Philip O'Brien

The Unified Theory suggests that sleep is a process that developed in eukaryotic animals from a relationship with an endosymbiotic bacterium. Over evolutionary time the bacterium evolved into the modern mitochondrion that continues to exert an effect on sleep patterns, e.g. the bacterium Wolbachia establishes an endosymbiotic relationship with Drosophila and many other species of insects and is able to change the host's behaviour by making it sleep. The hypothesis is supported by other host-parasite relationships, e.g., Trypanosoma brucei which causes day-time sleepiness and night-time insomnia in humans and cattle. For eukaryotes such as Monocercomonoids that don't contain mitochondria we find no evidence of them sleeping.

Mitochondria produce the neurotransmitter gamma aminobutyric acid (GABA), and ornithine a precursor of the neurotransmitter GABA, together with substances such as 3,4dihydroxy phenylalanine (DOPA) a precursor for the neurotransmitter dopamine: These substances have been shown to affect the sleep/wake cycles in animals such as Drosophilia and Hydra.

Eukaryote animals have traded the very positive side of having mitochondria providing aerobic respiration for them with the negative side of having to sleep. NREM (Quiet sleep) is the process endosymbionts have imposed upon their host eukaryotes and REM (Active sleep) is the push-back adaptation of eukaryotes with brains, returning to wakefulness.
•The Unified theory explains what sleep is, how it came about and why it persists in animals today. We also provide the context to explain what both NREM and REM sleep are.•Sleep is cellular and it is likely to be an endosymbiont occurrence. It occurs in all, if not most multi cellular eukaryote animals. Neurotransmitters predate sleep and sleep predates brains.

Powdery scab of potato, caused by the obligate biotrophic protozoan pathogen Spongospora subterranea f.sp. subterranea (Sss), is a major problem in potato growing areas throughout the world. It results in lesions (scabs) on the surface of the tubers which renders them unmarketable. In recent years there has been an increasing number of reports of the disease, many from new areas. Management of the disease has proved difficult and relies on the integrated application of a range of methods. Biocontrol is not currently used for the management of powdery scab although the results of preliminary studies have been encouraging. This review evaluates the potential for developing a biocontrol strategy for powdery scab.

Biological control is the control of disease by the application of biological agents to a host animal or plant that prevents the development of disease by a pathogen. With regard to plant diseases the biocontrol agents are usually bacterial or fungal strains isolated from the endosphere or rhizosphere. Viruses can also be used as biocontrol agents and there is a resurgent interest in the use of bacterial viruses for control of plant diseases. The degree of disease suppression achieved with biological agents can be comparable to that achieved with chemicals. Our understanding of the ways in which biocontrol agents protect plants from disease has developed considerably in recent years with the application of genomics and genetic modification techniques. We have uncovered mechanisms by which biocontrol agents interact with the host plant and other members of the microbial community associated with the plant. Understanding these mechanisms is crucial to the isolation of effective biocontrol agents and the development of biocontrol strategies for plant diseases. This review looks at recent developments in our understanding of biocontrol agents for plant diseases and how they work.

Phosphite application mitigates diseases caused by oomycete plant pathogens. Tissue concentrations of phosphite above 1 mM are generally required for disease protection. Determining the concentration of phosphite in plant material requires extensive extraction and derivatisation procedures prior to separation by gas–liquid chromatography (GLC). This paper describes a direct chemical method to estimate the concentration of phosphite using a silver nitrate reagent. Glass fiber filter papers were saturated with a 1 M aqueous solution of silver nitrate (adjusted to pH 2.5 with nitric acid) and dried for 2 h at 60 °C. 20 μL of polyvinylpolypyrrolidone treated aqueous plant extract was adsorbed onto the filter paper and incubated in the dark at room temperature (25 °C) for 1 h. The presence of phosphite in the extract reduces the silver ions to elemental silver resulting in a grey-black precipitate that is clearly visible. The method is rapid, sensitive and inexpensive, and can detect phosphite at concentrations of 1 mM in 20 μl of aqueous extract from 100 mg of fresh plant material. Samples analysed by this method gave similar results to analysis by GLC, indicating the method can be used in the field or the laboratory to determine uptake and distribution phosphite in the plant, the retention of phosphite over time and the timing of phosphite reapplication.

The application of either phosphite or calcium salts to plants that are susceptible to Phytophthora spp. protects them from infection and the development of disease symptoms. This suggests that there may be an additive protective-effect when they both are applied together. The combined effect of foliar phosphite and soil calcium levels on the health and survival of Banksia leptophylla seedlings infected with Phytophthora cinnamomi was investigated. Six month-old Banksia leptophylla plants grown in sand supplemented with 0, 3, 10 or 30 mM calcium sulphate were sprayed with 0, 0.1 or 0.3 % phosphite and inoculated with P. cinnamomi. Plant survival and health were recorded for 12 months after inoculation. The combination of foliar-phosphite spraying with the supplementation of sand with calcium sulphate significantly increased the survival and health of plants infected with P. cinnamomi. There was 2.7 % survival of plants with no phosphite or additional calcium, 8.3 % survival with 30 mM calcium alone, 53 % survival with 0.3 % phosphite alone and 100 % survival of plants given 0.3 % phosphite and 30 mM calcium. The pathogen survived in the sand of all treatments for the 12-month period of the trial. Combining foliar-application of phosphite with addition of calcium sulphate to soil is a cheap and practical way of significantly increasing the efficacy of phosphite in controlling the development and spread of Phytophthora dieback disease. A mechanism involving inhibition of calcium-dependent ATPases by phosphite and pyrophosphate, and the subsequent disruption of calcium ion signaling, is discussed.

Summary: Removal of living plants from an area of Eucalyptus marginata (jarrah) forest on black gravel sites infested with Phytophthora cinnamomi significantly reduced subsequent pathogen recovery. Vegetation, including trees and annual and herbaceous perennial plants, was killed on the sites by herbicide application. To determine whether this treatment efficiently eliminated P. cinnamomi, soil samples were seasonally collected and baited to test for the presence of the pathogen. There were no recoveries on treated sites in autumn, 28 months after removal of all vegetation by herbicide application. To test whether this was the result of the complete elimination of the pathogen or whether inoculum remained, regrowth on sites was not controlled after this period leading to the re-establishment of annual and herbaceous perennial species, some of which are hosts of P. cinnamomi. Recovery of P. cinnamomi after plant regrowth on the formerly treated sites indicated that for complete pathogen removal, sites need to remain free of vegetation for longer than 28 months. Overall, however, this study confirms that the pathogen is a weak saprophyte, and withdrawal of host material for a period of time may make eventual rehabilitation of these sites possible.

Phytophthora cinnamomi the agent of eucalypt dieback disease in Western Australia is a serious pathogen of many plant species around the world. The pathogen has a very wide host range. In Western Australia many species of native plants are susceptible, and a large number because they are of limited distribution are threatened with extinction. This paper reviews the mechanisms by which P. cinnamomi causes disease, together with the factors that contribute to the spread and survival of the pathogen allowing it cause new disease epidemics when the right conditions prevail. It also looks at possibilities for control of the pathogen by management, chemical application and biological control.

Resistant annual and herbaceous perennial plant species were identified as key hosts which allow Phytophthora cinnamomi to persist on severely impacted black gravel sites within the Eucalyptus marginata (jarrah) forest of southwest Western Australia. Of the annual and herbaceous perennial plant species present on black gravel sites, 15 out of 19 species were found to be hosts of P. cinnamomi, and 10 of these were symptomless hosts. In particular, the native annual Trachymene pilosa and the two native herbaceous perennials Stylidium diuroides and Chamaescilla corymbosa were commonly found to be hosts of the pathogen. Species from 12 new genera including three from new families (Crassulaceae, Droseraceae and Primulaceae) are reported for the first time to be hosts of P. cinnamomi. The species from which P. cinnamomi was recovered were the native species: Chamaescilla corymbosa, Crassula closiana, Drosera erythrorhiza, Hydrocotyle callicarpa, Levenhookia pusilla, Paracaleana nigrita, Podotheca angustifolia, Pterochaeta paniculata, Rytidosperma caespitosum, Siloxerus multiflorus, Stylidium diuroides and Trachymene pilosa, and the introduced annual weeds Hypochaeris glabra, Lysimachia arvensis and Pentameris airoides.

Phytophthora cinnamomi is a necrotrophic pathogen of woody perennials and devastates many biomes worldwide. A controlled perlite-hydroponic system with no other hyphae-producing organisms as contaminants present allowed rapid assessment of ten annual and herbaceous perennial plant species most of which have a wide distribution within the jarrah (Eucalyptus marginata) forest in Western Australia where this pathogen has been introduced. As some annuals and herbaceous perennials have recently been reported as symptomatic and asymptomatic hosts, laboratory screening of some of the field-tested annuals and herbaceous perennials and additional species was used to further evaluate their role in the pathogen's disease cycle. Nine of the species challenged with the pathogen were asymptomatic, with none developing root lesions; however, Trachymene pilosa died. The pathogen produced thick-walled chlamydospores and stromata in the asymptomatic roots. Furthermore, haustoria were observed in the roots, indicating that the pathogen was growing as a biotroph in these hosts.

Phosphite () induces a range of physiological and developmental responses in plants by disturbing the homeostasis of the macronutrient phosphate. Because of its close structural resemblance to phosphate, phosphite impairs the sensing, membrane transport, and subcellular compartmentation of phosphate. In addition, phosphite induces plant defence responses by an as yet unknown mode of action. In this study, the acclimation of Arabidopsis thaliana plants to a sustained phosphite supply in the growth medium was investigated and compared with plants growing under varying phosphate supplies. Unlike phosphate, phosphite did not suppress the formation of lateral roots in several Arabidopsis accessions. In addition, the expression of well-documented phosphate-starvation-induced genes, such as miRNA399d and At4, was not repressed by phosphite accumulation, whilst the induction of PHT1;1 and PAP1 was accentuated. Thus, a mimicking of phosphate by phosphite was not observed for these classical phosphate-starvation responses. Metabolomic analysis of phosphite-treated plants showed changes in several metabolite pools, most prominently those of aspartate, asparagine, glutamate, and serine. These alterations in amino acid pools provide novel insights for the understanding of phosphite-induced pathogen resistance.