Identification of Genes Involved in Resistance to Didymella pinodes in Pea by deepSuperSAGE Transcriptome Profiling

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• 作者：Sara Fondevilla (1) (3)
  Bj?rn Rotter (2)
  Nicolas Krezdorn (2)
  Ruth Jüngling (2)
  Peter Winter (2)
  Diego Rubiales (3)
  
• 关键词：Didymella pinodes ; Resistance ; Transcriptomics ; SuperSAGE ; Ascochyta blight ; Pisum sativum
• 刊名：Plant Molecular Biology Reporter
• 出版年：2014
• 出版时间：February 2014
• 年：2014
• 卷：32
• 期：1
• 页码：258-269
• 全文大小：369 KB
• 作者单位：Sara Fondevilla (1) (3)
  Bj?rn Rotter (2)
  Nicolas Krezdorn (2)
  Ruth Jüngling (2)
  Peter Winter (2)
  Diego Rubiales (3)
  
  1. Institute for Molecular Bioscience, University of Frankfurt, Max-von Laue Str. 9, 60438, Frankfurt am Main, Germany
  3. Institute for Sustainable Agriculture, CSIC, Apdo. 4084, 14080, Córdoba, Spain
  2. GenXPro, Altenh?ferallee 3, 60438, Frankfurt am Main, Germany
  
• ISSN：1572-9818

文摘

Didymella pinodes, causing ascochyta blight, is the most destructive foliar pathogen of dry peas. Despite the importance of this pathogen, very little is known about the mechanisms or genes that control host plant resistance against the fungus. Here we employed deepSuperSAGE genome-wide transcription profiling to identify pea genes involved in resistance to D. pinodes in the wild, resistant Pisum sativum ssp. syriacum accession P665. Two deepSuperSAGE libraries were constructed from leaf RNA of infected and control plants. A total of 17,561 different UniTags were obtained. Seventy per cent of them could be assigned to known sequences from pea or other plants. 509 UniTags were significantly differentially expressed (P-lt;-.05; fold change ?, ?) in inoculated versus control plants. Of these, 78?% could be assigned to known sequences from pea or other plants, and 58?% to proteins with known function. Our results suggest that a battery of genes contribute to resistance against D. pinodes in the wild pea accession P665. For example, genes encoding protease inhibitors are activated, and the corresponding proteins may contribute to a lower penetration success. The production of antifungal compounds and strengthening of host cell walls may interfere with the spread of the pathogen. In addition, detoxification of D. pinodes toxins and repair of cell walls could also reduce the damage produced by this devastating necrotroph. Hormones orchestrate metabolic adaptation to D. pinodes infection, since ethylene, ABA and indole-3-acetic acid pathways were up-, while the gibberellic acid pathway was down-regulated.