Watch presentations from the conference, including talks from Katie Peichel and Jonathan Pritchard.

Now that the dust has settled from the whirlwind of the first ever standalone GSA Population, Evolutionary, and Quantitative Genetics Conference (PEQG18), we’re delighted to be able to share the audio and synched slides from the Keynote and Crow Award sessions.

We’re gratified too that attendees got so much of value from the conference. Many have approached GSA staff and the conference organizers with rave reviews of their experience, and, despite the usual growing pains of a new conference, the results from the attendee survey have also been overwhelmingly positive.

We’re excited to incorporate some of the lessons we’ve learned into planning the next PEQG. It will be held April 22–26, 2020 in the metro Washington, DC, area at The Allied Genetics Conference (TAGC20). PEQG will join the C. elegans, Drosophila, mouse, Xenopus, yeast, and zebrafish research communities for a mix of community-specific and cross-community sessions.

Stay tuned for more announcements on the upcoming conference and for several more PEQG18 blog reports in the coming weeks. Enjoy the talks below!

PEQG18 Keynotes

Jonathan Pritchard Stanford University/HHMI

Omnigenic Architecture of Human Complex Traits

Catherine Peichel University of Bern

Genetics of Adaptation in Sticklebacks

Trudy Mackay North Carolina State University

Context-Dependent Effects of Alleles Affecting Genetic Variation of Quantitative Traits COMING SOON

Finalists for the 2018 Crow Award for Early Career Researchers

Amy Goldberg UC Berkeley

A mechanistic model of assortative mating in a hybrid population

Emily Josephs UC Davis

Detecting polygenic adaptation in maize

Jeremy Berg Columbia University 

Population genetic models for highly polygenic disease

Katherine Xue University of Washington 

Evolutionary dynamics of influenza across spatiotemporal scales

Alison Feder Stanford University 

Intra-patient evolutionary dynamics of HIV drug resistance evolution in time and space

Emily Moore North Carolina State University 

Genetic variation at a conserved non-coding element contributes to microhabitat-associated behavioral differentiation in Malawi African cichlid fishes

Videos

Jonathan Pritchard 

[youtube https://youtu.be/H18k55ruCOY&w=500&rel=0]

Catherine Peichel

[youtube https://youtu.be/QRCcLixjUtc&w=500&rel=0]

Amy Goldberg 

[youtube https://youtu.be/kccUNkF7SgY&w=500&rel=0]

Emily Josephs 

[youtube https://youtu.be/CxQOrK9h6D4&w=500&rel=0]

Jeremy Berg

[youtube https://youtu.be/HqA1H24LPZc&w=500&rel=0]

Katherine Xue

[youtube https://youtu.be/fTdaAwqdt0k&w=500&rel=0]

Alison Feder

[youtube https://youtu.be/ntM0448h2lA&w=500&rel=0]

Emily Moore

[youtube https://youtu.be/aX4_HS0K1kA&w=500&rel=0]

Corn feeds millions of people, and its low cost makes it particularly important in developing countries. However, it can’t be relied on as the sole source of protein for either humans or livestock because—like most cereals—corn is low in certain essential amino acids. In the 1960s, a type of corn was discovered with boosted levels of the essential amino acid lysine, which is typically found in small amounts in corn. But the variety had no practical use because it had a soft kernel that made it unfit for storage and transportation. To combat this problem, breeders developed Quality Protein Maize (QPM), a strain with restored kernel hardness—but there’s still room to improve corn’s nutritional profile.

In GENETICS, Planta and Messing describe how they constructed a strain that not only has more lysine, but also has an increased level of methionine, another essential amino acid found in insufficient amounts in corn. In addition to being more nutritious for humans, a strain with more methionine would make better feed for livestock; currently, synthetic methionine is often added to corn-based animal feed.

A key feature of QPM strains that makes them richer in lysine is a shift in the proportions of different proteins in the kernels, and the new strain is no exception. The lysine content is normally low in corn because most of the proteins in the mature kernel are from a group of proteins called zeins, the bulk of which contain few lysine residues. The original QPM strain has a mutation in the gene opaque-2 that decreases the production of many zeins, but there are other ways to achieve the same result.

Planta and Messing started with a strain carrying an RNAi gene that dampens the translation of RNA into a zein protein. Because this zein was known to be critical for kernel hardness, the strain had undesirably soft kernels, but the researchers serendipitously came upon a solution when they crossed the strain with their new high-methionine strain, called PE5. They had made PE5 by introducing a gene that increases flux through a biochemical pathway that produces sulfide, which is a precursor in the synthesis of methionine. To the researchers’ surprise, this cross produced a new strain that has a hard kernel and retains PE5’s superior methionine content, and it even has more lysine than its progenitors do, making it an excellent candidate for a new type of QPM.

Because the traits are dominant, it should be possible to add them to many existing strains of corn simply by crossing them with the new strain. Continued investigation of such enhanced corn strains is crucial—QPM strains are already in use, so an improved variety could make an even more significant dent in the malnutrition that plagues many regions where other protein sources are not readily available.

CITATION:
Planta, J.; Messing, J. Quality Protein Maize Based on Reducing Sulfur in Leaf Cells.
GENETICS, 207(4), 1687-1697.
DOI: 10.1534/genetics.117.300288
http://www.genetics.org/content/207/4/1687

If not for a single-nucleotide mutation, each kernel on a juicy corn cob would be trapped inside an inedible casing as tough as a walnut shell. In the July issue of GENETICS, Wang et al. identify an amino acid substitution that was key to the development of the so-called “naked” kernels that characterize modern corn (maize).

The domestication of maize has long fascinated biologists studying evolution. It can provide clues to how organisms change under selection — whether it’s natural selection or selection by humans choosing the most delicious and productive plants to grow in next year’s crop. Maize is a particularly powerful system because many methods and resources are available for its study and because it can be crossed with its wild progenitors for genetic analysis.

Maize was domesticated in Mexico around 9,000 years ago from the grass teosinte. Teosinte seeds are protected by a hard casing that makes them impractical to eat, but ancient plant breeders developed varieties with naked kernels. In these plants, the structures that form the seed case (technically a “fruitcase”) instead become the cob at the center of the ear, leaving the seed exposed for us to eat. Humans effectively turned the teosinte ear inside out, says study leader John Doebley (University of Wisconsin-Madison).

Left: Teosinte ear; right: maize ear; center: ear from the first generation hybrid of a cross between teosinte and maize. Photo credit: John Doebley.

Besides having lost the inconvenient fruitcase, corn kernels today remain firmly attached to the cob, rather than scattering easily as they do in teosinte. The cobs are also much larger, and maize has fewer leaf branches than its ancestor. All these changes evolved relatively quickly, within a few thousand years at most.

Over the last few decades, Doebley and his colleagues have mapped the genes responsible for these differences. They found that genes controlling many of these traits mapped to as few as six genomic locations. Fine-mapping revealed the major gene controlling naked kernel formation is tga1, a transcription factor from a family that regulates floral development.

The teosinte version of tga1 allows formation of an enclosed fruitcase. But maize tga1 disrupts this process, resulting in cases that are smaller and don’t fully enclose the kernel. But what exactly is different about the two versions of the tga1 gene?

To find out, the team compared the tga1 DNA sequence in 16 different maize varieties and 20 varieties of teosinte. They discovered only one variant fixed in all the maize samples but present in none of the teosinte: a single nucleotide change in the coding sequence of tga1 that changes one amino acid in the encoded protein from lysine to asparagine.

When the researchers tested the effect of this substitution on the TGA1 protein, they found that the maize version of the protein had a greater tendency to form dimers. The maize allele also seemed to turn TGA1 into a transcriptional repressor of its target genes, while the teosinte TGA1 did not act as a repressor in reporter assays.

This evidence suggests that repressing TGA target genes alters fruitcase development, contributing to the naked kernel trait.

Consistent with this idea, the researchers found that using RNAi to dampen expression of the maize tga1 gene itself—which should relieve repression of the target genes—enlarged the fruitcase remnant structures in maize. In other words, levels of the maize version of tga1 control the size of the maize structures that would normally form the seed case in teosinte.

These results provide an example of how selection by ancient plant breeders triggered profound structural change in an organism through relatively minor genetic alterations, allowing new traits to evolve rapidly.

“Twenty years ago, it was much harder to study evolution in such detail. It’s exciting that we can now understand complex examples like maize domestication at their most fundamental level,” says Doebley. He also acknowledged the major contributions of lead author Huai Wang for his “series of brilliant experiments that solved a big problem in maize evolution.”

CITATION

Evidence that the origin of naked kernels during maize domestication was caused by a single amino acid substitution in tga1 (2015). Huai Wang, Anthony J. Studer, Qiong Zhao, Robert Meeley, and John F. Doebley. Genetics 200(3): 965-974 doi: 10.1534/genetics.115.175752

http://genetics.org/content/200/3/965