Betül Kaçar

We varied the evolutionary distance, and then we kept the experimental conditions the same, and we propagated these populations every day for 150 days.

And we collected bacteria at every step of the way and looked at the sequence.

We wanted to understand what sort of changes may have happened in the genome to respond to the variation that we've introduced.

Exactly.

So we knew where we punched, right?

We punched right at the heart, right?

We punched the translation.

So we expected, is it going to be a translation?

Are we going to see a change?

Will translation respond to this by fixing itself right away?

Or will it be another, outside of translation, something completely different, a different module?

Because translation itself is a module.

Or will it be within elongation, a really sub-protein level translation?

So we had a strategy to identify the mutational pathways by categorizing what we expected to find or where.

It turned out that what we observed in general is that first of all, the harder we hit the cells, the more likely they were to respond by changes, right?

At where we hit it.

I like to think of it as hitting because we are, I like to think of this as breaking the cell, right?

I mean, not breaking enough to kill it, but we still, because they're still alive, they're not doing their job well.

Bigger the hammer, exactly.

That's what it turned out to be because that's what the data told us, that if the variation is higher, then the consequences will also be higher.