https://academic.oup.com/emph/article/2017/1/201/4911520

How many passages of the cell lines occurred before they were exposed to the treatments?

Please feel free to post questions and perspectives in the chat! We will open up for discussion at the end of Amanda’s talk.

I noticed that the figure that you showed in relation to the context-dependent eQTLs and associated diseases had mostly?/many auto-immune diseases and wondered what the significance of this might be

Why do you think that so many of the context dependent eQTLS were associated with *autoimmune* diseases? Because you used B cells? Could the higher positive selection signal on context-dependent eQTLs involved in immunity be a function of infectious disease-related selection, given that autoimmune loci are related to infectious disease risks? How does this fit in with mismatch and, say, obesity? Inflammation effects?

I am interested that you decided to use life span associated genes for this study. No one really knows how long flies live in nature. I think to would have been better to do this study on fecundity which would be more closely related to fitness in nature than life span.

Feel free to virtually raise your hand with any questions or perspectives!

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I also wondered why you chose as the "challenges" to the cell lines, environmental pollutants, but not in your Drosophila model? Isn't that a mismatch between the cell line work and the model organism?

We have time for 1-2 more questions or perspectives! Feel free to post in the chat or raise your hand.

What evidence would it take to prove the mismatch hypothesis? are there any “stubborn facts” that undermine the hypothesis? Or are we stuck with fuzzy science?