Associate Professor Paul Ebert

Reader

School of Biological Sciences
Faculty of Science
p.ebert@uq.edu.au
+61 7 336 52973

Overview

Molecular mechanisms of phosphine resistance

Genetic mapping of oxidative stress resistance genes. The fumigant phosphine disrupts oxidative metabolism, resulting in the production of reactive oxygen intermediates. This causes the premature ageing and death of targeted pests. Insect pests of stored grain in Australia now exhibit resistance to phosphine at levels more than 200 times the normal lethal dose.

We have genetically mappedf and identified the genes responsible for phosphine resistance in tall major insect pests of stored grain. We are using a systems biology approach in the model organism C. elegans to understand the molecular basis of phosphine action. Our genetic studies have recently shown that resistance to phosphine is associated with an extension of lifespan

Research Interests

  • Metabolic toxicology - fumigant toxicology
    I am interested in energy metabolism and mitochondrial function. My work is based around the toxicology of the agricultural fumigant, phosphine. The phosphine resistance gene, dld, not only results in phosphine resistance, but also modulates cellular energy metabolism.
  • Fumigant synergists - gasotransmitters
    To better understand phosphine toxicity and how the toxicity might be synergistically enhanced to improve pest control, we are comparing and contrasting phosphine toxicology with the toxicology of endogenous gasotransmitter signalling molecules.
  • Metabolic toxicology - ageing and diseases of ageing
    The dld gene not only influences phosphine resistance, but also can extend lifespan and protect against pathology in an animal model of Alzheimer's disease.
  • A phenotype first model to explain the evolution of phosphine resistance
    The evolution of resistance to agricultural pesticides poses a serious risk to global food security. Our observations regarding phosphine resistance has led us to a model by which a phenotype (e.g. resistance) is first created epigenetically and only subsequently stabilised via genetic change.

Research Impacts

Our discovery of the economically important phosphine resistance gene has allowed us to characterise resistance across Australia and India. It is now being use to monitor resistance management strategies in collaboration with major grain handling companies to improve commercial practice in Australia and India. This is the subject of a recent Australia-India AISRF project on which I was the UQ lead investigator. We have also used the gene marker to characterise resistance in Vietnam, China, Turkey. Others have used our work to characterise resistance in the USA and Brazil.

We have also sought to use our understanding of how phosphine works to identify synergistic gases that might be used to extend the useful life of phosphine as a grain fumigant. This work was supported by an ARC Discovery grant and a research grant from the Plant Biosecurity CRC.

We have also discovered the the phosphine resistance gene, dld, is a lifespan extending factor. Interestingly, it also protects against pathology in a C. elegans model of Alzheimer's disease, a serious ageing associated disease. Alzheimer's disease is a major disease of global importance with huge economic ramifications due to the level of care required by people who suffer from dementia. Our system allows us to explore the metabolic basis of the disease, an aspect that has until recently been largely neglected.

Qualifications

  • PhD, Washington State U (WSU)
  • MSc, U Washington (UW)
  • BSc, UC Riverside (UCR)

Publications

View all Publications

Supervision

  • Doctor Philosophy

  • Doctor Philosophy

  • Doctor Philosophy

View all Supervision

Available Projects

  • The evolution of resistance to agricultural pesticides poses a serious risk to global food security. Our observations regarding phosphine resistance have led us to a model by which a phenotype (e.g. resistance) is first created epigenetically and only subsequently stabilised via genetic change. This inverts the traditional model of eviolution in which phenotypes are selected from the existing genetic variability that exists in a population. Instead, we propose that the phenotype is first created epigenetically. This can occur rapidly, but epiphenotypes are not very stable. The epigentic proitotype can provide a sort of template for the subsequent selection of stably heritable genetic change.

  • This project is focused on energy metabolism and mitochondrial function as it relates to the toxicology of the agricultural fumigant, phosphine. This project employs a systems biology approach that ionvolves bioinformatics, genomics, metabolomics and functional genetics in the model organism, Caenorhabditis elegans.

  • We wish to better understand phosphine toxicity to learn how its toxicity can be synergistically enhanced to improve pest control. We are using small molecules and gene mutations that disrupt engergy metabolism to understand how phosphine works. We are also testing gases that alter energy metabolism to determine whether thay can be employed to synergistically enhance ophosphine toxicity. This project will employ pharmacology, gene expression profiling and genetic analysis.

View all Available Projects

Publications

Featured Publications

Book Chapter

  • Schlipalius, D., Ebert, P. R. and Hunt, G. J. (2008). Honeybee. Genome mapping and genomics in arthropods. (pp. 1-16) edited by Wayne Hunter and Chittaranjan Kole. Berlin, Germany: Springer. doi: 10.1007/978-3-540-73833-6_1

  • An, Gynheung, Ebert, Paul R., Mitra, Amitava and Ha, Sam B. (1989). Binary vectors. Plant molecular biology manual. (pp. 29-47) Dordrecht: Springer Netherlands. doi: 10.1007/978-94-009-0951-9_3

  • An, Gynheung, Ebert, Paul R., Mitra, Amitava and Ha, Sam B. (1988). Binary vectors. Plant molecular biology manual. (pp. 45-63) Dordrecht: Springer Netherlands.

Journal Article

Conference Publication

Edited Outputs

  • P. R. Ebert ed. (2004). Asia Pacific Journal of Clinical Nutrition. Nutrition Society of Australia 28th Annual Scientific Meeting, Brisbane Convention Centre, Brisbane, 11-13 August. Australia: H E C Press.

Grants (Administered at UQ)

PhD and MPhil Supervision

Current Supervision

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

Completed Supervision

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • The evolution of resistance to agricultural pesticides poses a serious risk to global food security. Our observations regarding phosphine resistance have led us to a model by which a phenotype (e.g. resistance) is first created epigenetically and only subsequently stabilised via genetic change. This inverts the traditional model of eviolution in which phenotypes are selected from the existing genetic variability that exists in a population. Instead, we propose that the phenotype is first created epigenetically. This can occur rapidly, but epiphenotypes are not very stable. The epigentic proitotype can provide a sort of template for the subsequent selection of stably heritable genetic change.

  • This project is focused on energy metabolism and mitochondrial function as it relates to the toxicology of the agricultural fumigant, phosphine. This project employs a systems biology approach that ionvolves bioinformatics, genomics, metabolomics and functional genetics in the model organism, Caenorhabditis elegans.

  • We wish to better understand phosphine toxicity to learn how its toxicity can be synergistically enhanced to improve pest control. We are using small molecules and gene mutations that disrupt engergy metabolism to understand how phosphine works. We are also testing gases that alter energy metabolism to determine whether thay can be employed to synergistically enhance ophosphine toxicity. This project will employ pharmacology, gene expression profiling and genetic analysis.

  • The phosphine resistance dld gene also can extend lifespan and protect against pathology in an animal model of Alzheimer's disease. This is not currently a primary focus of my lab, but it remains an area of interest.

  • Anorexia is the most deadly of all mental diosorders. This is likely due to the fact that anorexia results in severe malnutrition that is reinforced by maladaptive behaviours that restrict food intake and increase activity levels. Interestingly, the disorder can be triggered by a mental state that leads to restricted food intake, but is actually more frequently caused by restricted food intake, such as dieting, that triggers the maladaptive behaviours. We are investigating an hypothesis that anorexia is not actually a mental disorder int he traditional sense, but rather, is a suite of instinctual behaviours that have evolved as a starvation survival response.

    Our goal is to develop an animal model in which the genetics of anorexia can be studied and to use this model to indentify the metabolic switch that will allow the animals to escape the starvation response and resul=me normal food intake and behaviour. Ultimately, we wish to indentify therapeutic compounds that can be used to treat anorixia.