Interpretation of PRODIGY and SPOTON result

Hi!

Just want to ask for opinion on how to interpret the results from PRODIGY and SPOTON.

I’ve generated a pairwise protein A-B complex model and processed with both tools, both returned reasonable results but hotspots annotation is missed in SPOTON result. We have experimental data to back the affinity is not as high as nm level like antibody-antigen binding.

My question is should I report both or just take PRODIGY interface result, or I can still use SPOTON but state the affinity is not as high that’s why hotspot is not able to be characterized in such case? Had a hard time to understand how should I interpret and present the Null-spots only.

Many thanks for your help in this!

Just want to ask for opinion on how to interpret the results from PRODIGY and SPOTON.

I’ve generated a pairwise protein A-B complex model and processed with both tools, both returned reasonable results but hotspots annotation is missed in SPOTON result. We have experimental data to back the affinity is not as high as nm level like antibody-antigen binding.

Remember these are all prediction methods and as such not perfect.

How stable are your predictions if you use a slightly different model?
How did you generate the models?

Dear Prof. Bonvin,

Thank you for your prompt response.

The top models tried here were selected from two sets of docking models, generated by a knowledgeable collaborator using the latest Rosetta docking protocol based on how well each model accommodates the confident intermolecular cross-links between the two partner proteins. I will need to ask him for other highly ranked models from the same cluster, but I am certainly willing to explore whether SPOTON will predict any hotspots out of them.

In my last application of studying monoclonal antibody-antigen complex using SPOTON and PRODIGY, the derived interfaces, with hotspots annotated, aligned perfectly with the experimental HDX-MS epitope mapping data. This led me to hypothesize that the actual binding affinity might need to be strong enough to facilitate differential prediction of the hotspots in the binding interface. Curious to ask for your opinion on such assumption.

Interesting. But no idea is this is the case (sounds reasonable though).
Would need a good benchmark dataset to test this hypothesis