Skip to content

Author

Guotian Li

2 papers indexed here

We haven’t gathered this author’s papers yet. Follow them and we’ll fetch their work.

Not the right person? Other researchers publish under this name.

Open access Sep 2026

The rice cellulose synthase-like D4 gene (OsCSLD4) is required for resistance to Xanthomonas pv. oryzae

Plant cell walls serve as a physical support and a barrier to pathogen invasion. Cellulose is the main component of cell walls. The cellulose synthase-like D (CSLD) subfamily genes are required for plant normal development. In rice, Oscsld4 mutant plants are dwarfed and have narrow, rolled leaves. The role of OsCSLD4 in rice immune responses is unclear. We carried out a forward genetic screen using rice mutants expressing the XA21 immune receptor to identify components required for the resistance to Xanthomonas oryzae pv. oryzae (Xoo). One mutant from the screen carries a loss-of-function mutation in OsCSLD4. OsCSLD4 is required for resistance to Xoo mediated by both the XA21 and XA26 immune receptors and also participates in the basal resistance to Xoo. Hallmarks of the XA21-mediated immune response, including induction of the defense marker gene KO5, reactive oxygen species (ROS) burst and the phosphorylation of mitogen-activated protein kinases (MAPKs), are not compromised in the Oscsld4 mutant. These findings suggest that OsCSLD4 does not function as a core signaling component of the immune receptor pathway, but rather maintains the structural integrity of the cell wall as an effective physical barrier. This structural defense is essential for the full manifestation of both innate and receptor-mediated immunity.

Luo-De Shi, Guotian Li, Mawsheng Chern et al. · 0 citations
Jul 2026

A catalase-mediated redox-epigenetic switch governs rice immunity hijacked by a fungal effector.

Pathogen-induced reactive oxygen species (ROS) act as key signaling molecules in plant immunity, but their integration with epigenetic regulation remains unclear. Here, we identify the rice (Oryza sativa) histone deacetylase OsHDA705 as a redox sensor that coordinates immunity through oxidative post-translational modifications (PTMs). Pathogen-induced ROS oxidizes OsHDA705 at cysteine 256 (C256), blocking its deacylase activity. This oxidation promotes hyperacylation of the transcription factor OsIPA1 and histones, thereby activating defense gene expression. We further show that the catalase OsCATB functions as a redox mediator, reducing oxidized OsHDA705 to restore its deacetylase activity, thereby re-establishing the suppression of immunity. The fungal pathogen Ustilaginoidea virens hijacks this process via the secreted effector UvSE1, which physically interacts with the host catalase OsCATB to boost its ROS-scavenging activity, thereby reducing the oxidation level of OsHDA705. Genetic disruption of the OsCATB-OsHDA705 module enhances broad-spectrum disease resistance. Our findings reveal a pathogen strategy to reprogram the host's redox-epigenetic regulation and establish reversible histone deacetylase oxidation as a molecular switch regulating immune transcription in plants.

Yuan Fang, Rui Wang, Yuhang Duan et al. · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.