Pathotypes of Fusarium oxysporum f. sp. fragariae express discrete repertoires of accessory genes and induce distinct host transcriptional responses during root infection

Authors: JENNER, BRADLEY - University Of California; Henry, Peter

Submitted to: Fungal Genetics Conference
Publication Type: Abstract Only
Publication Acceptance Date: 3/18/2022
Publication Date: 3/18/2022
Citation: Jenner, B.N., Henry, P.M. 2022. Pathotypes of Fusarium oxysporum f. sp. fragariae express discrete repertoires of accessory genes and induce distinct host transcriptional responses during root infection. Fungal Genetics Conference, March 15-19, 2022, Pacific Grove, California.

Interpretive Summary:

Technical Abstract: Isolates classified as Fusarium oxysporum f. sp. fragariae are genetically diverse and cause one of two syndromes on strawberry. One syndrome includes symptoms of wilting and chlorosis and is caused by the “yellows-fragariae” pathotype, whereas only wilting symptoms are caused by the “wilt-fragariae” pathotype. Past work differentiated these pathotypes by symptoms and comparative genomics, but their effects on host transcription and the genomic organization of wilt-fragariae pathogenicity genes remain unexplored. To address these knowledge gaps, we challenged susceptible strawberry (Fragaria × ananassa) plants to root infection by five fungal isolates: three yellows-fragariae, one wilt-fragariae, and one that is not pathogenic to strawberry. The host and fungal transcriptomes were characterized at 6- and 13-days post inoculation and contrasted with non-inoculated plants or in vitro fungal growth. On average, >6 times more strawberry genes were differentially expressed (DE) in response to yellows-fragariae isolates than the other two isolates at each timepoint. Responses to yellows-fragariae infection were characterized by early induction of genes related to the jasmonic acid phytohormone pathway and widespread reprogramming of carbohydrate metabolism. The wilt-fragariae isolate induced few transcriptional responses at 6-days post-inoculation, when plants remained asymptomatic, but strongly induced ethylene production and response factors by the later timepoint. Pathotypes were not differentiated by conserved, fungal effector gene expression and few pathotype-specific differences were observed in the expression of conserved fungal genes. By contrast, fungal DE genes on accessory chromosomes were almost entirely distinct between pathotypes. An ~150 kbp ‘pathogenicity island’ on a wilt-fragariae accessory chromosome was enriched with DE genes, many of whose predicted functions were related to plant infection. Sequence conservation suggests this region was horizontally transferred between two wilt-fragariae lineages. There were 15 accessory genes expressed by all yellows-fragariae isolates during root infection, and only one of these genes was also DE by the wilt-fragariae isolate. These results support the conclusion that wilt- and yellows-fragariae cause physiologically distinct syndromes by the expression of discrete repertoires of genes on accessory chromosomes. Implications for our understanding of classification by ‘forma specialis’ will be discussed.