| Host plants are involved in endless co-evolutionary interactions for dominance with theirpathogens. Plants gained ability to detect invasions by pathogens and activate variousdefense responses. Meanwhile, pathogens evolved diverse mechanisms to suppress plantimmunity and thereby multiply and cause diseases. Phytophthora sojae, a casual agent ofsoybean root and stem rot, secretes a repertoire of highly divergent RXLR effectors into plantcells to suppress host immunity system during infection. RXLR effectors contain conservedRXLR-dEER bipartite motifs required for translocation into host cells and the C-terminaldomains that interact with plant resistance proteins. Large-scale investigation of RXLReffectors from P. sojae demonstrated that most of them are capable of suppressing PAMP(Pathogen Associated Molecular Patterns) and/or effector triggered immunities. However,the action of biochemical basis of RXLR effector proteins remains unclear.We aimed at understanding the biochemical basis of the virulence function of P. sojaeeffector Avr1b through Arabidopsis thaliana transformants that constitutively express Avr1bgene. Our results showed that the expression of Avr1b in Arabidopsis resulted in enhancedresistance to infection by P. parasitica and early flowering. The Avr1b transgenicArabidopsis showed weaker disease symptoms and restricted the growth of hyphae whenchallenged with P. parasitica. Compared to the wild-type Col-0, the transgenic Arabidopsisdisplayed enhanced callose deposition in response to treatment with flg22, a core activepeptide from the PAMP bacterial flagellin. Analysis of the growth and development showedthat transgenic expression of Avr1b in Arabidopsis induced faster flowering. Furtheranalysis showed that Avr1b might directly or indirectly repress expression of floweringrelated gene FLC. The functional characterization of Avr1b provided insights into theunderstanding of biochemical basis of functions of P. sojae RXLR effectors. |
