Abstract

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.

Highlights

  • Pseudocercospora fijiensis, causal agent of black Sigatoka disease (BSD) in Musa spp., was first recognized in 1963 in the South-Eastern Coast of Viti Levu in Fiji (Mourichon et al, 1997; Marin et al, 2003; Churchill, 2011)

  • MAP kinase Fus3 and Slt2 pathways are known to be responsible for regulating host penetration, infectious, invasive growth, and pathogenicity of several fungal pathogens including Mycosphaerella graminicola (Mehrabi et al, 2006; Cousin et al, 2007)

  • The fragments of MAP kinase genes PfSlt2 and PfFus3 were cloned into the RNA interference (RNAi) vector pKOIISD1

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Summary

Introduction

Pseudocercospora fijiensis, causal agent of black Sigatoka disease (BSD) in Musa spp. (banana and plantain), was first recognized in 1963 in the South-Eastern Coast of Viti Levu in Fiji (Mourichon et al, 1997; Marin et al, 2003; Churchill, 2011). (banana and plantain), was first recognized in 1963 in the South-Eastern Coast of Viti Levu in Fiji (Mourichon et al, 1997; Marin et al, 2003; Churchill, 2011). BSD has spread to sub-Saharan countries in the West African coast and to the Eastern African countries (Mourichon et al, 1997; Ploetz, 2001; Marin et al, 2003; Churchill, 2011). Pseudocercospora fijiensis is one of the most damaging and economically important pathogens of Musa spp. worldwide (Farr et al, 1995; Stewart et al, 1999; Carlier et al, 2000). P. fijiensis develops resistance to fungicides after many sprays and better strategies are needed to efficiently control this disease (Stover, 1990)

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