Abstract

Fusarium wilt caused by Fusarium oxysporum f. sp. conglutinans (FOC) is a destructive disease of Brassica crops, which results in severe yield losses. There is little information available about the mechanism of disease resistance. To obtain an overview of the transcriptome profiles in roots of R4P1, a Brassica oleracea variety that is highly resistant to fusarium wilt, we compared the transcriptomes of samples inoculated with FOC and samples inoculated with distilled water. RNA-seq analysis generated more than 136 million 100-bp clean reads, which were assembled into 62,506 unigenes (mean size = 741 bp). Among them, 49,959 (79.92%) genes were identified based on sequence similarity searches, including SwissProt (29,050, 46.47%), Gene Ontology (GO) (33,767, 54.02%), Clusters of Orthologous Groups (KOG) (14,721, 23.55%) and Kyoto Encyclopedia of Genes and Genomes Pathway database (KEGG) (12,974, 20.76%) searches; digital gene expression analysis revealed 885 differentially expressed genes (DEGs) between infected and control samples at 4, 12, 24 and 48 hours after inoculation. The DEGs were assigned to 31 KEGG pathways. Early defense systems, including the MAPK signaling pathway, calcium signaling and salicylic acid-mediated hypersensitive response (SA-mediated HR) were activated after pathogen infection. SA-dependent systemic acquired resistance (SAR), ethylene (ET)- and jasmonic (JA)-mediated pathways and the lignin biosynthesis pathway play important roles in plant resistance. We also analyzed the expression of defense-related genes, such as genes encoding pathogenesis-related (PR) proteins, UDP-glycosyltransferase (UDPG), pleiotropic drug resistance, ATP-binding cassette transporters (PDR-ABC transporters), myrosinase, transcription factors and kinases, which were differentially expressed. The results of this study may contribute to efforts to identify and clone candidate genes associated with disease resistance and to uncover the molecular mechanism underlying FOC resistance in cabbage.

Highlights

  • Fusarium wilt is a destructive disease that causes great losses to cabbage (Brassica oleracea L. var. capitata) production worldwide

  • A total of 33,767 unigenes were assigned to 49 Gene Ontology (GO) terms in three categories: BP (Biological process), CC (Cellular component) and MF (Molecular Function)

  • A high proportion of differentially expressed genes (DEGs) were assigned to cellular process and metabolic process in the BP category, to cell, cell part and organelle in CC and to binding and catalytic activity in MF (Fig 1)

Read more

Summary

Introduction

Fusarium wilt is a destructive disease that causes great losses to cabbage (Brassica oleracea L. var. capitata) production worldwide. This disease was first identified in the United States by Smith in the 1890s [1], and in the following decades was subsequently found in Japan and several other countries [2]. Conglutinans), which can remain in soil for years or even decades [6] This pathogen infects cabbage roots, colonizes and occludes the xylem vessels, and leads to leaf wilt or sometimes wilting of the entire plant, with stunted growth and eventually death. Traditional methods, such as crop rotation and chemical control, have almost no effect on the disease because this pathogen is ubiquitous in soil and is not eradicated by these methods. Developing resistant cultivars is considered to be the most effective measure to control fusarium wilt in cabbage [7]

Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.