Wirelessly powering: An enabling technology for zero-power sensors, IoT and D2D communication

Wireless power transfer (WPT) is foreseen as a key enabling technology for energy-autonomous wireless sensors, Internet of Things and Device to Device communication. RF energy, either scavenged from the ambient or intentionally provided to a wireless device, can be successfully exploited for autonomously sustaining its operations. In this paper we overview the main aspects to be addressed for a successful design of a far-field WPT system. The end-to-end circuit level co-design of the WPT link is described as the procedure to effectively address the system optimum efficiency. Specific selection of antenna elements and active sub-circuits are analyzed, depending on the power levels involved and on the specific application environment. The base-band design of the power management unit used to dynamically provide the receiver with optimum loading conditions is also analyzed

Abscisic acid-independent and abscisic acid-dependent regulation of proline biosynthesis following cold and osmotic stresses in Arabidopsis thaliana

The role of the phytohormone abscisic acid (ABA) in the regulation of proline synthesis was investigated by following the expression of the At-PSS and At-P5R proline biosynthesis genes in Arabidopsis thaliana wild type, in an ABA-deficient ubal-1 mutant as well as in ABA-insensitive abil-1 and abi2-1 mutants after ABA, cold and osmotic stress treatments. In wild-type and in ABA mutant seedlings, 50 mu M ABA or osmotic stress treatment triggered expression of At-P5S, whereas At-P5R accumulation was scarcely detectable. Expression of either gene was mediated by endogenous ABA since transcript levels were similar in wild-type and in ABA-deficient mutant plants. Proline accumulated to a greater extent after osmotic stress than upon ABA or cold treatment. Thus. ABA-treated abil-1 mutant plants accumulated less proline than the ABA-treated wild type. Upon salt stress, proline accumulated to a lesser extent in abal-1 and abil-1 mutant plants, suggesting an indirect role of ABA on proline accumulation during salt adaptation of the plant. These results indicate that the expression of the genes of the proline biosynthetic pathway is ABA independent upon cold and osmotic treatments, although their expression can be triggered by exogenously applied ABA. However, the endogenous ABA content may affect proline accumulation upon salt stress, suggesting post-transcriptional control of proline biosynthesis in response to NaCl

Abscisic acid independent and abscisic acid dependent regulation of the proline biosynthesis upon cold and osmotic stresses in Arabidopsis thaliana

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Current advances in abscisic acid action and signalling

International audienceAbscisic acid (ABA) participates in the control of diverse physiological processes. The characterization of deficient mutants has clarified the ABA biosynthetic pathway in higher plants. Deficient mutants also lead to a revaluation of the extent of ABA action during seed development and in the response of vegetative tissues to environmental stress. Although ABA receptor(s) have not yet been identified, considerable progress has been recently made in the characterization of more downstream elements of the ABA regulatory network. ABA controls stomatal aperture by rapidly regulating identified ion transporters in guard cells, and the details of the underlying signalling pathways start to emerge. ABA actions in other cell types involve modifications of gene expression. The promoter analysis of ABA-responsive genes has revealed a diversity of cis-acting elements and a few associated trans-acting factors have been isolated. Finally, characterization of mutants defective in ABA responsiveness, and molecular cloning of the corresponding loci, has proven to be a powerful approach to dissect the molecular nature of ABA signalling cascades

Cytosolic abscisic acid activates guard cell anion channels without preceding Ca(2+) signals

The phytohormone abscisic acid (ABA) reports on the water status of the plant and induces stomatal closure. Guard cell anion channels play a central role in this response, because they mediate anion efflux, and in turn, cause a depolarization-induced K(+) release. We recorded early steps in ABA signaling, introducing multibarreled microelectrodes in guard cells of intact plants. Upon external ABA treatment, anion channels transiently activated after a lag phase of ≈2 min. As expected for a cytosolic ABA receptor, iontophoretic ABA loading into the cytoplasm initiated a rise in anion current without delay. These ABA responses could be elicited repetitively at resting and at largely depolarized potentials (e.g., 0 mV), ruling out signal transduction by means of hyperpolarization-activated calcium channels. Likewise, ABA stimulation did not induce a rise in the cytosolic free-calcium concentration. However, the presence of ≈100 nM background Ca(2+) was required for anion channel function, because the action of ABA on anion channels was repressed after loading of the Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetate. The chain of events appears very direct, because none of the tested putative ABA-signaling intermediates (inositol 1,4,5 trisphosphate, inositol hexakisphosphate, nicotinic acid adenine dinucleotide phosphate, and cyclic ADP-ribose), could mimic ABA as anion channel activator. In patch-clamp experiments, cytosolic ABA also evoked anion current transients carried by R- and S-type anion channels. The response was dose-dependent with half-maximum activation at 2.6 μM ABA. Our studies point to an ABA pathway initiated by ABA binding to a cytosolic receptor that within seconds activates anion channels, and in turn, leads to depolarization of the plasma membrane

The abi1-1 mutation blocks ABA signaling downstream of cADPR action

Arabidopsis thaliana abscisic acid insensitive 1-1 (abi1-1) is a dominant mutant that is insensitive to the inhibition of germination and growth by the plant hormone, abscisic acid (ABA). The mutation severely decreases the catalytic activity of the ABI1 type 2C protein phosphatase (PP2C). However, the site of action of the abi1-1/ABI1 in the ABA signal transduction pathway has not yet been determined. Using single cell assays, we showed that microinjecting mutant abi1-1 protein inhibited the activation of RD29A-GUS and KIN2-GUS in response to ABA, cyclic ADP-ribose (cADPR), and Ca2+. The inhibitory effect of the mutant protein, however, was reversed by co-microinjection of an excess amount of the ABI1 protein. In transgenic Arabidopsis plants, overexpression of abi1-1 rendered the plants insensitive to ABA during germination, whereas overexpression of ABI1 did not have any apparent effect. Moreover, transgenic plants overexpressing abi1-1 were blocked in the induction of ABA-responsive genes; however, overexpression of ABI1 did not affect gene expression. Taken together, our results demonstrate that abi1-1 is likely to be a dominant negative mutation and ABI1 likely acts downstream of cADPR in the ABA-signaling pathway. Our results on ABI1 overexpression in Arabidopsis are not compatible with a negative regulatory role of this phosphatase in ABA responses