Abstract
Clubroot, caused by the soil-borne protist Plasmodiophora brassicae, is one of the most destructive disease for Brassica oleracea worldwide. However, the molecular mechanism of clubroot resistance still remains poorly elucidated. Therefore, we aim at identifying key genes responsive to P. brassicae infection and deducing possible molecular mechanism regulating clubroot resistance in cabbage. A clubroot-resistant line (XG) and a clubroot-susceptible line (JF) were employed to conduct histological observation and transcriptome analysis at 7 and 28 DAI (days after inoculation) following inoculation with P. brassicae. Differentially expressed genes (DEGs) obtained by comparing infected roots with mock-infected roots were assigned to Gene Ontology (GO) functions and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways for enrichment analysis. TEM observation showed obvious histological differences of root cells between JF and XG after inoculation with P. brassicae. At 7 DAI, the number of DEGs identified in JF was much higher than that of XG, and most of them were enriched in metabolic pathways, metabolites biosynthesis and starch, sucrose metabolism. More DEGs were identified at 28 DAI compared to 7 DAI in XG, and most of these DEGs involved in biosynthesis of secondary metabolites, plant-pathogen interaction and plant hormone transduction. Genes related to cell wall biosynthesis, pattern recognition receptors (PRRs), disease resistance proteins, SA signal transduction, calcium influx, respiratory burst oxidase homolog (RBOH), MAPK cascades, transcription factors and chitinase were mainly up-regulated in XG at 28 DAI, while most of them were repressed in JF. Our research work suggest drastic and complex defense response to P. brassicae infection at 28 DAI (secondary infection stage) at transcriptional level. Results generated in the present study could provide comprehensive insights into the transcriptomic landscape for better understanding of molecular regulatory mechanism of clubroot resistance in cabbage.
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