ArticleMicrobiome2026
MdUGT88F1 enhances plant resistance to Fusarium proliferatum f.sp. malus domestica MR5 via root exudate-mediated assembly of disease-suppressive rhizosphere microbiota.
Article in Microbiome, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundApple replant disease (ARD) is a major threat to the sustainable development of China's apple industry. It is primarily caused by the accumulation of phloridzin and the pathogen Fusarium proliferatum f.sp. malus domestica MR5 (Fpmd MR5). MdUGT88F1-mediated phloridzin biosynthesis is known to enhance disease resistance, but its role in shaping the rhizosphere microbiome and conferring resistance against Fpmd MR5 remains unclear. In this study, we used wild-type (WT) and MdUGT88F1 transgenic apple lines to systematically investigate the mechanism by which MdUGT88F1 regulates the rhizosphere microbiome to mitigate ARD.
resultsCompared with WT and MdUGT88F1-OE plants, MdUGT88F1-RNAi plants exhibited enhanced tolerance to ARD, as indicated by reduced disease severity, decreased abundance of Fpmd MR5 in the rhizosphere soil, and lower phloridzin content. Further greenhouse experiments demonstrated that the rhizosphere bacterial communities were triggered mainly by changes in community composition. Multi-omics joint analysis revealed that members of the family Bacillaceae with multiple plant growth-promoting traits were enriched in the MdUGT88F1-RNAi plant rhizosphere but only upon Fpmd MR5 invasion. MdUGT88F1-RNAi plants exhibited significantly higher exudation of D-tagatose, D-galactose, sucrose, 3-O-methyl-D-glucose, and maltitol. Interestingly, exogenous application of these compounds promoted the proliferation of Bacillus, enhancing plant resistance to Fpmd MR5. In vitro assays demonstrated that the recruited Bacillus significantly inhibited the hyphal growth and fumonisin B1 production of Fpmd MR5 and alleviated plant disease symptoms. We experimentally validated this observation by inoculating a synthetic microbial community (Bacillus velezensis, Bacillus mojavensis, Bacillus subtilis, Bacillus amyloliquefaciens, and Bacillus licheniformis) into replanted soil, which led to a significant reduction in pathogen Fusarium abundance and promoted plant growth.
conclusionOverall, these findings highlight that plant disease resistance is a complex trait driven by dynamic interactions among the host genetic background, rhizospheric microbial communities, and pathogens. Targeted modulation of the rhizospheric microbiome represents a potent "prebiotic" strategy. This approach can indirectly enhance plant disease resistance by fostering beneficial microbial activity in the rhizosphere. This study also provides a theoretical basis and practical solutions for the green control of ARD through prebiotics and synthetic microbial communities. Video Abstract.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.