Finally, thanks to all my collaborators & to the reviewers for their kind feedback that improved our manuscript!

Dominance reversals have long been hypothesized to help keep large-effect loci polymorphic under changing environments. Our results, further strengthened by laboratory measurements, offer some of the first empirical evidence. Read more in the November @natecoevo.nature.com issue:

At the same time, rapid growth under pesticide implies that dominance cannot be too low when alleles confer a fitness advantage. These observations are consistent with contextual dominance: alleles appear recessive when deleterious but dominant when beneficial.

These two independent measurements allowed us to estimate both the cost and dominance of pesticide resistance: decline in exposed cages after pesticide removal requires a fitness cost, while persistence at low frequency in unexposed cages suggests low dominance.

Simultaneously inferring both parameters is generally difficult, especially for deleterious alleles. In our experiment, however, costly resistant alleles remained low in unexposed cages; in exposed cages, they rose in frequency with pesticide application and began to decline once it was removed.

So excited for you and your group! Congrats!

Unfortunately not, but happy to chat offline!

Here we show that within-cell competition is key to plasmid evolution. Look at this photo of plasmids competing inside cells in a colony!!!

This allowed us to visualize the pattern of clones in the tumor! 10/16

Project scientist in computational population genetics (post PhD/postdoc experience usually expected). recruit.apo.ucla.edu/JPF10171

I am glad to see this work in print & on the cover! Read more at academic.oup.com/genetics/article/228/3/iyae145/7747749

Moving forward, we hope that our theoretical framework can be a starting point for understanding frequency-resolved linkage more broadly. We would love to hear your thoughts!

Our analytical results lead to several empirically relevant findings, e.g. that the dependence of homoplasy on the frequencies of the alleles can distinguish the effects of recombination from the confounding effects of recurrent mutation and epistasis.

We derive how these homoplasy measures depend on the rates of recombination and recurrent mutation, the strength of negative selection and genetic drift, and the present-day frequencies of the mutant alleles.