Bacterial diseases in plants pose significant challenges to crops, fruits, and vegetable production worldwide, leading to yield losses, reduced quality and economic loss. The management of bacterial diseases has relied on the application of antibiotics, antibacterial chemicals, biocontrol agents, and resistant varieties. Chemical control measures may negatively impact human health and the environment as some pesticides are toxic to living organisms and non-biodegradable. Moreover, these tactics are continuously challenged by the ever-evolving bacterial population. The recent advancements in understanding the pathobiology of bacterial pathogens and developing innovative management strategies have led to significant progress in mitigating the impact of these diseases. This review discusses the current practices for bacterial disease management and the recent breakthroughs in this field, including genetic resistance, biocontrol agents, targeting biofilms and quorum sensing, and precision agriculture techniques. It explores emerging technologies such as omics approaches and host resistance through genome modification for potential applications in bacterial disease management. Lastly, we discuss the research scope in the area to devise novel management strategies to control bacterial diseases in the future. Overall, this review is a valuable resource for researchers, agronomists, and vegetable growers seeking to enhance their knowledge and adopt sustainable practices for effectively managing bacterial diseases in vegetable crops.

Candida glabrata can thrive inside macrophages and tolerate high levels of azole antifungals. These innate abilities render infections by this human pathogen a clinical challenge. How C. glabrata reacts inside macrophages and what is the molecular basis of its drug tolerance are not well understood. Here, we mapped genome-wide RNA polymerase II (RNAPII) occupancy in C. glabrata to delineate its transcriptional responses during macrophage infection in high temporal resolution. RNAPII profiles revealed dynamic C. glabrata responses to macrophages with genes of specialized pathways activated chronologically at different times of infection. We identified an uncharacterized transcription factor (CgXbp1) important for the chronological macrophage response, survival in macrophages, and virulence. Genome-wide mapping of CgXbp1 direct targets further revealed its multi-faceted functions, regulating not only virulence-related genes but also genes associated with drug resistance. Finally, we showed that CgXbp1 indeed also affects fluconazole resistance. Overall, this work presents a powerful approach for examining host-pathogen interaction and uncovers a novel transcription factor important for C. glabrata’s survival in macrophages and drug tolerance.

Pathogenic fungi represent a diverse group of eukaryotic microorganisms that significantly impact human health and agriculture. In recent years, the role of epigenetic modifications, particularly histone modifications, in fungal pathobiology has emerged as a prominent area of interest. Among these modifications, methylation of histone H3 at lysine-4 (H3K4) has garnered considerable attention for its implications in regulating gene expression associated with diverse cellular processes. A body of literature has uncovered the pivotal roles of H3K4 methylation in multiple biological processes crucial for pathogenic adaptation in a wide range of fungal pathogens of humans and food crops. This review delves into the recent advancements in understanding the impact of H3K4 methylation/demethylation on fungal pathogenesis. We explore the roles of H3K4 methylation in various cellular processes, including fungal morphogenesis and development, genome stability and DNA repair, metabolic adaptation, cell wall maintenance, biofilm formation, antifungal drug resistance, and virulence. We also discuss the conservation of H3K4 methylation regulators and their potential as therapeutic targets to prevent fungal diseases. Collectively, this review underscores the intricate links between H3K4 methylation, fungal pathogenesis, and potential avenues for novel antifungal strategies.