Hi Varshit,
3. Regularisation of FBA solution: According to COBRA version 3.0 document, this is the recommended approach to find a unique solution for FBA. However, I am unable to understand the principle properly. Is there a prior publication which I can look into? Can anyone please explain on a non-mathematical level why this gives a unique solution. Can one use this solution to interpret biological phenomenon behind the solution vector?
It depends a bit on the regularisation you use. If you use an L1 regularisation (absolute flux minimization) or L0 normalization (minimial number of active fluxes), the resulting solution is still not guaranteed to be unique (2 alternative pathways of the same length can have any flux as long as their combination satisfies the maximal flux). If you use quadratic regularization (either directly, or as a secondary objective), then you will get a unique solution, since an optimal quadratic minimisation has a unique solution (see e.g. Grafahrend-Belau, E., Schreiber, F., Koschützki, D. & Junker, B. H. Flux balance analysis of barley seeds: a computational approach to study systemic properties of central metabolism. Plant Physiol. 149, 585–598 (2009).)
The biological reasoninig for either regularization is commonly
the assumption, that beside any other objective, an organism will
try to be efficient. And this efficiency is assumed to correspond
to a minimal enzyme usage (and therefore minimal required enzyme
amounts), which is reflected by the minimisation of fluxes.
As a side note here: a Quadratic solution tends to distribute
fluxes as much as possible, i.e. all alternative pathways will
carry flux. In contrast a L1 minimzation (i.e. absolute flux
minimisation) and of course an L0 normalization tend to create a
sparser solutions, which might be easier to interpret.
4. Geometric FBA: However, this also takes up a lot of time and does not provide solution all the time either.
What will be the most recommended method to use among the above options to identify unique flux solution. Also, are there more suitable alternatives as well?
My another question is what is the possible interpretation behind zero biomass growth rate. The most simplified interpretation is that the cell is dead. However, can it also refer to stationary, non-growth phase state of the cell as well? I inquire this because when I observe the flux solution after lethal knockout many reactions are free to choose any flux within their constraints. Should I interpret this as possible decoupling of these reactions with growth and explain this with modular architecture of metabolism?
From a pure FBA perspective, producing biomass is not 100%
equivalent to growing. This is mainly because even under non
growth, components have to be replaced, fixed etc pp, and if there
is no possible flux through the biomass function, this is
impossible for at least some parts of the biomass, which, to me,
indicates a dead or dying cell. There is a method called md-FBA
which takes this into account when checking for growth (i.e. it
assumes metabolic dilution, so all components being used for
growth have to be produced in some small amount to keep the
internal concentrations active). So from my point of view:
If a model cannot produce any biomass, it is dead, or dying. If it
can produce biomass but does not have any biomass flux with
md-FBA, it might still be viable, but it will definitely not grow
a lot any more.
Its not that they are necessarily decoupled. Its just, that enzymes will still do "their job" (i.e. catalyze reactions) as long as their products are not accumulating too much, and since FBA assumes a steady state, we don't incorporate this accumulation...
I hope this helps
Best
Thomas
Thank you!
Warm regards,Varshit Dusad
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optimizeCbModel(model,'max', 0, true, 'lp+')
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Hi Michel,
The call should be:
optimizeCbModel(model,'max',1)
The third argument is the min-norm, which is applied AFTER the original objective. What you suggested is an L0 norm approximation, and which version to use to approximate it.
Best
Thomas
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Hi Varshit,
Personally, I would consider a knockout that causes a
zero-biomass flux as detrimental enough for the system for it to
become inviable, always assuming, that the original model is
complete (i.e. contains all isozymes potentially running the
knocked out reactions), which in itself is a very big assumption.
Remember, that a knock-out would have to be a genetic modification
instead of a knock-down via e.g. shRNA/siRNA or similar processes.
Now, admittedly, such a phenotype might be rescuable by
supplementing the nutrition with those compounds that are being
produced by the knocked-out reaction, but without also adding this
to the model, you have a dying cell, which pretty surely will
throw in many regulatory effects, which are probably not modeled
by your FBA model, so I wouldn't know any good interpretation of
such flux distributions. (Which is not to say that there are
none).
Best
Thomas
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Dear Amanuel,
mdFBA is implemented in the Toolbox (the mdFBA function). Please be aware, that this function tries to solve a MILP problem, which will make it take a long time on larger models.
As for your second question:
If automated methods don't work, you have to adapt the model
manually using literature information. I.e. you will have to
determine which metabolites cannot be produced
(biomassPrecursorCheck), and investigate the network you extracted
the biomass function from with respect to their production
pathways to see, what might be missing in your model.
Also, if you take the biomass composition from a different model,
you need to check, that the ids used in that model are actually
compatible to the ones in your model.
Best
Thomas
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