The link between susceptibility to Macrophomina phaseolina and three phytohormones in Medicago truncatula

Abstract

Macrophomina phaseolina is a major agricultural pest causing the disease charcoal rot in many species of crops. The disease manifests as yellowing (chlorosis) and death (necrosis) of plant tissue by secreting plant toxins and clogging its vasculature with small black cellular aggregates called microsclerotia. This research aimed at identifying molecular mechanisms that can promote resistance to the pathogen. Using the exogenous application of phytohormones abscisic acid (ABA), ethylene (ET), and jasmonic acid (JA), we assessed the role of each of these hormones in promoting defense or susceptibility. In a previous study using M. truncatula as a model organism, application of ET and/or JA promoted resistance in the A17 ecotype but not in the R108 ecotype. To investigate the mechanism for this phenotypic difference, plants from each ecotype were treated with these hormones and their expression of ET and JA responsive genes were analyzed using real-time PCR. We investigated ABA for its role in defense because charcoal rot incidence is higher during hot, dry months and ABA is involved in defending plants against the symptoms of drought. Medicago truncatula plants were transferred to media containing ABA before being inoculated with the pathogen and then observed for the development of disease symptoms. The results of this study indicate that the expression of ET markers was similar between A17 and R108 plants treated with ethephon, while JA markers demonstrated a difference between these ecotypes following MeJA application. Thus, we speculate that the difference between R108 and A17's inducible resistance phenotypes results from misregulation of JA responsive gene in R108. Our results also indicated that exogenous ABA application can lead to increased susceptibility to M. phaseolina in A17 plants, as demonstrated by more rapid development of disease symptoms.