Antagonism between the defense hormones salicylic acid (SA) and jasmonic acid (JA) plays a central role in the modulation of the plant immune signaling network, but the molecular mechanisms underlying this phenomenon are largely unknown. Here, we demonstrate that suppression of the JA pathway by SA functions downstream of the E3 ubiquitin-ligase Skip-Cullin-F-box complex SCF COI1 , which targets JASMONATE ZIM-domain transcriptional repressor proteins (JAZs) for proteasomemediated degradation. In addition, neither the stability nor the JA-induced degradation of JAZs was affected by SA. In silico promoter analysis of the SA/JA crosstalk transcriptome revealed that the 1-kb promoter regions of JA-responsive genes that are suppressed by SA are significantly enriched in the JA-responsive GCC-box motifs. Using GCC:GUS lines carrying four copies of the GCC-box fused to the b-glucuronidase reporter gene, we showed that the GCC-box motif is sufficient for SA-mediated suppression of JA-responsive gene expression. Using plants overexpressing the GCC-box binding APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) transcription factors ERF1 or ORA59, we found that SA strongly reduces the accumulation of ORA59 but not that of ERF1. Collectively, these data indicate that the SA pathway inhibits JA signaling downstream of the SCF COI1 -JAZ complex by targeting GCC-box motifs in JA-responsive promoters via a negative effect on the transcriptional activator ORA59.

Plants adjust their development and architecture to small variations in ambient temperature. In a time in which temperatures are rising world-wide, the mechanism by which plants are able to sense temperature fluctuations and adapt to it, is becoming of special interest. By performing RNA-sequencing on two Arabidopsis accession and one Brassica species exposed to temperature alterations, we showed that alternative splicing is an important mechanism in ambient temperature sensing and adaptation. We found that amongst the differentially alternatively spliced genes, splicing related genes are enriched, suggesting that the splicing machinery itself is targeted for alternative splicing when temperature changes. Moreover, we showed that many different components of the splicing machinery are targeted for ambient temperature regulated alternative splicing. Mutant analysis of a splicing related gene that was differentially spliced in two of the genotypes showed an altered flowering time response to different temperatures. We propose a two-step mechanism where temperature directly influences alternative splicing of the splicing machinery genes, followed by a second step where the altered splicing machinery affects splicing of downstream genes involved in the adaptation to altered temperatures.

Root drench application of Trichoderma atroviride isolates R32, R33, R40 and R84 promoted the growth of potted radiata pine seedlings. After 6 weeks, seedlings treated with R33 and R84 had thicker stems and greater stem and root biomass (p < 0.05) than untreated controls. Treatment with R32 increased seedling root biomass whilst R40 increased stem diameter. None of the isolates affected seedling height. One isolate, R33, induced systemic resistance to stem inoculation with Diplodia pinea and reduced dieback incidence by 20% compared with untreated controls. To our knowledge, this is the first report of systemic induced resistance by Trichoderma in a pine species. Furthermore, seedlings that were treated with R33 (root drench) plus foliar application of methyl jasmonate (MeJA) expressed elevated peroxidase activity in their stems 2 weeks later, compared with seedlings treated only with MeJA. Because R33 itself did not affect peroxidase activity, this may be indicative of treatment synergy or defence potentiation by R33. Curiously, R33 + MeJA induced terpenoids but suppressed phenylalanine ammonia-lyase activity suggesting possible trade-offs between phenolic and terpenoid defence pathways in the treated seedlings.