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Reference Collections Management Reference: Usually dispatched within 1 week Details. About this book This book will awaken the interest of breeders, phytopathologists, environmentalists, extension services, plant virologists, entomologists and molecular biologists. The Bemisia tabaci complex: Survival of whiteflies during long distance transportation of agricultural products and plants; P. The Tomato yellow leaf curl virus genome; B.

Development of a New Molecular Marker for the Resistance to Tomato Yellow Leaf Curl Virus

Molecular biodiversity, taxonomy and nomenclature of Tomato yellow leaf curl-like viruses; M. Replication of geminiviruses and the use of rolling circle amplification for their diagnosis; H. Interactions of Tomato yellow leaf curl virus with its whitefly vector; H. Localization of Tomato yellow leaf curl virus in its whitefly vector; M. Localization of Tomato yellow leaf curl viruses in the infected plant; C. Biotic and abiotic stress responses in tomato breeding lines resistant and susceptible to Tomato yellow leaf curl virus; R. Integrated Pest Management measures and protection of tomato cultures.

The management of Tomato yellow leaf curl virus in greenhouses and the open field, a strategy of manipulation; Y. Introduction of Tomato yellow leaf curl virus into the Dominican Republic: Natural and engineered resistance. Sources of resistance, inheritance, and location of genetic loci conferring resistance to members of the tomato-infecting begomoviruses; Y. Exploitation of resistance genes found in wild tomato species to produce resistant cultivars; pile up of resistant genes; F. Gene silencing of Tomato yellow leaf curl virus; G. International networks to deal with Tomato yellow leaf curl disease: AVRDC's international networks to deal with the Tomato yellow leaf curl disease -- the needs of developing countries; S.

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1. Introduction

Be the first to review this book! Bestsellers in this subject. Supporting Conservation Your orders support book donation projects. Amazing Experience Fantastic service at a great price — I'll definitely use you again. Unique Product Range Search and browse over , wildlife and science products.

Rapid Global Service Multi-currency. Natural History Experts Wildlife, science and conservation since An interview with Brooke Bessesen. Conservation Volunteering at the Cornish Seal Sanctuary. This method has been successfully applied for the detection of plant virus-induced protein aggregates and their separation according to size 7 , Tomatoes grown at high temperature regime 2 showed a different CP pattern: In parallel to CP accumulation, we examined the patterns of several HS response proteins in infected and GF tomatoes. This heat-induced increase in the amounts of HS-dependent proteins was also observed in non-infected and GF tomatoes Supplementary Fig.

The OE33 chloroplast protein was used as protein loading control. The expression level of each gene was calculated in relation to leaves of susceptible line grown at high temperature.

Tomato Yellow Leaf Curl Virus Disease: Management, Molecular Biology, Breeding for Resistance

Bars represent the average and standard deviation of the relative expression from five independent biological repeats; pooled leaves of three different plants were taken for each sample. However, even in GF plants, HS-induced protein expression was diminished at the late stages of infection, when virus started to be detectable. However in line GF, the increase was higher than in the line. For example, HS induced a 2.

The expression of Apx genes was increased only in 0. Such differences might be caused by the virus ability to down-regulate the plant HS response, which prevailed in high-virus containing susceptible plants. Conversely, the behavior of HSP70 upon heat shock and recovery was similar in infected and in non-infected plants.

The stage of viral infection, but not virus amounts, influenced HS- protein expressions. Pooled leaves of three different plants were taken for each sample. During the recovery period, infected tomatoes did not show the same levels of stress gene expression as those observed in uninfected plants Fig. HSFs exist as inactive proteins mostly found in the cytoplasm. HSFA2 nuclear translocation was compared in tomato cells of uninfected vs. The heat shock caused the re-localization of the transcription factor from cytoplasm to nucleus in uninfected tomato cells.

Cytoplasmic HSP70 and nuclear Histone 3 were used as internal markers to assess the purity of the cellular fractions. The immunodetection in crude extracts was used as direct control D. Following elution, the two kinds of bound proteins described in Materials and Methods were immuno-detected with anti-HSFA2 antibodies Fig.

Electronic supplementary material

By comparison, HSP 70 interacted with only three viral proteins data not shown, except for CP, described in 7. To identify HSFA2-TYLCV complexes in the tomato leaf cellular compartments, proteins from separated cytoplasmic and nuclear fractions were passed through Ni resin columns bound to the viral proteins. Double in situ immuno-detection of HSFA2 and CP demonstrated their co-localized in cytoplasm yellow staining and nuclei pink staining. We expected that at this time the chaperones returned to their previous soluble state to regulate the protein quality control systems.


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Ultracentrifugation through sucrose gradients showed that in extracts of leaves incubated at normal temperatures, most HSP90 was detected in the gradient fractions containing soluble proteins fractions 1—2 and small protein complexes fractions 3—4. TYLCV infection induced the aggregation of some of the HSP90, which appeared in fraction 10 of the gradient, where large protein aggregates are present Fig. Similar results have been shown previously for HSP70 4 and Fig. Heat shock of TYLCV-infected leaves caused an increase in the amounts of chaperone present in gradient fraction 10 Fig.

It has to be noted that after recovery there is more HSPs in fraction 10 of infected plants than before heat shock. These aggregates contained viral CP together with at least two cellular chaperones. Restoration of initial chaperone patterns during recovery was impaired in viral infected plants. Extracts of native proteins were subjected to ultracentrifugation on sucrose gradients, which were subsequently divided in 10 fractions; aliquots were analyzed by western blots with anti-HSP90 and HSP70 antibodies.

The combination of extreme temperature and viral infection occurs quite often in the field in the Middle East and in many tropical regions, impairing crop productivity. It is well known that increasing temperatures facilitate pathogen spread in major food crops Temperature was identified as the dominant abiotic factor directly affecting herbivorous insects by changing their development, survival, range and abundance Moreover, many abiotic stresses were shown to weaken the defense mechanisms of plants and enhance their susceptibility to pathogen infection 33 , Current climate prediction models point to a gradual increase in ambient temperatures in the near future and to an enhancement in the frequency, length and amplitude of heat waves 35 , Therefore, there is a need to generate crops with enhanced combined tolerance to heat and pathogens.

Plants from line grown at high temperatures showed exacerbated symptoms compared to plants grown at milder temperatures Fig. Heat application significantly increased the amounts of viral DNA Fig. High temperatures regime 2 led to an increase in CP amounts.

Moreover, the size expansion of such aggregates was considered as a marker of a successful infection 7. In rice, the induction patterns of HSPs and HSFs following stress treatment such as drought, heat, cold, and salt showed some overlap, but also a specific response to each condition 13 One of the important results of the current study is the discovery that TYLCV infection is accompanied by a decreased activation of cellular HS response.

The current experiments do not completely exclude the possibility that the observed effect on HS response suppression is a secondary effect of changing cell metabolism in the aging infected cells. However, potential TYLCV capacity to suppress the HS response depended on the stage of infection, not on aging of the infected tomato plants. In uninfected tomatoes, some changes in the patterns of HS-inducible proteins during aging were observed Supplementary Fig. In uninfected tomatoes, during the recovery periods that followed heat shock, the key cellular chaperones HSP70 and HSP90 reverted to fractions containing soluble active proteins or protein complexes.

The mobilization of chaperones in large aggregates could weaken the HS response. They could be used by the virus as elements of the protein quality control machinery to reactivate cellular proteins needed for folding and assembly of multimeric protein complexes required for virus replication, transcription and encapsidation. In TYLCV infected tomatoes, a significant reduction in the levels of transcription and translation of the heat-inducible genes can lead to a decreased temperature tolerance, HS response and consequently to reduced cell death.

Likely, reduced stress responses supply enough time for successful viral replication. On the other hand, infected tomatoes become much more susceptible to various environmental stresses. HSF signaling is one of the main contributors to resistance against main abiotic stresses and is essential for the maintenance of normal growth and productivity under stress conditions Stable HSFA2 is expected to confer a stress resistance phenotype while maintaining yield productivity. The development of stable multiple stress tolerance traits in important crop plants will improve yields particularly in areas with adverse environmental conditions, and contributing to global food security.

It might be possible to increase the heat tolerance of TYLCV-susceptible plants by pre-inoculating by agroinfection seedlings with a TYLCV symptomless mutant lacking 20 amino acids near the N-terminus of the CP 42 , and therefore not transmissible by whiteflies, before planting in the field. We expect that the mutant will have the same capacity to suppress the HS response and to increase heat tolerance as the wild type virus, though this has to be proven experimentally.

How to cite this article: Tomato yellow leaf curl virus infection mitigates the heat stress response of plants grown at high temperatures. This research was supported by a grant from the U. All authors have read and approved the manuscript. National Center for Biotechnology Information , U. Published online Jan Received Oct 7; Accepted Dec This work is licensed under a Creative Commons Attribution 4. To view a copy of this license, visit http: This article has been corrected. This article has been cited by other articles in PMC. Heat treatment Plants were subjected to two types of treatment.

Open in a separate window. Discussion The combination of extreme temperature and viral infection occurs quite often in the field in the Middle East and in many tropical regions, impairing crop productivity. Additional Information How to cite this article: Supplementary Material Supplementary Information: Click here to view. Acknowledgments We thank K. Footnotes Author Contributions G.

Management, molecular biology, breeding for resistance. T omato yellow leaf curl viruses: Recruitment of the host plant heat shock protein 70 by Tomato yellow leaf curl virus coat protein is required for virus infection. PloS One 8 7 , e Tomato plant cell death induced by inhibition of HSP90 is alleviated by Tomato yellow leaf curl virus infection. Degradation mechanisms of the Tomato yellow leaf curl virus coat protein following inoculation of tomato plants by the whitefly Bemisia tabaci. Progressive aggregation of Tomato yellow leaf curl virus coat protein in systemically infected tomato plants, susceptible and resistant to the virus.

The Tomato yellow leaf curl virus V2 protein forms aggregates depending on the cytoskeleton integrity and binds viral genomic DNA. Suppression of tobacco mosaic virus-induced hypersensitive-type necrotization in tobacco at high temperature is associated with downregulation of NADPH oxidase and superoxide and stimulation of dehydroascorbate reductase.


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  • Development of a New Molecular Marker for the Resistance to Tomato Yellow Leaf Curl Virus!
  • Analysis of temperature modulation of plant defense against biotrophic microbes. Simultaneous application of heat, drought, and virus to Arabidopsis plants reveals significant shifts in signaling networks. Generating high temperature tolerant transgenic plants: Transcriptional profiling of maturing tomato Solanum lycopersicum L. The diversity of plant heat stress transcription factors. Arabidopsis heat shock transcription factor A2 as a key regulator in response to several types of environmental stress.