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Pseudocercospora fijiensis , causal agent of the black Sigatoka disease (BSD) of  Musa  spp., has spread globally since its discovery in Fiji 1963  to  all the banana and plantain growing areas across the globe. It is becoming the most damaging and economically important disease of this crop. The identification and characterization of genes that regulate infection processes and pathogenicity in  P. fijiensis  will provide important knowledge for the development of disease-resistant cultivars. In many fungal plant pathogens, the  Fus3  and  Slt2  are reported to be essential for pathogenicity.  Fus3  regulates filamentous-invasion pathways including the formation of infection structures, sporulation, virulence, and invasive and filamentous growth, whereas  Slt2  is involved in the cell-wall integrity pathway, virulence, invasive growth, and colonization in host tissues. Here, we used RNAi-mediated gene silencing to investigate the role of the  Slt2  and  Fus3  homologs in  P. fijiensis  in pathogen invasiveness, growth and pathogenicity. The  PfSlt2  and  PfFus3  silenced  P. fijiensis  transformants showed significantly lower gene expression and reduced virulence, invasive growth, and lower biomass in infected leaf tissues of East African Highland Banana (EAHB). This study suggests that  Slt2  and  Fus3  MAPK signaling pathways play important roles in plant infection and pathogenic growth of fungal pathogens. The silencing of these vital fungal genes through host-induced gene silencing (HIG) could be an alternative strategy for developing transgenic banana and plantain resistant to BSD.

Silencing of the Mitogen-Activated Protein Kinases (MAPK) Fus3 and Slt2 in Pseudocercospora fijiensis Reduces Growth and Virulence on Host Plants