Plant vascular pathogens such as Ralstonia solanacearum and Xanthomonas oryzae pv. oryzae are difficult to control because they invade xylem vessels, spread systemically, and interfere with water transport. Their biofilms act like protective shelters, helping bacteria withstand host defenses and persist inside plant tissues. Conventional resistance breeding and chemical control can be limited by pathogen diversity, soil persistence, and the internal location of infection. Biofilm eDNA has emerged as an attractive target because it helps stabilize the bacterial community and supports vascular colonization. Based on these challenges, deeper research is needed to develop precise strategies that directly dismantle bacterial biofilms inside plant vascular tissues.
The study was conducted by researchers from Huazhong Agricultural University, Hubei Hongshan Laboratory, and the National Key Laboratory of Crop Genetic Improvement, and was published (DOI: 10.1093/hr/uhag046) on February 19, 2026, in Horticulture Research. The article reports a biofilm-targeting approach for improving crop disease resistance. By replacing the native chloroplast transit peptide (CTP) of MOC1 with a secretory signal peptide (SP), the team redirected the enzyme from chloroplasts to the apoplast, enabling it to reach the site where vascular bacterial biofilms assemble.
The study began from a location problem. MOC1 is a conserved plant Holliday junction (HJ) resolvase with the ability to act on DNA structures, but in its natural state it is transported into chloroplasts and cannot contact bacterial biofilms in the xylem. The researchers first showed that recombinant tomato MOC1 reduced extracellular DNA (eDNA) released by R. solanacearum and disrupted the eDNA lattice within bacterial biofilms. They then engineered the tomato gene SlMOC1 by replacing its native CTP with an SP from tomato pathogenesis-related protein 1, producing a secreted MOC1 variant that accumulated in the apoplast.
In tomato, plants expressing secreted SlMOC1 showed milder bacterial wilt symptoms, lower disease severity, and reduced bacterial movement in xylem vessels. The researchers also found that this protection did not rely on broad activation of plant immune marker genes, suggesting that the main effect came from physical disruption of pathogen biofilms. To make the system more precise, they used the pathogen-inducible SlERF2b promoter to drive SlMOC1 expression mainly after R. solanacearum infection. These plants showed delayed wilting and less vascular blockage, while plant height and fruit weight remained comparable to wild type (WT).
The strategy also worked in rice. Secreted OsMOC1 reduced bacterial blight lesions caused by tested X. oryzae pv. oryzae strains. A synthetic promoter containing effector-binding elements (EBEs) responsive to transcription activator-like effectors (TALEs) further enabled pathogen-triggered OsMOC1 expression, reducing lesion length by more than 65% compared with WT plants and limiting biofilm accumulation observed by scanning electron microscopy (SEM).
The authors said the study shows that crop immunity can be improved by moving a useful plant enzyme to the exact battlefield where infection unfolds. Rather than forcing the whole plant into a heightened defense state, the design sends MOC1 into the apoplast, where vascular bacteria build biofilm shelters. They said this strategy attacks a structural weakness of the pathogen—the eDNA scaffold—while helping preserve normal plant growth. The results suggest that conserved plant proteins can be redesigned as precise tools for resistance breeding.
This work offers a new blueprint for controlling biofilm-dependent vascular diseases in crops. Because MOC1 is conserved across plant species and bacterial biofilms are central to many vascular infections, chloroplast-to-apoplast relocalization could inspire disease-resistance strategies beyond tomato and rice. The use of pathogen-inducible promoters is especially valuable because it limits enzyme production to infection-related contexts, potentially reducing fitness costs and unnecessary pressure on plant-associated microbes. Looking ahead, the authors suggest that clustered regularly interspaced short palindromic repeats (CRISPR)-based editing could replace native chloroplast-targeting sequences with secretion signals in situ, producing DNA-free edited germplasm with enhanced vascular immunity.
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References
DOI
10.1093/hr/uhag046
Original Source URL
https://doi.org/10.1093/hr/uhag046
Funding information
The study was supported by National Natural Science Foundation of China (32472512) and Fundamental Research Funds for the Central Universities (2662025ZKPY008), Hubei Special Project for Science Development (2024CSA060), and Funds of the National Key Laboratory of Agricultural Microbiology (AML2023C01).
About Horticulture Research
Horticulture Research is an open access journal of Nanjing Agricultural University and ranked number one in the Horticulture category of the Journal Citation Reports ™ from Clarivate, 2023. The journal is committed to publishing original research articles, reviews, perspectives, comments, correspondence articles and letters to the editor related to all major horticultural plants and disciplines, including biotechnology, breeding, cellular and molecular biology, evolution, genetics, inter-species interactions, physiology, and the origination and domestication of crops.