Combating the Sigatoka Disease Complex on Banana

Banana is the fourth most important staple food in the world, behind rice, wheat, and maize, with more than 100 million tons produced annually [1]. Although the majority of bananas produced are consumed locally, banana export is a multi-billion–dollar business [2]. Bananas are grown in more than 100 countries worldwide, largely in developing countries in tropical regions of Africa, Asia, and Latin America [1]. Black Sigatoka disease of banana is one of, if not the most, devastating disease of banana leaves [2]. Black Sigatoka disease is caused by the ascomycete fungus Pseudocercospora fijiensis, and this pathogen is part of the larger Sigatoka disease complex that is made up of P. fijiensis, P.musae (causal agent of Yellow Sigatoka disease), and P. eumusae (causal agent of eumusae leaf spot). Management of Black Sigatoka and the Sigatoka complex in general is currently almost completely dependent on frequent (weekly) fungicide treatments throughout the growing season (Fig 1) [3]. Arias et al. [4] estimated the cost of fungicide control at US$1,000/ha for large plantations. Such frequent application of fungicide control of these pathogens has significant socioeconomic impact that includes both environmental and human health hazards [5]. Additionally, the heavy use of fungicides as the primary means of disease management has resulted in resistance to several fungicide classes, reducing efficacy through the development of fungicide-resistant strains [2]. The levels of fungicide treatment used to control the Sigatoka disease complex is not a sustainable practice; therefore, other control solutions are desperately needed. Several labs from around the world have been working in collaboration to develop tools that are critical to combatting the Sigatoka disease complex. In the current issue, Arango and colleagues have sequenced, assembled, and begun to characterize the genome of P. fijiensis using full genome sequencing of two different P. fijiensis isolates [6]. The resulting 74 Mb assembly is currently one of the largest genomes sequenced in the Dothideomycete class, and Arango et al. have shown that this size is primarily due to the genome being highly expanded by long terminal repeat (LTR) retrotransposons. Due to the size of the genome compared to other phylogenetically related pathogens, Arango et al. have suggested that P. fijiensis and other banana pathogens may have undergone a genome expansion similar to, but independent of, that of the tomato pathogen Cladosporium fulvum [7]. The P. fijiensis genome also shows distinct differences in certain gene families compared to closely related necrotrophic pathogens such as Parastagonospora nodorum [8] and Pyrenophora tritic-repentis [9]. These gene families include several polyketide synthase and cell wall degrading enzymes that are likely beneficial to the necrotrophic lifestyle but detrimental to the stealth-like biotrophic phase of hemibiotrophic infection employed by P. fijiensis.