P58IPK, a Plant Ortholog of Double-Stranded RNA-Dependent Protein Kinase PKR Inhibitor, Functions in Viral Pathogenesis

AbstractP58IPK is a cellular inhibitor of the mammalian double-stranded RNA-activated protein kinase (PKR). Here we provide evidence for the existence of its homolog in plants and its role in viral infection at the organism level. Viral infection of P58IPK-silenced Nicotiana benthamiana and Arabidopsis knockouts leads to host death. This host cell death is associated with phosphorylation of the α subunit of eukaryotic translation initiation factor (eIF-2α). Loss of P58IPK leads to reduced virus titer, suggesting that wild-type P58IPK protein plays an important role in viral pathogenesis. Although our complementation results using mammalian P58IPK suggest conservation of the P58IPK pathway in plants and animals, its biological significance seems to be different in these two systems. In animals, P58IPK is recruited by the influenza virus to limit PKR-mediated innate antiviral response. In plants, P58IPK is required by viruses for virulence and therefore functions as a susceptibility factor

PLANTS HAVING INCREASED BOMASS AND METHODS FOR MAKING THE SAME

The impact of plastid size change in both monocot and dicot plants has been examined. In both, when plastid size is increased there is an increase in biomass relative to the parental lines. Thus, provided herein are methods for increasing the biomass of a plant, comprising decreasing the expression of at least one plastid division protein in a plant. Optionally, the level of chlorophyll in the plant is also reduced

PLANTS HAVING INCREASED BOMASS AND METHODS FOR MAKING THE SAME

The impact of plastid size change in both monocot and dicot plants has been examined. In both, when plastid size is increased there is an increase in biomass relative to the parental lines. Thus, provided herein are methods for increasing the biomass of a plant, comprising decreasing the expression of at least one plastid division protein in a plant. Optionally, the level of chlorophyll in the plant is also reduced

Biotic stress globally downregulates photosynthesis genes

To determine if damage to foliage by biotic agents, including arthropods, fungi, bacteria and viral pathogens, universally downregulates the expression of genes involved in photosynthesis, we compared transcriptome data from microarray experiments after twenty two different forms of biotic damage on eight different plant species. Transcript levels of photosynthesis light reaction, carbon reduction cycle and pigment synthesis genes decreased regardless of the type of biotic attack. The corresponding upregulation of genes coding for the synthesis of jasmonic acid and those involved in the responses to salicylic acid and ethylene suggest that the downregulation of photosynthesis-related genes was part of a defence response. Analysis of the sub-cellular targeting of co-expressed gene clusters revealed that the transcript levels of 84% of the genes that carry a chloroplast targeting peptide sequence decreased. The majority of these downregulated genes shared common regulatory elements, such as G-box (CACGTG), T-box (ACTTTG) and SORLIP (GCCAC) motifs. Strong convergence in the response of transcription suggests that the universal downregulation of photosynthesis-related gene expression is an adaptive response to biotic attack. We hypothesize that slow turnover of many photosynthetic proteins allows plants to invest resources in immediate defence needs without debilitating near term losses in photosynthetic capacity. © 2010 Blackwell Publishing Ltd.Fil: Bilgin, Damla D.. University of Illinois at Urbana; Estados UnidosFil: Zavala, Jorge Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. University of Illinois at Urbana; Estados Unidos. Universidad Catolica Argentina; Argentina. Universidad de Buenos Aires. Facultad de Agronomía; ArgentinaFil: Zhu, Jin. University of Illinois at Urbana; Estados UnidosFil: Clough, Steven J.. University of Illinois at Urbana; Estados UnidosFil: Ort, Donald R.. University of Illinois at Urbana; Estados UnidosFil: Delucia, Evan H.. University of Illinois at Urbana; Estados Unido

Impact of elevated levels of Atmospheric CO 2 and herbivory on Flavonoids of soybean (Glycine max Linnaeus)

Atmospheric levels of carbon dioxide (CO 2) have been increasing steadily over the last century. Plants grown under elevated CO 2 conditions experience physiological changes, particularly in phytochemical content, that can influence their suitability as food for insects. Flavonoids are important plant defense compounds and antioxidants that can have a large effect on leaf palatability and herbivore longevity. In this study, flavonoid content was examined in foliage of soybean (Glycine max Linnaeus) grown under ambient and elevated levels of CO 2 and subjected to damage by herbivores in three feeding guilds: leaf skeletonizer (Popillia japonica Newman), leaf chewer (Vanessa cardui Linnaeus), and phloem feeder (Aphis glycines Matsumura). Flavonoid content also was examined in foliage of soybean grown under ambient and elevated levels of O 3 and subjected to damage by the leaf skeletonizer P. japonica. The presence of the isoflavones genistein and daidzein and the flavonols quercetin and kaempferol was confirmed in all plants examined, as were their glycosides. All compounds significantly increased in concentration as the growing season progressed. Concentrations of quercetin glycosides were higher in plants grown under elevated levels of CO 2. The majority of compounds in foliage were induced in response to leaf skeletonization damage but remained unchanged in response to non-skeletonizing feeding or phloem-feeding. Most compounds increased in concentration in plants grown under elevated levels of O 3. Insects feeding on G. max foliage growing under elevated levels of CO 2 may derive additional antioxidant benefits from their host plants as a consequence of the change in ratios of flavonoid classes. This nutritional benefit could lead to increased herbivore longevity and increased damage to soybean (and perhaps other crop plants) in the future. © Springer Science+Business Media, LLC 2010.Fil: O'Neill, Bridget F.. University of Illinois; Estados UnidosFil: Zangerl, Arthur R.. University of Illinois; Estados UnidosFil: Dermody, Orla. Pioneer Hi-bred Switzerland S.A.; SuizaFil: Bilgin, Damla D.. University of Illinois; Estados UnidosFil: Casteel, Clare L.. University of Illinois; Estados UnidosFil: Zavala, Jorge Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Biociencias Agrícolas y Ambientales. Universidad de Buenos Aires. Facultad de Agronomía. Instituto de Investigaciones en Biociencias Agrícolas y Ambientales; ArgentinaFil: DeLucia, Evan H.. University of Illinois; Estados UnidosFil: Berenbaum, May R.. University of Illinois; Estados Unido

Complete Transcriptome of the Soybean Root Hair Cell, a Single-Cell Model, and Its Alteration in Response to Bradyrhizobium japonicum Infection1[C][W][OA]

Nodulation is the result of a mutualistic interaction between legumes and symbiotic soil bacteria (e.g. soybean [Glycine max] and Bradyrhizobium japonicum) initiated by the infection of plant root hair cells by the symbiont. Fewer than 20 plant genes involved in the nodulation process have been functionally characterized. Considering the complexity of the symbiosis, significantly more genes are likely involved. To identify genes involved in root hair cell infection, we performed a large-scale transcriptome analysis of B. japonicum-inoculated and mock-inoculated soybean root hairs using three different technologies: microarray hybridization, Illumina sequencing, and quantitative real-time reverse transcription-polymerase chain reaction. Together, a total of 1,973 soybean genes were differentially expressed with high significance during root hair infection, including orthologs of previously characterized root hair infection-related genes such as NFR5 and NIN. The regulation of 60 genes was confirmed by quantitative real-time reverse transcription-polymerase chain reaction. Our analysis also highlighted changes in the expression pattern of some homeologous and tandemly duplicated soybean genes, supporting their rapid specialization

Transcriptional program for nitrogen starvation-induced lipid accumulation in Chlamydomonas reinhardtii.

BackgroundAlgae accumulate lipids to endure different kinds of environmental stresses including macronutrient starvation. Although this response has been extensively studied, an in depth understanding of the transcriptional regulatory network (TRN) that controls the transition into lipid accumulation remains elusive. In this study, we used a systems biology approach to elucidate the transcriptional program that coordinates the nitrogen starvation-induced metabolic readjustments that drive lipid accumulation in Chlamydomonas reinhardtii.ResultsWe demonstrate that nitrogen starvation triggered differential regulation of 2147 transcripts, which were co-regulated in 215 distinct modules and temporally ordered as 31 transcriptional waves. An early-stage response was triggered within 12 min that initiated growth arrest through activation of key signaling pathways, while simultaneously preparing the intracellular environment for later stages by modulating transport processes and ubiquitin-mediated protein degradation. Subsequently, central metabolism and carbon fixation were remodeled to trigger the accumulation of triacylglycerols. Further analysis revealed that these waves of genome-wide transcriptional events were coordinated by a regulatory program orchestrated by at least 17 transcriptional regulators, many of which had not been previously implicated in this process. We demonstrate that the TRN coordinates transcriptional downregulation of 57 metabolic enzymes across a period of nearly 4 h to drive an increase in lipid content per unit biomass. Notably, this TRN appears to also drive lipid accumulation during sulfur starvation, while phosphorus starvation induces a different regulatory program. The TRN model described here is available as a community-wide web-resource at http://networks.systemsbiology.net/chlamy-portal.ConclusionsIn this work, we have uncovered a comprehensive mechanistic model of the TRN controlling the transition from N starvation to lipid accumulation. The program coordinates sequentially ordered transcriptional waves that simultaneously arrest growth and lead to lipid accumulation. This study has generated predictive tools that will aid in devising strategies for the rational manipulation of regulatory and metabolic networks for better biofuel and biomass production