The plant pathogen, Pseudomonas syringae (Ps), together with related Ps species, infects and attacks a wide range of agronomically important crops, including tomato, kiwifruit, pepper, olive and soybean, causing economic losses. Currently, chemicals and introduced resistance genes are used to protect plants against these pathogens but have limited success and may have adverse environmental impacts. Consequently, there is a pressing need to develop alternative strategies to combat bacterial disease in crops. One such strategy involves using narrow-spectrum protein antibiotics (so-called bacteriocins), which diverse bacteria use to compete against closely related species. Here, we demonstrate that one bacteriocin, putidacin L1 (PL1), can be expressed in an active form at high levels in Arabidopsis and in Nicotiana benthamiana in planta to provide effective resistance against diverse pathovars of Ps. Furthermore, we find that Ps strains that mutate to acquire tolerance to PL1 lose their O-antigen, exhibit reduced motility and still cannot induce disease symptoms in PL1-transgenic Arabidopsis. Our results provide proof-of-principle that the transgene-mediated expression of a bacteriocin in planta can provide effective disease resistance to bacterial pathogens. Thus, the expression of bacteriocins in crops might offer an effective strategy for managing bacterial disease, in the same way that the genetic modification of crops to express insecticidal proteins has proven to be an extremely successful strategy for pest management. Crucially, nearly all genera of bacteria, including many plant pathogenic species, produce bacteriocins, providing an extensive source of these antimicrobial agents.
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http://dx.doi.org/10.1111/pbi.13294 | DOI Listing |
Mol Plant Pathol
January 2025
Guangdong Provincial Key Laboratory of High Technology for Plant Protection, Plant Protection Research Institute, Guangdong Academy of Agricultural Sciences, Guangzhou, China.
Tomato yellow leaf curl Guangdong virus (TYLCGdV), a monopartite begomovirus first identified in 2004, remains poorly characterised. In this study, we demonstrate that TYLCGdV associates with a betasatellite, TYLCGdB, and the βC1 protein encoded by TYLCGdB is essential for symptom development. We also explore the role of TYLCGdV C4 protein by generating a C4-deficient infectious clone (TYLCGdV), revealing a dynamic role for TYLCGdV C4.
View Article and Find Full Text PDFEnviron Microbiome
January 2025
LMO Team, National Institute of Ecology, 1210 Geumgang-ro, Maseo-myeon, Seocheon, Republic of Korea.
Background: The anthosphere, also known as the floral microbiome, is a crucial component of the plant reproductive system. Therefore, understanding the anthospheric microbiome is essential to explore the diversity, interactions, and functions of wildflowers that coexist in natural habitats. We aimed to explore microbial interaction mechanisms and key drivers of microbial community structures using 144 flower samples from 12 different wild plant species inhabiting the same natural environment in South Korea.
View Article and Find Full Text PDFBMC Microbiol
January 2025
Microbiology and Immunology Department, October University for Modern Sciences and Arts (MSA), Giza, Egypt.
Background: Strain Cyp38S was isolated as an endophyte from the plant Cyperus alternifolius, collected along the banks of the River Nile in 2019. Preliminary analysis tentatively identified Cyp38S as belonging to the genus Pseudocitrobacter.
Methods: The preliminary identification of Cyp38S was performed using the VITEK2 identification system, MALDI-TOF-MS, and 16S rRNA gene sequencing.
BMC Plant Biol
January 2025
Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Background: Root rot is a major disease affecting alfalfa (Medicago sativa L.), causing significant yield losses and economic damage. The primary pathogens include Fusarium spp.
View Article and Find Full Text PDFNat Med
January 2025
Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Prion disease is a fatal neurodegenerative disease caused by the misfolding of prion protein (PrP) encoded by the PRNP gene. While there is currently no cure for the disease, depleting PrP in the brain is an established strategy to prevent or stall templated misfolding of PrP. Here we developed in vivo cytosine and adenine base strategies delivered by adeno-associated viruses to permanently modify the PRNP locus to achieve PrP knockdown in the mouse brain.
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