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Difference between revisions of "HP Modularity"

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(sketched an outline of what to touch on in the abstract/proposal)
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*Evolution of modularity in a host-pathogen system
*Evolution of modularity in a host-pathogen system
*Modularity: a pathogen's answer to host interactions
*Modularity: a pathogen's answer to host interactions
* Do host-pathogen interactions lead to the adaptive evolution for modularity?
*more here
*more here


=== ''Major'' Questions ===
=== ''Major'' Questions ===
#Does modularity in pathogen ''genes'' responsible for an interaction with a host increase its ability to adapt to a host?
#Does modularity in pathogen ''genes'' responsible for an interaction with a host increase its ability to adapt to a host?
# Is modularity in the host required for pathogen modularity to arise/emerge?
#under what conditions does pathogen modularity arise? specifically,
## Is modularity in the host required?
## what configurations of the interaction matrix?
## what influence does population structure have (in the hosts)?
#additional ones here
#additional ones here



Revision as of 21:48, 12 June 2008

Host-Pathogen Modularity

This is the working space for our project. Everything written is a work in progress.

Title Ideas

  • Evolution of modularity in a host-pathogen system
  • Modularity: a pathogen's answer to host interactions
  • Do host-pathogen interactions lead to the adaptive evolution for modularity?
  • more here

Major Questions

  1. Does modularity in pathogen genes responsible for an interaction with a host increase its ability to adapt to a host?
  2. under what conditions does pathogen modularity arise? specifically,
    1. Is modularity in the host required?
    2. what configurations of the interaction matrix?
    3. what influence does population structure have (in the hosts)?
  3. additional ones here

Questions to answer in proposal

  1. why are we studying host-pathogen interactions?
  2. what evidence suggests that modular allelic dependencies might be advantageous in such a host-pathogen system?
  3. give a one-line description of this type of modularity
  4. what conditions do we aim to test to show a benefit to modular dependencies/interaction structures?
  5. what are our null models, i.e. why is (this) result a surprise?
  6. what impact does this have for the understanding of host-pathogen interactions, and evolvability in general?


Model Details

Discrete or continuous?

  1. Pros for discrete: easier to run iterated simulations; possible to run experiments on explicit graph structures
  2. Pros for continuous: mathematical derivations cleaner

Glossary

Modularity Concepts

I'm quite sure that there is some overloading here; but these are the types of modularity that have come up in our discussions:

  1. Modularity for reassortment (Molly)
  2. Modularity for independence (Molly) (I call this 'functional decomposition' - Rob)
  3. Repeated modularity: eg where a body segment occurs many times in an organism (Rob)
  4. Modularity for robustness to antagonistic pleiotrophy (Molly)

Pathogen-related terms

  1. Epitope : the phenotype of a pathogen that interacts with a host
    1. only need to consider a portion of the host's genome since the pathogen only targets a specialised portion of that genome.