Functional analysis of the G-protein α subunits FGA1 and FGA3 in the banana pathogen Fusarium oxysporum f. sp. cubense

• The fungus Fusarium oxysporum f. sp. cubense (Foc) causes vascular wilt in bananas.
• The targeted deletion of the G-protein α subunit genes fga1 and fga3 were performed.
• FGA1, but not FGA3, plays vital roles in the growth, development and pathogenicity.
• Both FGA1 and FGA3 are involved in the modulation of heat resistance and cAMP levels.
• They may function partially through the cAMP-dependent protein kinase A pathway.

The asexual fungus Fusarium oxysporum f. sp. cubense (Foc) is the causal agent of fusarium wilt in bananas (Musa spp.). This fungus poses a threat to banana production throughout the world. Here, two Foc genes, fga1 and fga3, were functionally characterized. These genes encode proteins homologous to the G-protein α subunits GPA1 from Saccharomyces cerevisiae and MAGC from Magnaporthe grisea, respectively. The deletion of fga1 leads to a phenotypic defect in colony morphology and reductions in vegetative growth, conidiation and pathogenicity against the banana plant (Musa spp. cv. Brazil), which was not observed for the Δfga3 deletion mutant. Intriguingly, both Δfga1 and Δfga3 deletion mutants showed declines in intracellular cyclic AMP levels and increases in heat resistance, suggesting that FGA1 regulates growth, development, pathogenicity, and heat resistance, whereas FGA3 modulates heat resistance, potentially through the cAMP-dependent protein kinase A pathway. These findings offer insights into the roles of the G-protein α subunits in the development and pathogenicity of the fungus Foc.