Plants can reorient their organs in response to changes in environmental conditions. In some species, ethylene can induce resource-directed growth by stimulating a more vertical orientation of the petioles (hyponasty) and enhanced elongation. In this study on Arabidopsis (Arabidopsis thaliana), we show significant natural variation in ethylene-induced petiole elongation and hyponastic growth. This hyponastic growth was rapidly induced and also reversible because the petioles returned to normal after ethylene withdrawal. To unravel the mechanisms behind the natural variation, two contrasting accessions in ethylene-induced hyponasty were studied in detail. Columbia-0 showed a strong hyponastic response to ethylene, whereas this response was almost absent in Landsberg erecta (Ler). To test whether Ler is capable of showing hyponastic growth at all, several signals were applied. From all the signals applied, only spectrally neutral shade (20 mmol m 22 s 21) could induce a strong hyponastic response in Ler. Therefore, Ler has the capacity for hyponastic growth. Furthermore, the lack of ethylene-induced hyponastic growth in Ler is not the result of already-saturating ethylene production rates or insensitivity to ethylene, as an ethylene-responsive gene was up-regulated upon ethylene treatment in the petioles. Therefore, we conclude that Ler is missing an essential component between the primary ethylene signal transduction chain and a downstream part of the hyponastic growth signal transduction pathway.

The plant hormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) play crucial roles in the signaling network that regulates induced defense responses against biotic stresses. Antagonism between SA and JA operates as a mechanism to finetune defenses that are activated in response to multiple attackers. In Arabidopsis (Arabidopsis thaliana), NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) was demonstrated to be required for SA-mediated suppression of JA-dependent defenses. Because ET is known to enhance SA/NPR1-dependent defense responses, we investigated the role of ET in the SA-JA signal interaction. Pharmacological experiments with gaseous ET and the ET precursor 1-aminocyclopropane-1-carboxylic acid showed that ET potentiated SA/NPR1-dependent PATHOGENESIS-RELATED1 transcription, while it rendered the antagonistic effect of SA on methyl jasmonate-induced PDF1.2 and VSP2 expression NPR1 independent. This overriding effect of ET on NPR1 function in SA-JA cross talk was absent in the npr1-1/ein2-1 double mutant, demonstrating that it is mediated via ET signaling. Abiotic and biotic induction of the ET response similarly abolished the NPR1 dependency of the SA-JA signal interaction. Furthermore, JA-dependent resistance against biotic attackers was antagonized by SA in an NPR1-dependent fashion only when the plant-attacker combination did not result in the production of high levels of endogenous ET. Hence, the interaction between ET and NPR1 plays an important modulating role in the fine tuning of the defense signaling network that is activated upon pathogen and insect attack. Our results suggest a model in which ET modulates the NPR1 dependency of SA-JA antagonism, possibly to compensate for enhanced allocation of NPR1 to function in SA-dependent activation of PR genes.

The possible interference when measuring gas exchange with respiratory CO 2 produced under the gasket of commercially available clamp-on leaf chambers was investigated. Two of these chambers were compared with a leaf chamber that accommodated an entire leaf without clamping it under a gasket. An overestimation of dark respiration rate ( R D ) by 55% was found with Plantago major leaves, a species with homobaric leaves that have high resistance for lateral gaseous transport. The percentage was similar in the heterobaric Ficus benjamina , but was 32% in the highly porous homobaric Nicotiana tabacum . Net photosynthetic rate at low photon flux density was underestimated by 35% in the clamp-on chamber. However, the gasket effect was not detectable at light saturation because the error was small in comparison with the high photosynthetic rates. Estimation of respiration in the light ( R L ) in Nicotiana as derived from CO 2 exchange at low CO 2 concentrations was complicated by three factors. The inward diffusion of respiratory CO 2 from under the gasket was added to a diffusion of CO 2 from outside through the gasket material and through the leaf, which produced an even larger error in R L in comparison with R D at ambient CO 2 . These errors are significant for estimations of carbon gain at whole plant and canopy level and also at the leaf level when photosynthetic rates are low. Possible improvements in gasket design and corrections of CO 2 exchange measurements for the gasket effect are discussed.