Colletotrichum fructicola CfGti1 Transcriptionally Regulates Penetration, Colonization, and Pathogenicity on Apple

Glomerella leaf spot (GLS), mainly caused by <i>Colletotrichum fructicola</i>, is a destructive disease of apple. However, the underlying pathogenesis mechanisms of GLS are still largely obscure. Previous infection transcriptome analysis showed that transcription factor CfGti1 was induced during leaf infection. The present study confirms that the <i>CfGti1</i> gene is strongly expressed in conidia and early infection. To identify functions performed, we generated gene deletion mutant Δ<i>CfGti1</i> by homologous recombination. Phenotypic analysis revealed that Δ<i>CfGti1</i> lost pathogenicity to apple leaves by blocking appressorium-mediated host penetration, although penetration pegs still developed on cellophane. In addition, Δ<i>CfGti1</i> colonization and hyphal extension in wounded apple fruit were dramatically decreased. The Δ<i>CfGti1</i> mutant exhibited defects in growth and development of hyphae, which may be partly responsible for its inability to colonize apple. Comparative transcriptome and qRT-PCR analyses suggested that CfGti1 regulated appressorium-mediated host penetration by modulating genes related to metabolism of appressorial lipid droplets. Interestingly, CfGti1 also regulated the expression of <i>ybtS</i> and <i>AKT1</i> or <i>AFT1-1</i> related to biosynthesis of AK and AF host-specific toxins. This study demonstrated that CfGti1 is a pivotal regulator for apple GLS pathogenesis in <i>C. fructicola</i>.