RNA-Seq Analysis Reveals Transcriptomic and Alternative-Splicing Changes Associated with OsPHD1-Mediated Lesion Mimicry in Rice
TL;DR
These 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.
Abstract
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.