The Medicago truncatula–Mycosphaerella pinodes interaction: a new pathosystem for dissecting fungal-suppressor-mediated disease susceptibility in plants

A model pathosystem involving Mycosphaerella pinodes, causal agent of Mycosphaerella blight on pea and barrel medic(k) Medicago truncatula has been developed. Nineteen M. truncatula ecotypes were evaluated for disease susceptibility to M. pinodes strain OMP-1, using detached leaves inoculated with a pycnospore suspension. Inoculation of ecotype R108-1 with the pycnospores allowed direct penetration into the host’s epidermal cells, eventually causing leaf spots. Since pycnidia formed abundantly in infected tissues by 3 days post inoculation, M. pinodes is considered to have completed its infection cycle as on a natural host plant. Expression of phenylalanine ammonia-lyase (PAL)-, chalcone synthase (CHS)- and isoflavone reductase (IFR) mRNAs as well as subsequent accumulation of a major phytoalexin, medicarpin, was induced in ecotype R108-1 with an elicitor preparation from M. pinodes, whereas this phytoalexin response was markedly attenuated by supprescins from the same fungus. A transcriptional study of a salicylic acid (SA)-regulated gene encoding pathogenesis-related protein 10-1 (PR10-1) indicated that the suppressor likely interferes with the signal transduction process leading to inducible defenses in M. truncatula. Indeed, the suppressor rendered the host tissues (ecotype R108-1) susceptible to unrelated nonpathogenic fungi, probably through targeting ATPase activity of the host cells. Accordingly, the resistant and susceptible response of pea can be recapitulated in M. truncatula. This model pathosystem thus will allow us to verify the molecular basis underlying the fungal suppressor-mediated plant susceptibility.