Hijacking of the jasmonate pathway by the mycotoxin fumonisin B1 (FB1) to initiate programmed cell death in Arabidopsis is modulated by RGLG3 and RGLG4.

The mycotoxin fumonisin B1 (FB1) is a strong inducer of programmed cell death (PCD) in plants, but its underlying mechanism remains unclear. Here, we describe two ubiquitin ligases, RING DOMAIN LIGASE3 (RGLG3) and RGLG4, which control FB1-triggered PCD by modulating the jasmonate (JA) signalling pathway in Arabidopsis thaliana. RGLG3 and RGLG4 transcription was sensitive to FB1. Arabidopsis FB1 sensitivity was suppressed by loss of function of RGLG3 and RGLG4 and was increased by their overexpression. Thus RGLG3 and RGLG4 have coordinated and positive roles in FB1-elicited PCD. Mutated JA perception by coi1 disrupted the RGLG3- and RGLG4-related response to FB1 and interfered with their roles in cell death. Although FB1 induced JA-responsive defence genes, it repressed growth-related, as well as JA biosynthesis-related, genes. Consistently, FB1 application reduced JA content in wild-type plants. Furthermore, exogenously applied salicylic acid additively suppressed JA signalling with FB1 treatment, suggesting that FB1-induced salicylic acid inhibits the JA pathway during this process. All of these effects were attenuated in rglg3 rglg4 plants. Altogether, these data suggest that the JA pathway is hijacked by the toxin FB1 to elicit PCD, which is coordinated by Arabidopsis RGLG3 and RGLG4.

RGLG3 and RGLG4, novel ubiquitin ligases modulating jasmonate signaling.

JAs are important hormones for plant development and defense, and JA signaling is regulated by diverse mechanisms. We have recently identified two RING-type ubiquitin ligases, RGLG3 and RGLG4, as essential JA signaling regulators. In this addendum, we discuss some characters of RGLG3 and RGLG4, which further support their important roles in JA pathway. RGLG3 and RGLG4 didn't interact with known key factors of the core JA pathway, rather, it might target on unknown protein that negatively regulated JA signaling. RGLG3 and RGLG4 expression was suppressed by SA treatment in an NPR1-independent manner, and rglg3 rglg4 moderated SA-inhibited JA-responsive PDF1.2 expression, suggesting RGLG3 and RGLG4 took roles in SA-JA antagonism. RGLG3 and RGLG4 could be important players of a regulatory network and coordinated diverse signals to modulate JA signaling.