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Background Bois noir is an important disease of grapevine (Vitis vinifera L.), caused by phytoplasmas. An interesting, yet elusive aspect of the bois noir disease is “recovery”, i.e., the spontaneous and unpredictable remission of symptoms and damage. Because conventional pest management is ineffective against bois noir, deciphering the molecular bases of recovery is beneficial. The present study aimed to understand whether salicylate- and jasmonate-defence pathways might have a role in the recovery from the bois noir disease of grapevine.ResultsLeaves from healthy, bois noir-diseased and bois noir-recovered plants were compared, both in the presence (late summer) and absence (late spring) of bois noir symptoms on the diseased plants. Analyses of salicylate and jasmonate contents, as well as the expression of genes involved in their biosynthesis, signalling and action, were evaluated. In symptomatic diseased plants (late summer), unlike symptomless plants (late spring), salicylate biosynthesis was increased and salicylate-responsive genes were activated. In contrast, jasmonate biosynthesis and signalling genes were up-regulated both in recovered and diseased plants at all sampling dates. The activation of salicylate signalling in symptomatic plants might have antagonised the jasmonate-mediated defence response by suppressing the expression of jasmonate-responsive genes.ConclusionsOur results suggest that grapevine reacts to phytoplasma infection through salicylate-mediated signalling, although the resultant full activation of a salicylate-mediated response is apparently ineffective in conferring resistance against bois noir disease. Activation of the salicylate signalling pathway that is associated with the presence of bois noir phytoplasma seems to antagonise the jasmonate defence response, by failing to activate or suppressing both the expression of some jasmonate responsive genes that act downstream of the jasmonate biosynthetic pathway, as well as the first events of the jasmonate signalling pathway. On the other hand, activation of the entire jasmonate signalling pathway in recovered plants suggests the potential importance of jasmonate-regulated defences in preventing bois noir phytoplasma infections and the subsequent development of bois noir disease. Thus, on one hand, recovery could be achieved and maintained over time by preventing the activation of defence genes associated with salicylate signalling, and on the other hand, by activating jasmonate signalling and other defence responses.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-017-1069-4) contains supplementary material, which is available to authorized users.

The effect of iron (Fe) and sulphur (S) deprivation on sulphate uptake and assimilation pathways was investigated in durum wheat by analysing the expression of genes coding for major transporters and enzymes involved in sulphate assimilation and reduction: high-affinity sulphate transporters (TdSultr1.1 and TdSultr1.3), ATP sulphurylase (TdATPSul1 and TdATPSul2), APS reductase (TdAPR), sulphite reductase (TdSiR), O-acetylserine(thiol)lyase (TdOASTL1 and TdOASTL2), and serine acetyltransferase (TdSAT1 and TdSAT2). Further experiments were carried out to detect changes in the activities of these enzymes, together with the evaluation of growth parameters (fresh biomass accumulation, leaf green values, and total S, thiol, and Fe concentrations). Fe shortage in wheat plants under adequate S nutrition resulted in an S deficiency-like response. Most of the genes of the S assimilatory pathway induced by S deprivation (TdATPSul1, TdAPR, TdSir, TdSAT1, and TdSAT2) were also significantly up-regulated after the imposition of the Fe limitation under S-sufficient conditions. However, the differential expression of genes encoding the two high-affinity transporters (TdSultr1.1 and TdSultr1.3) indicates that the mechanisms of sulphate uptake regulation under Fe and S deficiency are different in wheat. Moreover, it was observed that the mRNA level of genes encoding ATPS, APR, and OASTL and the corresponding enzyme activities were often uncoupled in response to Fe and S availability, indicating that most probably their regulation involves a complex interplay of transcriptional, translational, and/or post-translational mechanisms induced by S and/or Fe deficiency.

Characterization of the relationship between sulfur and iron in both Strategy I and Strategy II plants, has proven that low sulfur availability often limits plant capability to cope with iron shortage. Here it was investigated whether the adaptation to iron deficiency in tomato (Solanum lycopersicum L.) plants was associated with an increased root sulfate uptake and translocation capacity, and modified dynamics of total sulfur and thiols accumulation between roots and shoots. Most of the tomato sulfate transporter genes belonging to Groups 1, 2, and 4 were significantly upregulated in iron-deficient roots, as it commonly occurs under S-deficient conditions. The upregulation of the two high affinity sulfate transporter genes, SlST1.1 and SlST1.2, by iron deprivation clearly suggests an increased root capability to take up sulfate. Furthermore, the upregulation of the two low affinity sulfate transporter genes SlST2.1 and SlST4.1 in iron-deficient roots, accompanied by a substantial accumulation of total sulfur and thiols in shoots of iron-starved plants, likely supports an increased root-to-shoot translocation of sulfate. Results suggest that tomato plants exposed to iron-deficiency are able to change sulfur metabolic balance mimicking sulfur starvation responses to meet the increased demand for methionine and its derivatives, allowing them to cope with this stress.

This study addresses the question of the interference between iron (Fe) nutrition and cadmium (Cd) toxicity at the level of growth performance, phytosiderophores (PS) release, micronutrient accumulation and expression of genes involved in Fe homeostasis in barley seedlings, a plant with strategy II-based response to Fe shortage. Cd exposure induced responses similar to those of genuine Fe deficiency also in Fe-sufficient plants. Most genes involved in PS biosynthesis and secretion (HvNAS3, HvNAS4, HvNAS6, HvNAS7, HvNAAT-A, HvDMAS1 and HvTOM1) induced by Fe deprivation were also significantly upregulated in the presence of Cd under Fe sufficient conditions. Accordingly, the enhanced expression of these genes in roots under Cd exposure was accompanied by an increase of PS release. However, induced expression of HvIRO2 and the downregulation of HvIDEF1 and HvIRT1, after Cd exposure, suggested the presence of a pathway that induces HvIRO2-mediated PS biosynthesis under Cd stress, which probably is not simply caused by Fe deficiency. The downregulation of HvIRT1 and HvNramp5 may represent a protective mechanism at transcriptional level against further Cd uptake by these transporters. These results likely indicate that Cd itself may be able to activate Fe acquisition mechanism in an Fe-independent manner.