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Abstract

Transcriptional profiling of Medicago truncatula roots after infection with Aphanomyces euteiches (oomycota) identifies novel genes upregulated during this pathogenic interaction.

Common root rot of pea caused by Aphanomyces euteiches has been the major yield-reducing factor for pea production during the last decades. In this study, a systematic sequencing of expressed sequence tags (ESTs) was chosen to ubtain a first global picture of the assembly of genes involved in pathogenesis. For this purpose, a pathosystem between the model legume Medicago truncatula and A. euteiches was established. Typical symptoms of this disease such äs root discoloration and a redtiction of root mass were observed in the model legume. Significant transcriptional changes in the host plant occurred already 6 days after inoculation. To identify a large number of plant ESTs, which are induced at this lime point, a cDNA-library was established by Suppression Subtractive Hybridization. Five hundred and sixty ESTs have been generated of this library. On the one hand, EST-annotations showed homologies to a number of classical pathogenesis-related (FR) and defense genes. A notable number of the ESTs, however, were derived from novel genes not matching entries of the large-scale M. truncatula sequence collection. Hybridization experiments showed that also within these new ESTs, 21% are induced after pathogen infection. Hence, the here presented transcriptomic approach demonstrates that classical pathogenesis mechanisms as well as new specific gene regulations are involved in root rot disease development caused by A. euteiches.
Keywords: Aphanomyces euteiches, Medicago truncatula, Pisum sativum, Expressed sequence tags; Suppression subtractive hybridization; cDNA-AFLP



Nyamsuren, O.; Colditz, F.; Tamasloukht, M.; Rosendahl, S.; Bekel, T.; Meyer, F.; Kuester, H.; Franken, P.; Krajinski, F. 2003. Transcriptional profiling of Medicago truncatula roots after infection with Aphanomyces euteiches (oomycota) identifies novel genes upregulated during this pathogenic interaction. Physiological and molecular plant pathology 63, 17-26.