was assessed by Oil Red O microscopy and quantitative analysis. Glucose uptake was measured before and after insulin challenge. Additionally, expression of relevant genes regulating cholesterol, lipoprotein, and glucose metabolism was assessed by qPCR, and apoptosis was examined by Annexin V/PI flow cytometry and Western blotting for apoptotic markers. Results: The ATO-curcuminoid combination markedly reduced ApoB expression and secretion compared with control (p < 0.01). In contrast, the combination significantly increased intracellular lipid accumulation compared with control, ATO, and CUR (p < 0.001). Additionally, CUR and the ATO-curcuminoid combination significantly reduced glucose uptake before and after insulin challenge (p < 0.01; p < 0.001, respectively). Consistent with the impaired glucose uptake, the ATO-curcuminoid combination significantly reduced GLUT2 protein expression compared with control and ATO (p < 0.05 and p < 0.01, respectively). The ATO-curcuminoid combination also significantly increased early and late apoptosis and reduced viable-cell populations (p < 0.05; p < 0.01, respectively). Molecular docking and molecular dynamics simulations revealed that curcuminoids occupied the catalytic domain of HMG-CoA reductase and maintained conserved interactions with key residues, including GLY656, ASN658, and GLY808. Conclusions: ATO-curcuminoid co-treatment suppressed ApoB secretion but was accompanied by increased intracellular lipid accumulation, altered glucose uptake and GLUT2 expression, and apoptosis, indicating a discordant hepatic response. Computational analyses suggested potential interactions between curcuminoids and the catalytic region of HMG-CoA reductase; however, these findings are hypothesis-generating and require direct enzyme-inhibition and kinetic validation.