My new Genetics paper just came out [link]! This paper represent my final dissertation chapter and a whole lot of hard work and learning. It’s also cool to be in such an exciting issue of Genetics. My google reader just exploded with this new issue, so I have now expanded my RSS to show my 10 most recent starred items.
Brief summary: Although strict maternal symbiont acquisition will create a strong association between a maternally inherited organelle and a symbiont, rare non-maternal transmission erases population-level signatures of maternal symbiont transmission more.
How I feel: Publishing a paper is a lot of work, but most papers go unread and uncited, or are met by heavy criticism. Thus with every publication, I feel like Navin R. Johnson opening up the new phonebook.
but I’m optimistic that this paper will be useful for population geneticists.
Background: Our nuclear genome consists of two copies of 23 chromosomes. We inherit one copy of each chromosome from our mother (a mix of our maternal grandparents), and father (a mix of our paternal grandparents). However, we inherit our mitochondria exclusively from our mother, and therefore the mitochondria provides a view into our matrilineal heritage. In fact we often inherit numerous things from our mother an not our father [belated (or early) mother’s day song].
Motivation: Because of our close relationship with our mothers, and because some microbes insert themselves into eggs, we (e.g. eukaryotes) often inherit a large complement of microbes maternally. But this maternal symbiont transmission is often incomplete – that is,we can pick up copies of microbes from someone other than mom. With my PhD advisor, Mike Wade, and collaborator, Charles Goodnight, I asked how if we could get a sense of how often we ended up with a copy of our mom’s microbes by looking at the genetics coupling (i.e. linkage disequilibrium) between our mitochondria and a microbe that we get from our mom sometimes.
Methods and Results: With some math and some computer simulations [simulation code in R], we examined the covariation between mitochondrial and symbiont genotypes as a function of how often we inherit a microbe maternally. We find that nearly any degree of non-maternal symbiont inheritance destroys any population level association between mitochondrial and symbiont loci.
Assumptions: Our major assumptions are that a population mixes randomly (i.e. panmixis)*, that generations are non-overlapping, and that both mitochondrial and symbiont genomes are evolving neutrally. These assumptions are (obviously) nearly all wrong, but I think that this model provides a nice heuristic view, and very weird biology would need to be happening to get anything different form our qualitative conclusions.
Interpretation and conclusions: Unlike meiosis, which is semi-conservative, and provides detailed signals of history at partially linked loci, horizontal symbiont transmission demolishes all past history. Therefore, it seems unlikely that we will be able to generate a high resolution view of the joint history of hosts and symbionts [compared to the detailed view of demographic history that we get from considering partially linked nuclear loci]…. bummer. Rather, we’ll probably need to rely on old methods in which we look at how well symbiont and host phylogenetic trees line up. In fact, our paper implies that even those methods won’t provide an accurate measurement of the histories of hosts and symbionts, because rare transmission between species can erase the signal built up by generations of evolution.
* In an earlier draft, we included a more complex model in which there was a metapopulation of hosts with arbitrary rates of migration between demes. On the whole, our results weren’t super sensitive to this, and the math was pretty ugly looking, so we ditched it. The major thing that we missed out on is that strong population structure can maintain some association between symbiont and mitochondrial genome. This earlier draft is available upon request.