Coordinator: Luis Eduardo Aranha
FUNCTIONAL'OMICS OF THE RATOON STUNTING DISEASE OF SUGARCANE
Ratoon stunting disease (RSD), caused by the vascular, xylem limited and fastidious gram-positive bacterium Leifsonia xyli subsp. xyli (Lxx), is one of the main diseases of sugarcane worldwide. Control of the bacterium relies primarily on using healthy heat-treated stalks as planting material. However, this approach is not 100% effective and given the perennial nature of sugarcane and the prevalent mechanic mode of transmission of the bacterium, the disease can reach epidemic levels during successive ratoon crops starting from a small amount of initial infected planting material.
The main objectives are to establish a time course of colonization of sugarcane by Lxx and to use this information to monitor gene and protein expression of a resistant and a susceptible sugarcane variety based on global gene expression profiles and 2-D LC-MS/MS protein analysis and sequencing. In addition, we propose to characterize the biological effects of a putative toxin-like compound secreted by Lxx on sugarcane plantlets and to clone and express the genes supposedly involved in its production in E. coli.
The proposal explores available genomic data both on the host and on the pathogen and will lead to the identification of sugarcane defense genes involved in the reaction to Lxx. This set of genes comprises a valuable source of candidate resistance genes so that the effects of these genes on resistance can be further assessed by the scientific community either by a transgenic approach or by the candidate marker mapping approach. Regarding the latter approach it should be emphasized that this project is connected with a linkage mapping proposal submitted to the BIOEN so that our results will be of use in the near future.
Significance and relevance to the Bioenergy program
Ratoon stunting disease is regarded as the main disease of sugarcane worldwide. Losses due to RSD are of considerable size but like any other plant disease, depend on environmental conditions. Yields can be reduced by 15-30% in commercial varieties grown under good irrigated conditions and by 20-40% under average rainfall conditions. Losses of 50% were reported for highly susceptible genotypes. Annual losses were estimated at US$ 11 million in Australia and US$ 36 million in Florida. In Brazil, a recent study with ten varieties developed by the Sugarcane Breeding Program of the Federal University of São Carlos including six ranked among the top ten most planted varieties in the 2004 census, indicated a loss of 15% in productivity (ton/ha) averaged over varieties and over the first, second, and third harvests.
Assuming an incidence of 4% of infected plants in Brazilian commercial fields which totaled 7 million hectares in 2006 and an average productivity of 80 ton/ha, losses in biomass of sugarcane due to RSD can be estimated to be around 3.3 million tons/yr or R$ 107 million/yr given the actual price of R$ 32/ton. This figure is underestimated if one considers that the bacterium is present in the liquids of infected plants and can be mechanically disseminated after contamination of the cane knives used in harvesting. Thus, the incidence of infected plants increases during successive ratoon crops, reaching levels as high as 10% in Brazil.
Expected results and products in the short and long runs
From the host perspective, in the short run we will define genes of sugarcane that are differentially expressed during the colonization by Lxx thus uncovering defense pathways and disease resistance candidate genes. In the long run (10 yrs), it will be possible to associate genotypes (allelic variations) at candidate loci with disease resistance phenotypes by analyzing linkage disequilibrium among a panel of accessions of commercial sugarcane aiming to identify key genes and their variants which have great phenotypic effects on resistance.
From the pathogen perspective, we expect to dissect two potential mechanisms of pathogenicity of Lxx which as of today represent new strategies of plant attack. In the long run, we might be able to inhibit these mechanisms perhaps by modifying the host environment using transgenic approaches.