The jasmonate‐insensitive mutant jin1 shows increased resistance to biotrophic as well as necrotrophic pathogens

Abstract

SUMMARY Jasmonic acid and related oxylipin compounds are plant signalling molecules that are involved in the response to pathogens, insects, wounding and ozone. To explore further the role of jasmonates in stress signal transduction, the response of two jasmonate-signalling mutants, jin1 and jin4, to pathogens and ozone was analysed in this study. Upon treatment with the biotrophic bacterial pathogen Pseudomonas syringae, endogenous jasmonate levels increased in jin1 and jin4 similar to wild-type, demonstrating that these mutants are not defective in jasmonate biosynthesis. Jin1 but not jin4 is more resistant to P. syringae and this higher resistance is accompanied by higher levels of salicylic acid. Jin1 is also more resistant to the necrotrophic fungal pathogen Botrytis cinerea and shows wild-type sensitivity to ozone whereas jin4 is more susceptible to B. cinerea and ozone. These results indicate that the mutations in jin1 and jin4 affect different branches of the jasmonate signalling pathway. Additionally, in this combination of phenotypes, jin1 is unique among all other jasmonate-related mutants described thus far. These data also provide support for a crosstalk between the jasmonate and salicylate pathways.

Arabidopsis WRKY33 Is a Key Transcriptional Regulator of Hormonal and Metabolic Responses toward Botrytis cinerea Infection

“…Interestingly, the mutants opr3, jar1-1, jrg21, and ein2, corresponding to genes associated with the JA and ET pathways, were also resistant. These findings partly contrast with previous studies demonstrating the enhanced susceptibility of jar1-1 and ein2 toward this fungal pathogen (Thomma et al, 1999;Ferrari et al, 2003;Nickstadt et al, 2004;Van Baarlen et al, 2007) and highlight the fact that defenses against B. cinerea can be dependent on the fungal isolate . Additionally, mutants in genes shown to act in fungal penetration resistance, pen1-1, pen3-3, and pen4-1 (Collins et al, 2003), were resistant, as was cyp81F2 (Pfalz et al, 2009), a key component in glucosinolate toxification.…”

Architecture and Dynamics of the Jasmonic Acid Gene Regulatory Network

“…The best-known example of such a regulator is MYC2, a key positive regulator of MYC branch genes and associated defenses against chewing insects (e.g., Helicoverpa armigera and Spodoptera littoralis) (Dombrecht et al, 2007;Fernández-Calvo et al, 2011). By contrast, MYC2 negatively regulates defenses against necrotrophic pathogens (e.g., B. cinerea and Plectosphaerella cucumerina) (Lorenzo et al, 2004;Nickstadt et al, 2004). JA-inducible NAC TF family paralogs ANAC019 and ANAC055 show the same effect: they positively regulate MYC branch-associated genes and defenses to S. littoralis, while they antagonize ERF branch-associated resistance to B. cinerea (Bu et al, 2008;Schweizer et al, 2013).…”

Ethylene: traffic controller on hormonal crossroads to defense

“…The ERF and MYC branches of the JA pathway act as communicating vessels in which the relative balance is dependent on the relative strength of the concomitantly activated ET and ABA pathways (Lorenzo et al, 2004;Verhage et al, 2011;Vos et al, 2013b). This is exemplified by the fact that ABA-deficient mutants are more resistant to necrotrophic pathogens and more susceptible to certain insects, whereas ET-deficient mutants are more susceptible to necrotrophs and more resistant to certain insects (Berrocal-Lobo et al, 2002;Lorenzo et al, 2003Lorenzo et al, , 2004Nickstadt et al, 2004;van Loon et al, 2006;Bodenhausen and Reymond, 2007;Kazan and Manners, 2012;Dinh et al, 2013). However, it should be noted that there are exceptions; for example, an ETinsensitive mutant of N. attenuata displayed reduced JA-mediated defenses against M. sexta caterpillars (Onkokesung et al, 2010).…”