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BAPG schedule

BAPG schedule.

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The Coop Lab will be hosting the sixth Bay area population genomics (BAPG) meeting at UC Davis on May 26th. This is a great informal meeting 2-3 times a year of the Bay area evolutionary and population geneticists. The signup sheet for the sixth Bay area population genomics meeting at UC Davis is here http://tinyurl.com/72wd9xr. Details below. Please signup to give talks and posters, as this offers a great opportunity to present your work to a friendly audience of fellow evolutionary and population geneticists. Details below.

Best wishes,
Yaniv Brandvain, Alisa Sedghifar, Peter Ralph, Jeremy Berg, Graham Coop

BAPG VI: May 26, 2012

1322 Storer Hall (map: http://campusmap.ucdavis.edu/?b=145 ), UC Davis

Tentative Schedule:

9:00-10:00 – Morning reception and poster set-up, Coffee, and snacks provided
10:00-11:00 – Talks
11:00-11:30 – break
11:30-12:30 – Talks
12:30-1:30 – Lunch and Poster session
1:30-2:30 – Talks
2:30-4:00 – Hangin out

Tentative talk format:…

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[Kummerspeck: literally grief bacon in German. The excess weight gained from from over eating.]

In the Coop lab we’ll be piling on the kummerspeck due to our sadness at Torsten leaving the lab to return to Germany.

For the past 6 months we’ve been hosting Torsten Gunther a PhD student from Hohenheim. Torsten has been working on a variety of projects on detecting adaptation and gene flow in A. thaliana during his time with us. One of his projects has been to extend Bayenv to more robustly identify local adaptation through environmental correlations, we hope to have that program and a paper out shortly.

It’s been really great fun having Torsten in the lab – both scientifically and socially – and we’ll miss him hugely. (Yaniv and he had a running argument over who ate the last of the cookies and cakes, and Torsten was constantly amazed about…

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Looking to spruce up both my actual and virtual homes, I was cruising through sally harless’ blog late one night. In her post, ‘things i am obsessed with‘, sally pointed out some work by elly mackay [website, blog]. I thought elly’s work was awesome, and purchased two pictures for my house (right).

elly kindly gave me permission to share her work on my site. So, if you see a new or unfamiliar image in my header above, relax and enjoy. If you like it, do check out elly’s website.

Her work/process is super cool. In brief, she cuts out small pieces of plastic paper, and then she colors, bends, and arranges them into amazing images. Next, she puts them in a small ‘theater’ to hold all of the paper together, and takes pictures of her work under differing light conditions, giving the similar creations very different feels (Compare the lively, springtime picture below, to the warm, autumnal image above).

Thanks elly mackay

Here’s a picture of elly setting up the theater (super cool)

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Although I study conflict, I like to avoid it in real life, and  in my professional work. However, I recently had a small dispute over a recent paper of mine. In brief, Phil Hedrick considered it incorrect to discuss ‘inbreeding’ at haploid, uni-parentally inherited loci. Here I briefly review my original paper, Hedrick’s comment, and our response. On the whole I think the debate was fun, although I’d rather be doing science than nitpicking about words, it is important that scientists form a common language to best communicate with one another and the greater community.

Mother’s curse – or ‘What’s in it for a mitochondrion in a male’: Since anything that is strictly inherited maternally is never transmitted by males, it seems like mitochondrial influences male fitness should be invisible to selection. This has been called ‘Mother’s curse’ by Gemmell et al, and Frank and Hurst argued that it may explain some diseases that preferentially strike males and may involve the mitochondria (e.g. Leber’s hereditary optic neuropathy).

Reversing Mother’s curse: The idea of mothers’ curse seems compelling, but my graduate co-advisor, Mike Wade and I thought that some proceses could reverse mother’s curse. Specifically, we argued that when maternal sibs depend on each other for help (i.e. kin selection) or mating (i.e. inbreeding)  the success of a mitochondria in a female may depend on her brother. We argued that this indirect selection could act to maintain mitochondrial which function well in males. At the same time my friend, Rob Unckless and his collaborator Jeremy K. Herren came to the same conclusion.

Inbreeding and mitochondria: Recently, Phil Hedrick argued that since mitochondria are haploid, individuals cannot inbreed at mitochondrial loci. His argument is based on a common definition of the inbreeding level as the deviation in genotype frequencies from Hardy-Weinberg expectations (i.e. binomial sampling). With this definition of inbreeding, we cannot measure inbreeding at haploid loci, and therefore mitochondria cannot be inbred. Although this makes some sense, we countered that individuals cannot be inbred at haploid loci, they can inbreed with respect to mitochondrial loci. That is we consider mating between relatives tobe inbreeding, while Hedrick considers the deviation from Hardy Weinberg to be inbreeding. In our response we pointed out a few benefits of our ‘process’ rather than ‘outcome’ – oriented approach.

comments/thoughts appreciated


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Best Commercial Ever.

At NESCENT, I hung out with my friend, jon wilkins. Jon maintains a broad internet presence including his cartoon, Darwin eats cake,  and his blog, Lost in transcription. Jon pointed out the most incredible commercial ever on his blog.

So, this is apparently an actual television ad for Burger King in Russia, which is soooo much better than Burger King in America.

At Burger King in Russia, you ride on unicorn. At Burger King in Capitalist America, unicorn rides you!

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Imprinting @ NESCENT

Imprinting @ NESCENT I am back from a week long trip to The National Evolutionary Synthesis Center (NESCENT), where I was discussing the evolution of parent of origin dependent gene expression (i.e. genomic imprinting). Genomic imprinting is special to me, as it is one of the amazing things that first excited me about studying evolutionary biology.

The kinship theory

The most widely accepted theory of the evolution of genomic imprinting (articulated by David Haig), is known as the kinship theory. According to the kinship theory, a major force influencing the evolution of imprinting is the selective pressure arising from the fact that individuals may have different degrees of relatedness via maternally and paternally inherited alleles (e.g. my maternally inherited alleles are more likely to be present in my maternal aunt, Alice than in my paternal aunt, Rifka).

Since relatedness plays a major role in the evolution of cooperative behavior, the selectively favored level of cooperation may differ at maternally and paternally inherited loci. This idea is largely born out by considering the phenotypic effect of many imprinted genes: alleles expressed when paternally inherited are often growth promoters, while alleles expressed when maternally inherited are often growth enhancers. I have previously argued that this conflict can generate reproductive isolation between plant species, I have also extended the theory to more complex interactions, and suggested how our an extended kinship theory can be evaluated in light of next-gen transcriptome data.

However, not all imprinted genes work this way, and it was clear from the meeting that not everyone in the field is on board with this theory. Hopefully, this discontent will lead to novel tests of the kinship theory, careful evaluation of alternative  ideas (e.g. the coadaptation theory), and new theoretical proposals.

Genomic imprinting in the transcriptomic era

Historically, most imprinted regions were discovered by observing gross phenotypic effects in reciprocal crosses. This phenotypic work was then followed up with careful genetic experiments. This laborious method has taught us much about imprinting, but is a lot of work and leaves us with a biased view of imprinting – only imprinted genes with large and observable phenotypic effects can be easily identified. But now we can identify imprinted genes by quantitative RNA sequencing. This new technology provides the potential to discover all imprinted genes in the genome without bias, across many species, cell types, and development.

However, I there are some hazards associated with these data. Andy Clark pointed out that since most RNA-Seq data is associated with an amplification step, there is an extra round of sampling. Thus asking whether there is a significant difference in read counts of alternative alleles from a single locus (without biological replicates, or numerous independent amplifications) is not great evidence for diferences in allelic expression. It seems that the safest way forward is to conduct numerous replicates and to confirm candidate alleles with other technologies (e.g. pyrosequencing).

I also learned a few other things to be cautious about when studying imprinting. Specifically, Ueli Grossniklaus pointed out that it is not always easy to differentiate between maternally contributed RNAs and imprinted loci. In fact, if you’re using inbred lines, it is not possible to tell the differences between these explanations without having some hunch (or data) suggesting that candidate imprinted alleles are not maternally derived RNAs. In animals, this problem could be adressed by using heterozygous parents; however, this makes it more difficult to uncover imprinted loci. Even worse, using heterozygous maternal plants does not solve this issue because maternal RNAs are derived from the haploid mega-gametophyte, which is genotypically equivalent to maternally derived chromosomes in the embryo and endosperm.

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