Development of a hemibiotroph within its host: Transcriptomic and histological studies of the Colletotrichum graminicola-maize pathosystem

Walter A. Vargas, José M. Sanz Martín, Lina P. Rivera, Michael R. Thon and Serenella A. Sukno. 11th  European Congress on Fungal Genetics. Marburg,  Germany, 30 March-2 april 2012

Abstract

Hemibiotrophic plant pathogens first establish a biotrophic interaction with the host plant, and later switch to a destructive necrotrophic lifestyle. The molecular mechanisms and the biochemical events involved in this process are poorly understood. Studies of biotrophic pathogens have shown that they actively suppress plant defenses after they have penetrated the host cell.  To determine whether C. graminicola also suppresses host defenses during its biotrophic stage, we performed comprehensive transcriptomic, histological and biochemical studies of the early stages of C. graminicola infection of maize leaves, a model pathosystem for the study of hemibiotrophy. We identified novel putative fungal effectors differentially expressed during host colonization. Our findings also show the presence of a fungal respiratory burst in fungal tips during the transition from biotrophic into necrotrophic lifestyle. Additionally, time-course experiments revealed a strong induction of defense-related genes, as well as the accumulation of reactive oxygen species and antimicrobial compounds in host cells during the biotrophic stage.  We demonstrate the production of maize-derived vesicular bodies containing H2O2 targeted to the fungal hyphae. These results demonstrate a strong induction of defense mechanisms occurring in maize cells during C. graminicola infection, even during the biotrophic development of the pathogen. Overall, these results demonstrate a complex molecular and metabolic interaction between C. graminicola and maize cells, with a strong induction on plant defense mechanisms at early stages of infection. We hypothesize that the switch into the necrotrophic lifestyle is an adaptive response by the fungus that enables it to evade the host immune system, kill the host cells and complete its life-cycle after host infection.

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