Academic journal article Genetics

Beautiful Piles of Bones: An Interview with 2017 Genetics Society of America Medal Recipient David M. Kingsley

Academic journal article Genetics

Beautiful Piles of Bones: An Interview with 2017 Genetics Society of America Medal Recipient David M. Kingsley

Article excerpt

The Genetics Society of America Medal is awarded to an individual for outstanding contributions to the field of genetics in the last 15 years. Recipients of the GSA Medal are recognized for elegant and highly meaningful contributions to modern genetics, exemplifying the ingenuity of GSA membership. The 2017 recipient is David M. Kingsley, whose work in mouse, sticklebacks, and humans has shifted paradigms about how vertebrates evolve. Kingsley first fell in love with genetics in graduate school, where he worked on receptor mediated endocytosis with Monty Krieger. In his postdoctoral training he was able to unite genetics with his first scientific love: vertebrate morphology. He joined the group of Neal Copeland and Nancy Jenkins, where he led efforts to map the classical mouse skeletal mutation short ear. Convinced that experimental genetics had a unique power to reveal the inner workings of evolution, Kingsley then established the stickleback fish as an extraordinarily productive model of quantitative trait evolution in wild species. He and his colleagues revealed many important insights, including the discoveries that major morphological differences can map to key loci with large effects, that regulatory changes in essential developmental control genes have produced advantageous new traits, and that nature has selected the same genes over and over again to drive the stickleback's skeletal evolution. Recently, Kingsley's group has been using these lessons to reveal more about how our own species evolved.

This is an abridged version of the interview. The full interview is available on the Genes to Genomes blog, at genestogenomes. org/kingsley/.

What inspired you to become a scientist?

My dad died of cancer when he was 34. As a little kid I was aware that you don't know how long you have left, and I grew up wanting to make sure I spent the time I have doing something interesting and important. I thought that tackling ageold mysteries about life's origin and mechanisms was a good way to spend my life.

What did you learn from your first mentors?

I was a kid who loved dinosaurs and skeletons. That interest was nurtured by a great high school teacher, Jack Koch at Roosevelt High School in Des Moines, Iowa. In his advanced biology class we memorized the names of every bone and muscle in the cat and human skeleton. A lot of people hated it, but I loved it because you could see so much about the function and lifestyle ofthe organisms from the size and shapes and patterns ofbones.

In graduate school I fell in love with the power ofgenetics. I had a set of teachers at MIT, including David Botstein and Monty Krieger, who helped me learn that with genetics you didn't have to assume anything about the answer to your question. You didn't have guess that you were looking for a particular type of molecule or anything like that. Genetics was an algorithm that would take you to the key components controlling a biological system no matter what they were.

Why did you choose to work on the short ear gene?

Vertebrate genetics takes a long time, so you should pick your problem carefully. I didn't want to pick something that was better studied in bacteria, yeast, or powerful invertebrate systems. The skeleton was perfect; it's the defining feature of vertebrates. It also plays such an important role in animals' external appearance that many classic mutants had already been picked up in simple morphological screens.

After World War II there had been a lot of interest in the effects of radiation on the mammalian germline, and there were two big mouse forward mutation experiments in the UK and US. They both used a test strain carrying seven homozygous recessive mutations with visible phenotypes. These were six pigment mutations and short ear. Millions of wild type mice were mutagenized and crossed with the test strain to measure the rate that new alleles were recovered at any of the seven loci. As a result, there were lots of newly induced mutations, including a whole set of deficiency chromosomes that took out both short ear and one of the closely linked pigmentation loci. …

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