Explore the vast range of titles available.

Diverse and rapidly evolving pathogens cause plant disease and epidemics that threaten crop yield and food security around the world. Research over the last 25 years has led to an increasingly clear conceptual understanding of the molecular components of the plant immune system. Combined with ever-cheaper DNA-sequencing technology and the rich diversity of germ plasm manipulated for over a century by plant breeders, we now have the means to begin development of durable (long-lasting) disease resistance beyond the limits imposed by conventional breeding and in a manner that will replace costly and unsustainable chemical controls.

We investigated whether lines of transgenic tomato (Solanum lycopersicum) expressing the Bs2 resistance gene from pepper, a close relative of tomato, demonstrate improved resistance to bacterial spot disease caused by Xanthomonas species in replicated multi-year field trials under commercial type growing conditions. We report that the presence of the Bs2 gene in the highly susceptible VF 36 background reduced disease to extremely low levels, and VF 36-Bs2 plants displayed the lowest disease severity amongst all tomato varieties tested, including commercial and breeding lines with host resistance. Yields of marketable fruit from transgenic lines were typically 2.5 times that of the non-transformed parent line, but varied between 1.5 and 11.5 fold depending on weather conditions and disease pressure. Trials were conducted without application of any copper-based bactericides, presently in wide use despite negative impacts on the environment. This is the first demonstration of effective field resistance in a transgenic genotype based on a plant R gene and provides an opportunity for control of a devastating pathogen while eliminating ineffective copper pesticides.

Crop diseases are a dangerous and recurring threat to food production that are poorly recognized by the general public or lost in the big picture by global priority setting organizations, such as the World Bank and United Nations. Moreover, disease incidence is on the rise due to increasing food production needs, climate change, and expanding international trade and travel. In developing countries, up to 80% of people are involved in farming (World Bank) under conditions of limited resources, and they are especially vulnerable to damage from crop disease. With more than 2.2 billion additional people to feed by 2050, the demands on modern agriculture are enormous, and preventing losses caused by plant diseases is a key factor for ensuring global food security. The most infamous crop disease episode in history was the Irish Potato Famine, caused by the water mold, Phytophthora infestans, whose name means the \"Plant Destroyer\". More commonly, the disease it causes is known as Late Blight. The severe multi-year Late Blight outbreak and the political conditions of the 1840s resulted in famine and the deaths of more than one million people and the emigration of more than another million. To this day, the population of Ireland has not returned to pre-Late Blight levels. Outbreaks of Phytophthora and numerous other plant pathogens continue around the world, causing average losses of 15% of global food production every year. Of particular concern are diseases that can cause pandemics and entire crop failure, such as wheat stem rust, wheat blast, bacterial wilt of banana and late blight of potato. Disease losses can be limited with agronomic management, agrochemicals, and breeding for varieties with disease resistance. Unfortunately, farming practices designed to maximize production efficiency and yield create opportunities for pathogens to spread, mutate, and overcome chemical sprays and genetic resistance based on single genes as seen with numerous fungal and bacterial pathogens. Disease resistance is a major goal of conventional breeding, because genetic resistance is the most effective means of disease control. Yet developing finished varieties that balance multiple yield, flavor, and other traits while achieving disease resistance is very challenging, and durable examples are few. And though the global crop protection industry develops agrochemicals to aid in disease control, in 2014 growers spent more than $14 billion on crop protection compounds to control diseases, however these were only partially effective. Whereas the combination of improved seeds and chemistry has generally produced reliable harvests in developed countries, serious unmanaged diseases of crops exist today in these areas, including stripe rust of wheat (Puccinia striiformis), citrus greening (Candidatus liberibacter asiaticus), corn stalk and ear rots (many different pathogens), and Xylella. Additionally the world's 500 million smallholder farmers, who feed one third of the world's people, have insufficient resources and access to these tools to address their very serious disease threats, including late blight of potato, maize lethal necrosis disease, and cassava brown streak disease.

Citrus bacterial canker (CBC), caused by Xanthomonas citri subsp. citri ( Xcc ), causes dramatic losses to the citrus industry worldwide. Transcription activator‐like effectors (TALEs), which bind to effector binding elements ( EBEs ) in host promoters and activate transcription of downstream host genes, contribute significantly to Xcc virulence. The discovery of the biochemical context for the binding of TALEs to matching EBE motifs, an interaction commonly referred to as the TALE code, enabled the in silico prediction of EBEs for each TALE protein. Using the TALE code, we engineered a synthetic resistance ( R ) gene, called the Xcc‐TALE‐trap , in which 14 tandemly arranged EBEs , each capable of autonomously recognizing a particular Xcc TALE, drive the expression of Xanthomonas avrGf2 , which encodes a bacterial effector that induces plant cell death. Analysis of a corresponding transgenic Duncan grapefruit showed that transcription of the cell death‐inducing executor gene, avrGf2 , was strictly TALE‐dependent and could be activated by several different Xcc TALE proteins. Evaluation of Xcc strains from different continents showed that the Xcc ‐ TALE ‐ trap mediates resistance to this global panel of Xcc isolates. We also studied in planta ‐evolved TALEs (eTALEs) with novel DNA‐binding domains and found that these eTALEs also activate the Xcc‐TALE‐trap , suggesting that the Xcc‐TALE‐trap is likely to confer durable resistance to Xcc . Finally, we show that the Xcc‐TALE‐trap confers resistance not only in laboratory infection assays but also in more agriculturally relevant field studies. In conclusion, transgenic plants containing the Xcc‐TALE‐trap offer a promising sustainable approach to control CBC.

Currently, hunger affects nearly 12 per cent of the world’s population — 4 per cent more than in 2015, when the United Nations launched the 2030 Agenda for Sustainable Development. If all scientific knowledge and technological innovation in crop development were readily available and globally adopted, could zero hunger have been achieved by 2030? Most people recognize the potential for agricultural biotechnology to contribute to food security. However, there has been limited application and adoption of new crop varieties in countries that are disproportionately affected by malnutrition and food insecurity.

Transgenic tobacco plants carrying a number of regulatory sequences derived from the cauliflower mosaic virus 35S promoter were tested for their response to treatment with salicylic acid (SA), an endogenous signal involved in plant defense responses. beta-Glucuronidase (GUS) gene fusions with the full-length (-343 to +8) 35S promoter or the -90 truncation were found to be induced by SA. Time course experiments revealed that, in the continuous presence of SA, the -90 promoter construct (-90 35S-GUS) displayed rapid and transient induction kinetics, with maximum RNA levels at 1 to 4 hr, which declined to low levels by 24 hr. Induction was still apparent in the presence of the protein synthesis inhibitor cycloheximide (CHX). Moreover, mRNA levels continued to accumulate over 24 hr rather than to decline. By contrast, mRNA from the endogenous pathogenesis-related protein-1 alpha (PR-1 alpha) gene began to accumulate at later times during SA treatment and steadily increased through 24 hr; transcription of this gene was almost completely blocked by the presence of CHX. Further dissection of the region from -90 and -46 of the 35S promoter revealed that the SA-responsive element corresponds to the previously characterized activation sequence-1 (as-1). These results represent a definitive analysis of immediate early responses to SA, relative to the late induction of PR genes, and potentially elucidate the early events of SA signal transduction during the plant defense response

In a large trial, the estimated incidence of stroke, systemic embolism, hemorrhage, or death was 2.8 percentage points lower to 0.5 percentage points higher with early than with later use of direct oral anticoagulants.

On detecting viral RNAs, the RNA helicase retinoic acid‐inducible gene I (RIG‐I) activates the interferon regulatory factor 3 (IRF3) signalling pathway to induce type I interferon (IFN) gene transcription. How this antiviral signalling pathway might be negatively regulated is poorly understood. Microarray and bioinformatic analysis indicated that the expression of RIG‐I and that of the tumour suppressor CYLD (cylindromatosis), a deubiquitinating enzyme that removes Lys 63‐linked polyubiquitin chains, are closely correlated, suggesting a functional association between the two molecules. Ectopic expression of CYLD inhibits the IRF3 signalling pathway and IFN production triggered by RIG‐I; conversely, CYLD knockdown enhances the response. CYLD removes polyubiquitin chains from RIG‐I as well as from TANK binding kinase 1 (TBK1), the kinase that phosphorylates IRF3, coincident with an inhibition of the IRF3 signalling pathway. Furthermore, CYLD protein level is reduced in the presence of tumour necrosis factor and viral infection, concomitant with enhanced IFN production. These findings show that CYLD is a negative regulator of RIG‐I‐mediated innate antiviral response.