Answers are grounded in this paper and cite their sources.
Lesion-mimic mutants provide tractable systems for linking metabolic disruption to cell death and immunity in plants. OsPHD1 encodes a plastidial UDP-glucose/UDP-galactose 4-epimerase, and its disruption causes a lesion-mimic phenotype in the rice mutant lm212. Here, we compared the leaf transcriptomes of lm212 and wild-type plants by RNA sequencing and identified 999 differentially expressed genes. Enriched functions included redox regulation, cell-wall organization, plant–pathogen interaction, MAPK signaling, glutathione metabolism, phenylpropanoid biosynthesis and alpha-linolenic acid metabolism. Alternative-splicing analysis revealed gene-dependent changes, and selected intron-retention events were supported by genome-browser inspection and isoform-specific RT-qPCR. Together, our findings associate OsPHD1 disruption with coordinated transcriptional and post-transcriptional differences and identify candidate pathways potentially related to lesion formation and defense responses in rice.
No takes yet. Share an insight, caveat, or question.
Cao et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: