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لقد تكاثرت اليوم وسائل التربية في من الخلافة الألعاب الرسوم والصور، أدوات التلوين، أنواع الدف الدفاتر والأقلام، وتقابلها الأغراءات التي : قد تشوه نفسية الطفل، والتي ينشر منها التلفزيون أشكالا عدة، فموقف الأهل من الطفل حاسم إذا عرفوا كيف بر جهونه دون قسر أو بحد أدني من القسر. الواقع أن الأم التي تهب ذاتها كلها لطفلها وهذا نادر يمكن ان تكشف تلقائيا حاجات الطفل تقريبا كلها، يلزمها فقط مسعف في كشوفها، وكتابنا هذا هو دليلها ودليل الأب إلى أطفالهما، وفيه ما يستفهما في التعرف على أطفالهما عندما تتكاثر اشغالهما فلا يعيران للطفل الوقت اللازم لتربيته.
Book
Glutamate triggers long-distance, calcium-based plant defense signaling
A plant injured on one leaf by a nibbling insect can alert its other leaves to begin anticipatory defense responses. Working in the model plant Arabidopsis , Toyota et al. show that this systemic signal begins with the release of glutamate, which is perceived by glutamate receptor–like ion channels (see the Perspective by Muday and Brown-Harding). The ion channels then set off a cascade of changes in calcium ion concentration that propagate through the phloem vasculature and through intercellular channels called plasmodesmata. This glutamate-based long-distance signaling is rapid: Within minutes, an undamaged leaf can respond to the fate of a distant leaf. Science , this issue p. 1112 ; see also p. 1068 Wounded plant cells leak l -glutamate, triggering plant-wide Ca 2+ signaling events through glutamate receptor–like channels. Animals require rapid, long-range molecular signaling networks to integrate sensing and response throughout their bodies. The amino acid glutamate acts as an excitatory neurotransmitter in the vertebrate central nervous system, facilitating long-range information exchange via activation of glutamate receptor channels. Similarly, plants sense local signals, such as herbivore attack, and transmit this information throughout the plant body to rapidly activate defense responses in undamaged parts. Here we show that glutamate is a wound signal in plants. Ion channels of the GLUTAMATE RECEPTOR–LIKE family act as sensors that convert this signal into an increase in intracellular calcium ion concentration that propagates to distant organs, where defense responses are then induced.
Journal Article
Regulation of growth–defense balance by the JASMONATE ZIM-DOMAIN (JAZ)-MYC transcriptional module
The plant hormone jasmonate (JA) promotes the degradation of JASMONATE ZIM-DOMAIN (JAZ) proteins to relieve repression on diverse transcription factors (TFs) that execute JA responses. However, little is known about how combinatorial complexity among JAZ–TF interactions maintains control over myriad aspects of growth, development, reproduction, and immunity.
We used loss-of-function mutations to define epistatic interactions within the core JA signaling pathway and to investigate the contribution of MYC TFs to JA responses in Arabidopsis thaliana.
Constitutive JA signaling in a jaz quintuple mutant (jazQ) was largely eliminated by mutations that block JA synthesis or perception. Comparison of jazQ and a jazQ myc2 myc3 myc4 octuple mutant validated known functions of MYC2/3/4 in root growth, chlorophyll degradation, and susceptibility to the pathogen Pseudomonas syringae. We found that MYC TFs also control both the enhanced resistance of jazQ leaves to insect herbivory and restricted leaf growth of jazQ. Epistatic transcriptional profiles mirrored these phenotypes and further showed that triterpenoid biosynthetic and glucosinolate catabolic genes are up-regulated in jazQ independently of MYC TFs.
Our study highlights the utility of genetic epistasis to unravel the complexities of JAZ–TF interactions and demonstrates that MYC TFs exert master control over a JAZ-repressible transcriptional hierarchy that governs growth–defense balance.
Journal Article
Rewiring of jasmonate and phytochrome B signalling uncouples plant growth-defense tradeoffs
Plants resist infection and herbivory with innate immune responses that are often associated with reduced growth. Despite the importance of growth-defense tradeoffs in shaping plant productivity in natural and agricultural ecosystems, the molecular mechanisms that link growth and immunity are poorly understood. Here, we demonstrate that growth-defense tradeoffs mediated by the hormone jasmonate are uncoupled in an
Arabidopsis
mutant (
jazQ phyB
) lacking a quintet of Jasmonate ZIM-domain transcriptional repressors and the photoreceptor phyB. Analysis of epistatic interactions between
jazQ
and
phyB
reveal that growth inhibition associated with enhanced anti-insect resistance is likely not caused by diversion of photoassimilates from growth to defense but rather by a conserved transcriptional network that is hardwired to attenuate growth upon activation of jasmonate signalling. The ability to unlock growth-defense tradeoffs through relief of transcription repression provides an approach to assemble functional plant traits in new and potentially useful ways.
Plant immune responses are often associated with reduced growth. Here, the authors show that combining mutations in transcriptional repressors of the defense and light perception pathways can confer both robust growth and strong herbivore defense, demonstrating that growth-defense tradeoffs can be uncoupled.
Journal Article
Two Abscisic Acid-Responsive Plastid Lipase Genes Involved in Jasmonic Acid Biosynthesis in Arabidopsis thaliana
Chloroplast membranes with their unique lipid composition are crucial for photosynthesis. Maintenance of the chloroplast membranes requires finely tuned lipid anabolic and catabolic reactions. Despite the presence of a large number of predicted lipid-degrading enzymes in the chloroplasts, their biological functions remain largely unknown. Recently, we described PLASTID LIPASE1 (PLIP1), a plastid phospholipase A1 that contributes to seed oil biosynthesis. The Arabidopsis thaliana genome encodes two putative PLIP1 paralogs, which we designated PLIP2 and PLIP3. PLIP2 and PLIP3 are also present in the chloroplasts, but likely with different subplastid locations. In vitro analysis indicated that both are glycerolipid A1 lipases. In vivo, PLIP2 prefers monogalactosyldiacylglycerol as substrate and PLIP3 phosphatidylglycerol. Overexpression of PLIP2 or PLIP3 severely reduced plant growth and led to accumulation of the bioactive form of jasmonate and related oxylipins. Genetically blocking jasmonate perception restored the growth of the PLIP2/3-overexpressing plants. The expression of PLIP2 and PLIP3, but not PLIP1, was induced by abscisic acid (ABA), and plip1 plip2 plip3 triple mutants exhibited compromised oxylipin biosynthesis in response to ABA. The plip triple mutants also showed hypersensitivity to ABA. We propose that PLIP2 and PLIP3 provide a mechanistic link between ABA-mediated abiotic stress responses and oxylipin signaling.
Journal Article
Insect herbivory antagonizes leaf cooling responses to elevated temperature in tomato
As global climate change brings elevated average temperatures and more frequent and extreme weather events, pressure from biotic stresses will become increasingly compounded by harsh abiotic stress conditions. The plant hormone jasmonate (JA) promotes resilience to many environmental stresses, including attack by arthropod herbivores whose feeding activity is often stimulated by rising temperatures. How wound-induced JA signaling affects plant adaptive responses to elevated temperature (ET), however, remains largely unknown. In this study, we used the commercially important crop plant Solanum lycopersicum (cultivated tomato) to investigate the interaction between simulated heat waves and wound-inducible JA responses. We provide evidence that the heat shock protein HSP90 enhances wound responses at ET by increasing the accumulation of the JA receptor, COI1. Wound-induced JA responses directly interfered with short-term adaptation to ET by blocking leaf hyponasty and evaporative cooling. Specifically, leaf damage inflicted by insect herbivory or mechanical wounding at ET resulted in COI1-dependent stomatal closure, leading to increased leaf temperature, lower photosynthetic carbon assimilation rate, and growth inhibition. Pharmacological inhibition of HSP90 reversed these effects to recapitulate the phenotype of a JA-insensitive mutant lacking the COI1 receptor. As climate change is predicted to compound biotic stress with larger and more voracious arthropod pest populations, our results suggest that antagonistic responses resulting from a combination of insect herbivory and moderate heat stress may exacerbate crop losses.
Journal Article
COI1 is a critical component of a receptor for jasmonate and the bacterial virulence factor coronatine
Jasmonate (JA) is a lipid-derived hormone that regulates diverse aspects of plant immunity and development. An amino acid-conjugated form of JA, jasmonoyl-isoleucine (JA-Ile), stimulates binding of the F-box protein coronatine-insensitive 1 (COI1) to, and subsequent ubiquitin-dependent degradation of, jasmonate ZIM domain (JAZ) proteins that repress transcription of JA-responsive genes. The virulence factor coronatine (COR), which is produced by plant pathogenic strains of Pseudomonas syringae, suppresses host defense responses by activating JA signaling in a COI1-dependent manner. Although previous data indicate that COR acts as a molecular mimic of JA-Ile, the mechanism by which JA-Ile and COR are perceived by plant cells remains unknown. Here, we show that interaction of tomato COI1 with divergent members of the JAZ family is highly specific for JA-Ile and structurally related JA conjugates and that COR is [almost equal to]1,000-fold more active than JA-Ile in promoting this interaction in vitro. JA-Ile competes for binding of COR to COI1-JAZ complexes, demonstrating that COR and JA-Ile are recognized by the same receptor. Binding of COR to the COI1-JAZ complex requires COI1 and is severely impaired by a point mutation in the putative ligand-binding pocket of COI1. Finally, we show that the C-terminal region of JAZ3 containing the highly conserved Jas motif is necessary and sufficient for hormone-induced COI1-JAZ interaction. These findings demonstrate that COI1 is a critical component of the JA receptor and that COR exerts its virulence effects by functioning as a potent agonist of this receptor system.
Journal Article
Cytochrome P450 CYP94B3 mediates catabolism and inactivation of the plant hormone jasmonoyl-L-isoleucine
The phytohormone jasmonoyl-L-isoleucine (JA-Ile) signals through the COI1-JAZ coreceptor complex to control key aspects of plant growth, development, and immune function. Despite detailed knowledge of the JA-Ile biosynthetic pathway, little is known about the genetic basis of JA-Ile catabolism and inactivation. Here, we report the identification of a wound- and jasmonate-responsive gene from Arabidopsis that encodes a cytochrome P450 (CYP94B3) involved in JA-Ile turnover. Metabolite analysis of wounded leaves showed that loss of CYP94B3 function in cyp94b3 mutants causes hyperaccumulation of JA-Ile and concomitant reduction in 12-hydroxy-JA-Ile (12OH-JA-Ile) content, whereas overexpression of this enzyme results in severe depletion of JA-Ile and corresponding changes in 12OH-JA-Ile levels. In vitro studies showed that heterologously expressed CYP94B3 converts JA-Ile to 12OH-JA-Ile, and that 12OH-JA-Ile is less effective than JA-Ile in promoting the formation of COI1-JAZ receptor complexes. CYP94B3-overexpressing plants displayed phenotypes indicative of JA-Ile deficiency, including defects in male fertility, resistance to jasmonate-induced growth inhibition, and susceptibility to insect attack. Increased accumulation of JA-Ile in wounded cyp94b3 leaves was associated with enhanced expression of jasmonate-responsive genes. These results demonstrate that CYP94B3 exerts negative feedback control on JA-Ile levels and performs a key role in attenuation of jasmonate responses.
Journal Article