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SUMMARY:Plenary Lecture 12: The causes and consequences of metabolic speci
 alization - Johnson\, D (ETH Zrich)
DTSTART:20141031T115500Z
DTEND:20141031T123000Z
UID:TALK55846@talks.cam.ac.uk
CONTACT:Mustapha Amrani
DESCRIPTION:Co-authors: Elin E Lilja (ETH Zrich and Eawag)\, Felix Goldsch
 midt (ETH Zrich and Eawag)\, Martin Ackermann (ETH Zrich and Eawag) \n\nCo
 nsider a microbial cell residing within a lake\, soil\, or the human gut. 
 This cell encounters a myriad of different substrates that could theoretic
 ally satisfy its growth requirements. Yet\, even if this cell were near st
 arvation\, it would only consume a subset of the available substrates. Why
  is this? What is the advantage of consuming only a subset of the availabl
 e substrates rather than all of them? We hypothesize that particular metab
 olic processes are in biochemical conflict with each other\, thus causing 
 those processes to be more effectively performed by different strains than
  by the same strain. A biochemical conflict could occur\, for example\, if
  different metabolic processes compete for the same pool of limiting intra
 cellular resources or if different metabolic processes produce products th
 at inhibit other metabolic processes. In this talk\, I first present a gen
 eral theoretical model that uses information about biochemical conflicts t
 o predict whether any two metaboli c processes will be retained by a singl
 e metabolic generalist strain or will segregate into different metabolic s
 pecialist strains over evolutionary time. I next present empirical evidenc
 e of specific environmental conditions when consortia of metabolically spe
 cialized strains consume substrates more rapidly than a single metabolic g
 eneralist strain. Our findings are potentially relevant for any pair of me
 tabolic processes and could therefore be useful for predicting how best to
  distribute different metabolic processes among different cells in order t
 o maximize the conversion of a substrate into a desired product.\n
LOCATION:Seminar Room 1\, Newton Institute
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