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  • Title: Identification and differential induction of ABCG transporter genes in wheat cultivars challenged by a deoxynivalenol-producing Fusarium graminearum strain.
    Author: Muhovski Y, Jacquemin JM, Batoko H.
    Journal: Mol Biol Rep; 2014 Sep; 41(9):6181-94. PubMed ID: 24973883.
    Abstract:
    Fusarium head blight (FHB), predominantly caused by Fusarium graminearum, is a devastating disease that poses a serious threat to wheat (Triticum aestivum L.) production worldwide. A suppression subtractive hybridization cDNA library was constructed from F. graminearum infected spikes of a resistant Belgian winter wheat, Centenaire, exhibiting Type II resistance to FHB in order to identify differentially expressed members of full-size ABCG family. Members of the ABCG family are pleiotropic drug transporters allowing the movement of structurally unrelated metabolites, including pathogens-derived virulent compounds, across biological membranes and could be potentially involved in resistance to plant pathogens. In this study, five new full-size ABCG transporter expressed sequence tags TaABCG2, TaABCG3, TaABCG4, TaABCG5 and TaABCG6 have been identified. Time-course gene expression profiling between the FHB resistant Centenaire and the susceptible Robigus genotype showed that the newly isolated transcripts were differentially expressed up to 72 h-post inoculation. The respective genes encoding these transcripts were mapped to corresponding wheat chromosomes or chromosomal arms known to harbor quantitative trait loci for FHB resistance. Interestingly, these ABCG transcripts were also induced by deoxynivalenol (DON) treatment of germinating wheat seeds and the toxin treatment inhibited root and hypocotyl growth. However, the hypocotyl of the FHB resistant cultivar Centenaire was less affected than that of the susceptible cultivar Robigus, reflecting more likely the genotype-dependent differential expression pattern of the identified ABCG genes. This work emphasizes the potential involvement of ABCG transporters in wheat resistance to FHB, at least in part through the detoxification of the pathogen-produced DON.
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