Rapid modification of the insect elicitor N-linolenoyl-glutamate via a lipoxygenase-mediated mechanism on Nicotiana attenuata leaves

<p>Abstract</p> <p>Background</p> <p>Some plants distinguish mechanical wounding from herbivore attack by recognizing specific constituents of larval oral secretions (OS) which are introduced into plant wounds during feeding. Fatty acid-amino acid conjugates (FACs) are major constituents of <it>Manduca sexta </it>OS and strong elicitors of herbivore-induced defense responses in <it>Nicotiana attenuata </it>plants.</p> <p>Results</p> <p>The metabolism of one of the major FACs in <it>M. sexta </it>OS, <it>N</it>-linolenoyl-glutamic acid (18:3-Glu), was analyzed on <it>N. attenuata </it>wounded leaf surfaces. Between 50 to 70% of the 18:3-Glu in the OS or of synthetic 18:3-Glu were metabolized within 30 seconds of application to leaf wounds. This heat-labile process did not result in free α-linolenic acid (18:3) and glutamate but in the biogenesis of metabolites both more and less polar than 18:3-Glu. Identification of the major modified forms of this FAC showed that they corresponded to 13-hydroxy-18:3-Glu, 13-hydroperoxy-18:3-Glu and 13-oxo-13:2-Glu. The formation of these metabolites occurred on the wounded leaf surface and it was dependent on lipoxygenase (LOX) activity; plants silenced in the expression of <it>NaLOX2 </it>and <it>NaLOX3 </it>genes showed more than 50% reduced rates of 18:3-Glu conversion and accumulated smaller amounts of the oxygenated derivatives compared to wild-type plants. Similar to 18:3-Glu, 13-oxo-13:2-Glu activated the enhanced accumulation of jasmonic acid (JA) in <it>N. attenuata </it>leaves whereas 13-hydroxy-18:3-Glu did not. Moreover, compared to 18:3-Glu elicitation, 13-oxo-13:2-Glu induced the differential emission of two monoterpene volatiles (β-pinene and an unidentified monoterpene) in ir<it>lox2 </it>plants.</p> <p>Conclusions</p> <p>The metabolism of one of the major elicitors of herbivore-specific responses in <it>N. attenuata </it>plants, 18:3-Glu, results in the formation of oxidized forms of this FAC by a LOX-dependent mechanism. One of these derivatives, 13-oxo-13:2-Glu, is an active elicitor of JA biosynthesis and differential monoterpene emission.</p

Small-Signal Stability Analysis for Droop-Controlled Inverter-based Microgrids with Losses and Filtering

An islanded microgrid supplied by multiple distributed energy resources (DERs) often employs droop-control mechanisms for power sharing. Because microgrids do not include inertial elements, and low pass filtering of noisy measurements introduces lags in control, droop-like controllers may pose significant stability concerns. This paper aims to understand the effects of droop-control on the small-signal stability and transient response of the microgrid. Towards this goal, we present a compendium of results on the small-signal stability of droop-controlled inverter-based microgrids with heterogeneous loads, which distinguishes: (1) lossless vs. lossy networks; (2) droop mechanisms with and without filters, and (3) mesh vs. radial network topologies. Small-signal and transient characteristics are also studied using multiple simulation studies on IEEE test system

Silencing COI1 in Rice Increases Susceptibility to Chewing Insects and Impairs Inducible Defense

The jasmonic acid (JA) pathway plays a key role in plant defense responses against herbivorous insects. CORONATINE INSENSITIVE1 (COI1) is an F-box protein essential for all jasmonate responses. However, the precise defense function of COI1 in monocotyledonous plants, especially in rice (Oryza sativa L.) is largely unknown. We silenced OsCOI1 in rice plants via RNA interference (RNAi) to determine the role of OsCOI1 in rice defense against rice leaf folder (LF) Cnaphalocrocis medinalis, a chewing insect, and brown planthopper (BPH) Nilaparvata lugens, a phloem-feeding insect. In wild-type rice plants (WT), the transcripts of OsCOI1 were strongly and continuously up-regulated by LF infestation and methyl jasmonate (MeJA) treatment, but not by BPH infestation. The abundance of trypsin protease inhibitor (TrypPI), and the enzymatic activities of polyphenol oxidase (PPO) and peroxidase (POD) were enhanced in response to both LF and BPH infestation, but the activity of lipoxygenase (LOX) was only induced by LF. The RNAi lines with repressed expression of OsCOI1 showed reduced resistance against LF, but no change against BPH. Silencing OsCOI1 did not alter LF-induced LOX activity and JA content, but it led to a reduction in the TrypPI content, POD and PPO activity by 62.3%, 48.5% and 27.2%, respectively. In addition, MeJA-induced TrypPI and POD activity were reduced by 57.2% and 48.2% in OsCOI1 RNAi plants. These results suggest that OsCOI1 is an indispensable signaling component, controlling JA-regulated defense against chewing insect (LF) in rice plants, and COI1 is also required for induction of TrypPI, POD and PPO in rice defense response to LF infestation

Stat3 controls cell death during mammary gland involution by regulating uptake of milk fat globules and lysosomal membrane permeabilization.

We have previously demonstrated that Stat3 regulates lysosomal-mediated programmed cell death (LM-PCD) during mouse mammary gland involution in vivo. However, the mechanism that controls the release of lysosomal cathepsins to initiate cell death in this context has not been elucidated. We show here that Stat3 regulates the formation of large lysosomal vacuoles that contain triglyceride. Furthermore, we demonstrate that milk fat globules (MFGs) are toxic to epithelial cells and that, when applied to purified lysosomes, the MFG hydrolysate oleic acid potently induces lysosomal leakiness. Additionally, uptake of secreted MFGs coated in butyrophilin 1A1 is diminished in Stat3-ablated mammary glands and loss of the phagocytosis bridging molecule MFG-E8 results in reduced leakage of cathepsins in vivo. We propose that Stat3 regulates LM-PCD in mouse mammary gland by switching cellular function from secretion to uptake of MFGs. Thereafter, perturbation of lysosomal vesicle membranes by high levels of free fatty acids results in controlled leakage of cathepsins culminating in cell death.This work was supported by a grant from the Medical Research Council programme grant no. MR/J001023/1 (T.J.S. and B. L-L.) and a Cancer Research UK Cambridge Cancer Centre PhD studentship (H.K.R.).This is the accepted manuscript. The final version is available from Nature Publishing at http://www.nature.com/ncb/journal/vaop/ncurrent/full/ncb3043.html

Face to Facebook: Social media and the learning and teaching potential of symmetrical, sychronous communication

Social networking offers teachers and learners exciting opportunities to communicate. Web 2.0 and its synchronous communications platforms provide new avenues for teachers to deliver curriculum and facilitate learning. Further, they provide new avenues for students to engage and intensify their own learning. Being able to chat in real-time with a teacher, usually via face-to-face discussions, is something that many students studying in on-campus (or day) mode take for granted, and is something that distance or off-campus students are generally unable to experience. In the evolving, flexible-learning tertiary environment, viable and effective computer mediated communication (CMC) alternatives to face-to-face teaching need to be explored. These alternatives will only work if they prove useful to students. This article considers student reactions to social media as a teaching tool, probing its benefits and limitations. Over the course of a semester, third year on- and off-campus students communicated with an academic, outside lecture times, via the social networking site facebook®. Students were allowed to ask any questions they had that related to the unit. At the end of the semester students were provided with a 10-item questionnaire asking them to evaluate their experience. This study looked at a specific aspect of social networking — synchronous text-based chat — and the students’ perceptions of its usefulness for their learning

Whiteflies glycosylate salicylic acid and secrete the conjugate via their honeydew

During insect feeding, a complex interaction takes place at the feeding site, with plants deciphering molecular information associated with the feeding herbivore, resulting in the upregulation of the appropriate defenses, and the herbivore avoiding or preventing these defenses from taking effect. Whiteflies can feed on plants without causing significant damage to mesophyll cells, making their detection extra challenging for the plant. However, whiteflies secrete honeydew that ends up on the plant surface at the feeding site and on distal plant parts below the feeding site. We reasoned that this honeydew, since it is largely of plant origin, may contain molecular information that alerts the plant, and we focused on the defense hormone salicylic acid (SA). First, we analyzed phloem sap from tomato plants, on which the whiteflies are feeding, and found that it contained salicylic acid (SA). Subsequently, we determined that in honeydew more than 80% of SA was converted to its glycoside (SAG). When whiteflies were allowed to feed from an artificial diet spiked with labeled SA, labeled SAG also was produced. However, manually depositing honeydew on undamaged plants resulted still in a significant increase in endogenous free SA. Accordingly, transcript levels of PR1a, an SA marker gene, increased whereas those of PI-II, a jasmonate marker gene, decreased. Our results indicate that whiteflies manipulate the SA levels within their secretions, thus influencing the defense responses in those plant parts that come into contact with honeydew