Poster

Nicholas Rhoades^1,2, Todd Naumann¹, Susan McCormick¹, HyeSeon Kim¹, and Guixia Hao¹
1. USDA, Agricultural Research Service, National Center for Agricultural Utilization Research, Mycotoxin Prevention and Applied Microbiology Research Unit., Peoria, IL. 61604, USA.
2. Oak Ridge Institute for Science and Education, USDA, Agricultural Research Service, National Center for Agricultural Utilization Research, Mycotoxin Prevention and Applied Microbiology Research Unit, Peoria, IL 61604, USA.
Corresponding Author: Nicholas Rhoades, Nicholas.Rhoades@usda.gov

Rhodes, Nicholas

Nicholas.Rhoades@usda.gov

Fusarium graminearum is the primary causal agent of Fusarium Head Blight (FHB), a devastating fungal disease on wheat, barley, and other economically relevant grains. Upon infection of a host plant, F. graminearum secretes hundreds of small proteins called effectors that can interfere with host immunity, promote infection and disease spread. Our recent study identified and characterized an effector, FGSG_04848 encoding a rhamnogalacturonan acetylesterase (FgRGAE1) that is involved in initial infection of both wheat and barley hosts. In this study, we have identified a second RGAE ortholog (FGSG_11280; FgRGAE2) in the F. graminearum genome and characterized its general biochemical activity and role in FHB establishment. Similar to FgRGAE1, FgRGAE2 is involved in initial F. graminearum infection, but FgRGAE1/2 double mutants do not have an additive effect on FHB reduction. Investigation of catalytically-null alleles of FgRGAE1 (S29A) and FgRGAE2 (S36A) reveals that FgRGAE1 does not require enzymatic activity to participate in FHB infection, while FgRGAE2 is dependent upon this activity. The mechanisms by which FgRGAE1 and FgRGAE2 influence FHB establishment are not fully elucidated, however we show that both FgRGAE1 and its catalytically-null allele are able to suppress a chitin-induced ROS burst on leaves of Arabidopsis and barley, supporting the observation that catalytic activity is not the driving factor of this effector. In contrast, both FgRGAE2 and its catalytically-null allele do not suppress chitin-induced ROS burst, and expression of catalytically-null FgRGAE2 is unable to complement FgRGAE2 deletion mutants. In silico analysis of FgRGAE1 and FgRGAE2 reveal potential differences in host-pathogen interactions that may explain these functional differences.

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