The septin protein Sep4 facilitates host infection by plant fungal pathogens via mediating initiation of infection structure formation.
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Many phytopathogenic fungi use infection structures (IFSs, i.e., appressoria and infection cushions) to penetrate host cuticles. However, the conserved mechanisms that mediate initiation of IFS formation in divergent pathogens upon sensing the presence of host plants remain obscure. Here, we demonstrate that a conserved septin gene SEP4 plays crucial roles in this process. Disruption of SEP4 in the plant grey mould fungus Botrytis cinerea completely blocked IFS formation and abolished the virulence of Bcsep4 mutants on unwounded hosts. During IFS formation, mutants lacking SEP4 could produce reactive oxygen species (ROS) normally. Inhibition of ROS production in strains harbouring the SEP4 gene resulted in disordered assembly of Sep4 and the subsequent failure to form infection cushions, suggesting that proper Sep4 assembly regulated by ROS is required for initiation of IFS formation and infection. Moreover, loss of SEP4 severely impaired mutant conidiation, melanin and chitin accumulation in hyphal tips and lesion expansion on wounded hosts, but significantly promoted germ tube elongation and sclerotium production. SEP4-mediated fungal pathogenic development, including IFS formation, was validated in the hemibiotroph Magnaporthe oryzae. Our findings indicate that Sep4 plays pleiotropic roles in B. cinerea development and specifically facilities host infection by mediating initiation of IFS formation in divergent plant fungal pathogens in response to ROS signaling.
