Difference between revisions of "Long Range Dpp Gradient Formation"

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<newstitle> Understanding Dpp gradient formation mechanism </newstitle>
 
<newstitle> Understanding Dpp gradient formation mechanism </newstitle>
 
     <teaser>
 
     <teaser>
In collaboration with the Basler group (University of Zurich), we developed a theoretical model allowing to understand which is the leading mechanism involved in the Dpp long range gradient formation.
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In collaboration with the Basler group (University of Zurich), we developed a theoretical model allowing to understand which is the leading mechanism involved in the Dpp long range gradient formation. The article appeared online in <a href="http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001111">PLoS Biology</a> on 26 July 2011.
 
 
The article appeared online in [http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001111 PLoS Computational Biology] on 26 Juli 2011.
 
 
     <date>18 October 2011 — 11:13</date>
 
     <date>18 October 2011 — 11:13</date>
 
     </teaser>
 
     </teaser>
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In a recent paper (for more details [http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001111 click here]), we developed a rigorous theoretical model which involves three Dpp components: extracellular Dpp, receptor-bound Dpp and internalized Dpp. Providing a different parameter choice, this model allows to describe both the RMT and RED mechanism.
 
In a recent paper (for more details [http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001111 click here]), we developed a rigorous theoretical model which involves three Dpp components: extracellular Dpp, receptor-bound Dpp and internalized Dpp. Providing a different parameter choice, this model allows to describe both the RMT and RED mechanism.
Comparing our analytical model to wild-type and receptor mutant clone experimental data, we conclude that \\
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Comparing our analytical model to wild-type and receptor mutant clone experimental data, we conclude that  
(1) the RMT mechanism is not consistent with our experimental data\\
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(1) the RMT mechanism is not consistent with our experimental data
 
(2) a RED mechanism where most of the Dpp is unbound to the receptor leads to the expected Dpp profiles.
 
(2) a RED mechanism where most of the Dpp is unbound to the receptor leads to the expected Dpp profiles.
  

Latest revision as of 17:06, 20 August 2012



Decapentaplegic (Dpp) is a key morphogen which is expressed in a stripe of cells along the anteriorposterior (A-P) boundary of the Drosophila wing imaginal discs and diffuses along the A-P axis forming, at steady-state, a "quasi exponential" profile. The mechanisms by which this profile is formed has however long been controversal and two distinct mechanisms involving Dpp receptors have been proposed: Receptor-Mediated Transcytosis (RMT) and Restricted Extracellular Diffusion (RED).

In a recent paper (for more details click here), we developed a rigorous theoretical model which involves three Dpp components: extracellular Dpp, receptor-bound Dpp and internalized Dpp. Providing a different parameter choice, this model allows to describe both the RMT and RED mechanism. Comparing our analytical model to wild-type and receptor mutant clone experimental data, we conclude that (1) the RMT mechanism is not consistent with our experimental data (2) a RED mechanism where most of the Dpp is unbound to the receptor leads to the expected Dpp profiles.


Gerald Schwank, Sascha Dalessi, Schu-Fee Yang, Ryohei Yagi, Aitana Morton de Lachapelle, Markus Affolter, Sven Bergmann, Konrad Basler
Formation of the long range Dpp morphogen gradient.
PLoS Biol.: 2011, 9(7);e1001111
[PubMed:21814489] [WorldCat.org] [DOI]