Abstract
BACKGROUND: Fusarium wilt disease of banana is one of the most devastating diseases and was responsible for destroying banana plantations in the late nineteenth century. Fusarium oxysporum f. sp. cubense is the causative agent. Presently, both race 1 and 4 strains of Foc are creating havoc in the major banana-growing regions of the world. There is an urgent need to devise strategies to control this disease; that is possible only after a thorough understanding of the molecular basis of this disease. RESULTS: There are a few regulators of Foc pathogenicity which are triggered during this infection, among which Sge1 (Six Gene Expression 1) regulates the expression of effector genes. The protein sequence is conserved in both race 1 and 4 strains of Foc indicating that this gene is vital for pathogenesis. The deletion mutant, FocSge1 displayed poor conidial count, loss of hydrophobicity, reduced pigmentation, decrease in fusaric acid production and pathogenicity as compared to the wild-type and genetically complemented strain. Furthermore, the C-terminal domain of FocSge1 protein is crucial for its activity as deletion of this region results in a knockout-like phenotype. CONCLUSION: These results indicated that FocSge1 plays a critical role in normal growth and pathogenicity with the C-terminal domain being crucial for its activity.