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Novel Secretory Protein Ss-Caf1 of the Plant-Pathogenic Fungus Sclerotinia sclerotiorum Is Required for Host Penetration and Normal Sclerotial Development

Xiao, Xueqiong, Xie, Jiatao, Cheng, Jiasen, Li, Guoqing, Yi, Xianhong, Jiang, Daohong, Fu, Yanping
Molecular plant-microbe interactions 2014 v.27 no.1 pp. 40-55
EF hand motifs, Nicotiana benthamiana, Sclerotinia sclerotiorum, appressoria, cell death, genes, leaves, mutants, oxalic acid, pathogenicity, phenotype, plant pathogenic fungi, proteins, rapeseed, sclerotia, signal peptide, tissues, tobacco, transfer DNA
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 Ca²⁺-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.