The global temperatures are predicted to rise due to climate change. However, knowledge on the mechanisms underlying the effect of high temperature (HT) on plant pathogen interaction is limited. We investigated the effect of elevated temperature on host phenotypic, biochemical and gene expression patterns in the rice-Magnaporthe oryzae (Mo) pathosystem using two genetic backgrounds, Co39 (Oryzae sativa-indica) and LTH (O. sativa-japonica) with (CO and LT) and without (Co39 and LTH) R gene (Pi54). After exposure to 28°C and 35°C the two genetic backgrounds showed contrasting responses to Mo. At 28°C, CO, Co39 and LTH displayed a more severe disease phenotype than LT. Surprisingly, CO became resistant to Mo after exposure to 35°C. CO and LT were used for further analysis to determine the defence related biochemical and transcriptome changes associated with HT induced resistance. Pre-exposure to 35°C triggered intense callose deposits and cell wall fluorescence of the attacked epidermal cells, as well as, increased hydrogen peroxide (HO) and salicylic acid (SA) levels. Transcriptional changes due to combined stress (35°C+Mo) were largely overridden by pathogen infection in both backgrounds, suggesting that the plants tended to shift their response to the pathogen. However, significant differences in global gene expression patterns occurred between CO and LT in response to both single (35°C and Mo) and double stress (35°C+Mo). Collectively, our results suggest that rice lines carrying Pi54 respond to Mo by rapid induction of callose and HO, and that these resistance mechanisms are amplified at HT. The relative difference in disease severity between CO and LT at 28°C suggests that the genetic background of japonica rice facilitates the function of Pi54 more than the background of indica rice. The phenotypic plasticity and gene expression differences between CO and LT reveal the presence of intricate background specific molecular signatures that may potentially influence adaptation to plant stresses.

Iron nutrition in plants is highly regulated in order to supply amounts sufficient for optimal growth while preventing deleterious effects. In response to iron deficiency, plants induce either reduction-based or chelation-based mechanisms to enhance iron uptake from the soil. Major physiological traits and genes involved in these mechanisms have been fairly well described in model plants like Arabidopsis thaliana (L. Heynh.) and rice (Oryza sativa L.). However, for rice, iron toxicity presents a major challenge worldwide and causes yield reductions because rice is widely cultivated in flooded soils. Nonetheless, rice employs different mechanisms of adaptation to iron-toxicity, which range from avoidance to tissue tolerance. The physiological and molecular bases of such mechanisms have not been fully investigated and their use in breeding for iron-toxicity tolerance remains limited. Efforts to precisely characterise iron-toxicity control mechanisms may help speed-up the development of tolerant rice varieties. Considering how far the understanding of iron dynamics in the soil and plants has progressed, we consider it valuable to exploit such knowledge to improve rice tolerance to iron toxicity. Here we present the mechanisms that regulate iron uptake from the rhizosphere to the plant tissues together with the possible regulators involved. In addition, a genetic model for iron-toxicity tolerance in rice, which hypothesises possible modulation of key genes involved in iron nutrition and regulation is presented. The possibility of incorporating such relevant regulators in breeding is also discussed.

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