title: Novel secretory protein Ss-Caf1 of the plant-pathogenic fungus Sclerotinia sclerotiorum is required for host penetration and normal sclerotial development.
abstract: To decipher the mechanism of pathogenicity in Sclerotinia sclerotiorum, a pathogenicity-defective mutant, Sunf-MT6, was isolated from a T-DNA insertional library. Sunf-MT6 could not form compound appressorium and failed to induce lesions on leaves of rapeseed though it could produce more oxalic acid than the wild-type strain. However, it could enter into host tissues via wounds and cause typical necrotic lesions. Furthermore, Sunf-MT6 produced fewer but larger sclerotia than the wild-type strain Sunf-M. A gene, named Ss-caf1, was disrupted by T-DNA insertion in Sunf-MT6. Gene complementation and knockdown experiments confirmed that the disruption of Ss-caf1 was responsible for the phenotypic changes of Sunf-MT6. Ss-caf1 encodes a secretory protein with a putative Ca(2+)-binding EF-hand motif. High expression levels of Ss-caf1 were observed at an early stage of compound appressorium formation and in immature sclerotia. Expression of Ss-caf1 without signal peptides in Nicotiana benthamiana via Tobacco rattle virus-based vectors elicited cell death. These results suggest that Ss-caf1 plays an important role in compound appressorium formation and sclerotial development of S. sclerotiorum. In addition, Ss-Caf1 has the potential to interact with certain host proteins or unknown substances in host cells, resulting in subsequent host cell death.
authors.forename: Xueqiong
authors.initials: X
authors.lastname: Xiao
authors.forename: Jiatao
authors.initials: J
authors.lastname: Xie
authors.forename: Jiasen
authors.initials: J
authors.lastname: Cheng
authors.forename: Guoqing
authors.initials: G
authors.lastname: Li
authors.forename: Xianhong
authors.initials: X
authors.lastname: Yi
authors.forename: Daohong
authors.initials: D
authors.lastname: Jiang
authors.forename: Yanping
authors.initials: Y
authors.lastname: Fu
mesh_terms: D020816:Amino Acid Motifs; D017360:Arabidopsis / Q000382:microbiology* / Q000502:physiology; D001203:Ascomycota / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology / Q000648:ultrastructure; D016923:Cell Death; D018552:Daucus carota / Q000382:microbiology / Q000502:physiology; D048690:Fruiting Bodies, Fungal; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism*; D015723:Gene Library; D020868:Gene Silencing; D054884:Host-Pathogen Interactions; D008958:Models, Molecular; D016254:Mutagenesis, Insertional; D019815:Oxalic Acid / Q000378:metabolism; D010641:Phenotype; D010802:Phylogeny; D010935:Plant Diseases / Q000382:microbiology*; D018515:Plant Leaves / Q000382:microbiology / Q000502:physiology; D018517:Plant Roots / Q000382:microbiology / Q000502:physiology; D036226:Seedlings / Q000382:microbiology / Q000502:physiology; D013312:Stress, Physiological; D014026:Nicotiana / Q000382:microbiology* / Q000502:physiology
chemical_list: D005656:Fungal Proteins; D019815:Oxalic Acid