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[Nathalie Vanden Hautte]

CORRECTION

 

Event time: 09:30 am - 10:30 am 

 

 

iCal Calendar Event Reminder 

12:00 - 13:00 

Tuesday, March 10, 2009 

 

Go to the: psbsem Calendar <http://157.193.202.9:88/psbsem> 

 

Event Text:

   Dr. Etienne H. Meyer ARC Centre of Excellence in Plant Energy Biology
The University of Western Australia Australia "Effect of complex I
mutation on mitochondria and its consequences for growth and cellular
functions"

Event Date:

  Tuesday, March 10, 2009

Event Time:

  09:30 - 10:30

Popup Text:

  ABSTRACT 

Respiratory oxidative phosphorylation is a cornerstone of cellular
metabolism allowing the development of eukaryotic and ultimately aerobic
multi-cellular organisms. Being the largest of the energy-transducing
complexes of the respiratory chain, Complex I is composed of 44 subunits
in Arabidopsis. These subunits are encoded either by nuclear or
mitochondrial genes; remarkably, over 20% of them are plant-specific. 
We characterized an Arabidopsis mutant, ndufs4, lacking complex I, which
has constitutively lowered phosphorylation efficiency. The lack of
complex I has no pleiotropic effects on other respiratory components but
promotes broad changes in the nuclear transcriptome governing growth and
photosynthetic function. We observed large increases in organic acid and
amino acid pools in the mutant, especially at night, concomitant with
large increases in the cellular inorganic phosphate pool s. While
germination is delayed this can be rescued by application of GA, and
root growth assays of seedlings show enhanced tolerance to cold, mild
salt and osmotic stress. Our data suggest that the absence of complex I
alters the adenylate control of cellular metabolism and provide insights
into how cellular metabolism flexibly adapts to reduced phosphorylation
efficiency and why this state may benefit the plant by providing
moderate stress tolerance. 
My future research will build on this analysis of the effects of altered
phosphorylation efficiency on cellular metabolism and plant growth. A
set of Arabidopsis mutants with different degrees of respiration
impairment will provide a system in which the role of respiration on
redox homeostasis, cellular metabolism and ROS signalling can be
studied. I intend to characterize these mutants in order to understand
how a respiratory defect can influence other metabolic pathways such as
glycolysis, photosynthesis or photorespi ration. I will moreover
investigate the assembly of complex I and its functions, especially a
plant-specific role in exporting CO2 produced during photorespiration. 

 

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