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Plants activate a myriad of signaling cascades to tailor adaptive responses under environmental stresses, such as salinity. While the roles of exogenous karrikins (KARs) in salt stress mitigation are well comprehended, genetic evidence of KAR signaling during salinity responses in plants remains unresolved. Here, we explore the functions of the possible KAR receptor KARRIKIN-INSENSITIVE2 (KAI2) in Arabidopsis thaliana tolerance to salt stress by investigating comparative responses of wild-type (WT) and kai2 -mutant plants under a gradient of NaCl. Defects in KAI2 functions resulted in delayed and inhibited cotyledon opening in kai2 seeds compared with WT seeds, suggesting that KAI2 played an important role in enhancing seed germination under salinity. Salt-stressed kai2 plants displayed more phenotypic aberrations, biomass reduction, water loss and oxidative damage than WT plants. kai2 shoots accumulated significantly more Na+ and thus had a lower K+/Na+ ratio, than WT, indicating severe ion toxicity in salt-stressed kai2 plants. Accordingly, kai2 plants displayed a lower expression of genes associated with Na+ homeostasis, such as SALT OVERLY SENSITIVE (SOS) 1, SOS2, HIGH-AFFINITY POTASSIUM TRANSPORTER 1;1 (HKT1;1) and CATION–HYDROGEN EXCHANGER 1 (NHX1) than WT plants. WT plants maintained a better glutathione level, glutathione-related redox status and antioxidant enzyme activities relative to kai2 plants, implying KAI2's function in oxidative stress mitigation in response to salinity. kai2 shoots had lower expression levels of genes involved in the biosynthesis of strigolactones (SLs), salicylic acid and jasmonic acid and the signaling of abscisic acid and SLs than those of WT plants, indicating interactive functions of KAI2 signaling with other hormone signaling in modulating plant responses to salinity. Collectively, these results underpin the likely roles of KAI2 in the alleviation of salinity effects in plants by regulating several physiological and biochemical mechanisms involved in ionic and osmotic balance, oxidative stress tolerance and hormonal crosstalk. [ABSTRACT FROM AUTHOR]

Calcium (Ca2+) mobilization is a central theme in various plant signal transduction pathways. We demonstrate that Arabidopsis thaliana cyclic nucleotide-gated channel 2 (AtCNGC2) is involved in jasmonic acid (JA)-induced apoplastic Ca2+ influx in Arabidopsis epidermal cells. Ca2+ imaging results showed that JA can induce an elevation in the cytosolic cAMP concentration ([cAMP]cyt), reaching a maximum within 3 min. Dibutyryl cAMP (db-cAMP), a cell membrane-permeable analogue of cAMP, induced an increase in the cytosolic Ca2+ concentration ([Ca2+]cyt), with a peak at 4 min. This [Ca2+]cyt increase was triggered by the JA-induced increase in [cAMP]cyt. W-7[N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide], an antagonist of calmodulin, positively modulated the JA-induced increase in [Ca2+]cyt, while W-5[N-(6-aminohexyl)-1-naphthalenesulfonamide], an inactive antagonist of calmodulin, had no apparent effect. db-cAMP and JA positively induced the expression of primary (i.e. JAZ1 and MYC2) and secondary (i.e. VSP1) response genes in the JA signalling pathway in wild-type Arabidopsis thaliana, whereas they had no significant effect in the AtCNGC2 mutant 'defense, no death (dnd1) plants. These data provide evidence that JA first induces the elevation of cAMP, and cAMP, as an activating ligand, activates the AtCNGC2 channel, resulting in apoplastic Ca2+ influx through AtCNGC2. [ABSTRACT FROM AUTHOR]

Levels of the enzymes that produce wound response mediators have to be controlled tightly in unwounded tissues. The Arabidopsis (Arabidopsis thaliana) fatty acid oxygenation up-regulated8 (fou8) mutant catalyzes high rates of α-linolenic acid oxygenation and has higher than wild-type levels of the α-linolenic acid-derived wound response mediator jasmonic acid QA) in undamaged leaves. fou8 produces a null allele in the gene SAL1 (also known as FIERY1 or FRY1). Overexpression of the wild-type gene product had the opposite effect of the null allele, suggesting a regulatory role of SAL1 acting in JA synthesis. The biochemical phenotypes in fous were complemented when the yeast (Saccharomyces cerevisiae) sulfur metabolism 3' (2'), 5' -bisphosphate nucleotidase MET22 was targeted to chloroplasts in fou8. The data are consistent with a role of SAL1 in the chioroplast-localized dephosphorylation of 3' -phospho-5' -adenosine phosphosulfate to 5' -adenosine phosphosulfate or in a closely related reaction (e.g. 3' ,5' -bisphosphate dephosphorylation). Furthermore, the fou8 phenotype was genetically suppressed in a triple mutant (fou8 apk1 apk2) affecting chloroplastic 3'-phospho-5'-adenosine phosphosulfate synthesis. These results show that a nucleotide component of the sulfur futile cycle regulates early steps of JA production and basal JA levels. [ABSTRACT FROM AUTHOR]