Pre-harvest sprouting (PHS) is one of the most important factors having adverse effects on yield and grain quality all over the world, particularly in wet harvest conditions. PHS is controlled by both genetic and environmental factors and the interaction of these factors. Breeding varieties with high PHS resistance have important implications for reducing yield loss and improving grain quality. The rapid advancements in the wheat genomic database along with transcriptomic and proteomic technologies have broadened our knowledge for understanding the regulatory mechanism of PHS resistance at transcriptomic and post-transcriptomic levels. In this review, we have described in detail the recent advancements on factors influencing PHS resistance, including grain color, seed dormancy, α-amylase activity, plant hormones (especially abscisic acid and gibberellin), and QTL/genes, which are useful for mining new PHS-resistant genes and developing new molecular markers for multi-gene pyramiding breeding of wheat PHS resistance, and understanding the complicated regulatory mechanism of PHS resistance.

Bacteria use cholesterol-dependent cytolysins (CDCs) to damage eukaryotes. While well-studied in mammals, the mechanisms by which CDCs bind to and kill protozoans remain unclear. CDCs bind to the human pathogen Leishmania major but only kill in the absence of sphingolipids. The contribution of other leishmanial membrane components to CDC binding and cytotoxicity remains unknown. Here, we used genetic knockouts and inhibitors to determine the contribution of key membrane components to CDC binding and killing in L. major. We analyzed toxin binding and killing using flow cytometry and Western blotting. Loss of the virulence factor GP63 enhanced toxicity of perfringolysin O but not streptolysin O. Plasmenylethanolamine and lipophosphoglycan had minimal contributions to CDC binding and cytotoxicity. Removal of sterols protected cells from CDCs yet failed to reduce binding. We used CDCs defective in engaging glycans or cholesterol to confirm that CDCs deficient in sterol binding, but not glycan binding, could bind to L. major. Thus, in non-mammalian systems, CDCs may rely on glycans for binding, while using sterols for pore formation. This suggests that CDCs may not be sterol-specific probes in some non-mammalian systems. We conclude that early-branching eukaryotes use distinct mechanisms from mammals to limit CDC pore formation and killing.

Staphylococcus aureus (S. aureus), a leading cause of nosocomial infections, contributes significantly to increased morbidity and mortality, especially when it forms biofilms on medical devices. This pathogen, specifically methicillin-resistant S. aureus (MRSA), remains a challenge to treat due to its ability to form biofilms and rapidly develop resistance against antibiotics. Biofilm formation allows bacteria to adhere to biotic and abiotic surfaces, creating a protective matrix that shields them from immune responses and antibiotic therapies. The widespread prevalence of multidrug-resistant S. aureus biofilms poses a significant therapeutic challenge in clinical settings. Several novel therapeutic strategies have been developed to combat S. aureus biofilm-associated infections. Accumulating evidence suggests that natural plants and their derivatives possess antimicrobial and chemo preventive properties that can disrupt established biofilms. Several plant-derived compounds with anti-biofilm activities have been reported to target the regulatory proteins involved in the Agr quorum sensing (Agr-QS) system, underscoring their potential as therapeutic candidates for the prevention and treatment of biofilm-associated infections. However, despite these encouraging findings, clinical validation of these plant-based agents is essential to ensure their efficacy, safety, and optimal application in treating S. aureus biofilm infections. The continued exploration of natural biofilm inhibitors anticipates the urgent need for new treatments to combat biofilm-associated infections and multidrug-resistant pathogens like MRSA. This review provides a detailed overview of preventive and therapeutic interventions to eradicate biofilm-forming S. aureus infections.