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SUMMARY:Biochemistry Friday Seminars - Using yeast to model human diseases
 : parasites to paralysis - Professor Steve Oliver\, Department of Biochemi
 stry\, University of Cambrige
DTSTART:20190906T140000Z
DTEND:20190906T150000Z
UID:TALK113854@talks.cam.ac.uk
CONTACT:13388
DESCRIPTION:The unity of molecular and cell biology across the Eukaryotes 
 makes yeasts favourable organisms with which to model both infectious and 
 systemic diseases of humans. \n\nIn order to model infectious diseases\, w
 e have set up systems in which the infectious agent and the human host are
  modelled either within the same or separate yeast cells. For instance\, m
 any tropical diseases are caused by eukaryotic pathogens\, including proto
 zoa and nematode worms\, with a very similar biochemistry to humans. This 
 makes it difficult to identify agents that will kill the parasite but not 
 the patient. The search for such drugs is also hampered by the fact that m
 any of these parasites are difficult or impossible to culture in the labor
 atory. This is where yeast comes in. We have developed a robust\, fully au
 tomated method to screen for potential anti-parasitic drugs. This system u
 ses separate yeast strains whose growth is dependent on the expression of 
 coding sequences specifying target enzymes from either the parasite or the
  human host. The yeast system thus permits multiple parasite targets to be
  screened in parallel and is also able to exclude compounds that do not di
 scriminate between host and parasite enzymes. \n\nWe have also used yeast 
 to model the interactions between pathogenic bacteria and their plant and 
 animal hosts\; in this case both pathogen and host are modelled by a singl
 e yeast construct. We have engineered yeast to inducibly synthesise unusua
 l nucleotides that are involved bacterial pathogenesis. Interactions betwe
 en these bacterial signalling molecules and the yeast cell can result in g
 rowth inhibition or death. We find that cdiGMP functions through a mechani
 sm that must be compensated by ribonucleotide reductase activity or by fun
 ctionally competent mitochondria. Synthesis of the human Mesh1 protein in 
 yeast indicates that it may be required to protect human cells from the da
 maging effects of ppGpp during bacterial infection.\n\nThe forgoing experi
 ments generated data on yeast purine nucleotide metabolism that could not 
 be accurately predicted by existing models of yeast metabolism. Investigat
 ion of this deficiency led us to increase the representation of iron metab
 olism in the model and to discover that yeast has potential for modelling 
 the cellular processes in involved in the onset and early progression of P
 arkinson’s disease. I shall discuss other examples of using yeast to mod
 el neurodegenerative diseases\, including Friedreich’s Ataxia and motor 
 neurone disease. \n\n
LOCATION:Department of Biochemistry\, Sanger Building Jean Thomas Lecture 
 Theatre
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