ArticleMolecular plant pathology2025
A Lrp/AsnC Family Transcriptional Regulator Lrp Is Essential for the Pathogenicity of Dickeya oryzae.
Article in Molecular plant pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Identification of biofilm-associated genes inBiofilm · 2026Article
- The MarR Family Transcriptional Regulator EmrR Negatively Regulates the Type III Secretion System (T3SS) and Positively Modulates Pathogenicity in Dickeya oryzae.Molecular plant pathology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Dickeya oryzae causes severe soft rot diseases in a range of important crops. To understand its complicated pathogenic mechanisms, we tried to identify the key virulence regulators through transposon mutagenesis. This led to the identification of a member of the Lrp/AsnC family transcriptional regulators in D. oryzae EC1, designated as Lrp. Phenotype analyses showed that Lrp positively regulated biofilm formation and the production of zeamines, proteases and polygalacturonases, but negatively regulated bacterial swimming motility. Deletion of lrp caused a drastic attenuation in bacterial virulence, indicating that Lrp is a key regulator in the modulation of D. oryzae pathogenicity. We further showed that the transcription of the lrp gene was negatively regulated by the transcriptional regulators SlyA, Fis and OhrR, and the transcriptional expression of tzpA, ohrR and fis was positively modulated by Lrp. Moreover, we demonstrated that Lrp can directly bind to the promoter regions of zmsA, zmsK, prtG, prtX, pehK, pehX, fis, tzpA and ohrR. DNase I footprinting assay determined that Lrp was capable of binding to a specific site (5'-GTGTAATTATGGGCGTGCTCCGGG-3') in the promoter of zmsA. Furthermore, we found that four amino acid residues of Lrp, L20, L23, G111 and T146, are essential to the biological function of Lrp. Overall, this study demonstrated that Lrp is an essential virulence modulator in D. oryzae and suggested that Lrp can be a potent target for controlling the soft rot diseases caused by D. oryzae.
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.