The receptor-like kinase SlSOBIR1 is differentially modulated by virus infection but its overexpression in tobacco has no significant impact on virus accumulation.

ABSTRACT

KEY MESSAGE The role of the tomato receptor-like kinase SlSOBIR1 in antiviral defense was investigated. SlSOBIR1 was transcriptionally modulated by unrelated viruses but its ectopic expression had no effect on virus accumulation. Leucine-rich repeat receptor-like kinases (LRR-RLK) constitute a diverse group of proteins allowing the cell to recognize and respond to the extracellular environment. In the present study we focused on a gene encoding a tomato LRR-RLK (named SlSOBIR1) involved in the host defense against fungal pathogens. Curiously, SlSOBIR1 has been previously reported to be down-regulated by Pepper yellow mosaic virus (PepYMV) infection. Here, we show that SlSOBIR1 is responsive to wounding and differentially modulated by unrelated virus infection, i.e., down-regulated by PepYMV and up-regulated by Tomato chlorotic spot virus (TCSV). Despite these divergent expression profiles, SlSOBIR1 overexpression in transgenic tobacco plants had no evident effect on TCSV and PepYMV accumulation. On the other hand, overexpression of SlSOBIR1 significantly increased the expression of selected defense genes (PR-1a and PR-6) and exacerbated superoxide production in wounded leaves. Our data indicate that the observed modulation of SlSOBIR1 expression is probably triggered by secondary effects of the virus infection process and suggest that SlSOBIR1 is not directly involved in antiviral signaling response.