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SUMMARY:BMI Seminar // Analysis of Parkinson's disease genes using Drosoph
 ila: mitophagy and transport
DTSTART:20130626T121500
DTEND:20130626T131500
DTSTAMP:20260916T014014Z
UID:7e1b12cd909aa09031397234343c0d5db60df190a65bbb8685c38969
CATEGORIES:Conferences - Seminars
DESCRIPTION:Alex Whitworth\nDepartment of Biomedical Science\nThe Universi
 ty of Sheffield\, UK\nMitochondria are a nexus of life and death of the ce
 ll and have long been implicated in the pathogenesis of neurodegenerative 
 diseases such as Parkinson’s disease (PD). Genetic analysis of PD has id
 entified single-gene mutations responsible for rare\, heritable forms of P
 D.  Understanding the consequence of these mutations can potentially illu
 minate the pathogenic mechanisms underlying many forms of PD. These mutati
 ons can be modelled in genetically tractable model systems\, such as the f
 ruit fly\, Drosophila melanogaster\, which has proven a remarkably informa
 tive model. \nLoss of function in parkin and PINK1 cause the majority of 
 early onset PD.  It was established using Drosophila that PINK1 and parki
 n act in a common pathway to maintain mitochondrial homeostasis. Mitochond
 ria localised PINK1 is required to signal parkin translocation to dysfunct
 ional mitochondria where ubiquitination of multiple outer membrane targets
 \, such as Mitofusins\, promotes their isolation and degradation by autoph
 agy (mitophagy). In neurons\, these mitochondria must also be transported 
 large distances for degradation.\nThe inability to properly regulate mitoc
 hondrial turnover will impact on the long-term maintenance of the mitochon
 drial network and ultimately on neuronal survival\, suggesting a possible 
 pathogenic mechanism for PD\, however\, the physiological in vivo evidence
  is limited. In addition\, many details of the molecular mechanism and oth
 er pathway components are unclear. Our work aims to addresses these defici
 encies using Drosophila as a model system.
LOCATION:SV1717A
STATUS:CONFIRMED
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