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Accession IconSRP131078

OsDCL1a activation impairs phytoalexin biosynthesis and compromises disease resistance in rice [RNA-seq]

Organism Icon Oryza sativa
Sample Icon No Downloadable Samples
Technology Badge IconIllumina HiSeq 2500

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Description
MicroRNAs (miRNAs) are small non-coding RNAs that act as post-transcriptional regulators of gene expression via sequence-specific cleavage or translational repression of target transcripts. They are transcribed as long single-stranded RNA precursors with unique stem-loop structures that are processed by a DICER-Like (DCL) ribonuclease, typically DCL1, to produce mature miRNA sequences. Here, we investigated the contribution of OsDCL1 to innate immunity in rice. Activation-tagged dcl1a mutants (dcl1a-Ac) showed enhanced susceptibility to infection by the fungal pathogens Magnaporthe oryzae and Fusarium fujikuroi. Susceptibility to pathogen infection in dcl1a-Ac plants was associated with weaker induction of defence gene expression. Plant growth and development were not affected in dcl1a-Ac plants in the absence of pathogen challenge. To analyse the impact of OsDCL1a activation on the host transcriptome, we compared the mRNA and miRNA transcriptomes of dcl1a-Ac and wild-type plants. OsDCL1a activation misregulated genes involved in detoxification of reactive oxygen species (ROS) and accumulation of O2•- in leaves. Consequently, dcl1a-Ac plants were more sensitive to oxidative stress caused by methyl viologen treatment. Notably, transcriptome analysis revealed downregulation of diterpenoid phytoalexin biosynthetic genes in dcl1a-Ac, the expression of these genes also being weakly induced during pathogen infection in these plants. Finally, OsDCL1a activation resulted in marked alterations in the rice miRNAome, including both upregulation and downregulation of miRNAs. Our findings support that OsDCL1a plays an important role in regulating innate immunity in rice. Overall design: 2 different replicates of RNA seq from mock and M. oryzae inculated rice leaves are included in this study. They correspond to wild type and DCL1a activation mutants.
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