Molly Schumer
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Princeton University
2018 Rising Star in Evolutionary Biology, Atwood Colloquium
Molly Schumer | |
|---|---|
| Alma mater | Reed College Princeton University |
| Known for | Biological hybrids |
| Awards | 2019 Rosalind Franklin Young Investigator, Genetics Society of America 2018 Rising Star in Evolutionary Biology, Atwood Colloquium |
| Scientific career | |
| Fields | Ecology, Evolution |
| Website | https://schumerlab.com/ |
Molly Schumer is an American scientist who studies evolution, hybridization, and population genetics. She is an assistant professor of biology at Stanford University.[1] She is a member of Stanford Bio-X and a Hannah H. Grey Fellow at the Howard Hughes Medical Institute.[2][3]
Schumer completed her Bachelor of Arts in 2009 at Reed College, earning Phi Beta Kappa.[4][5] She went on to pursue her PhD in Ecology and Evolutionary Biology at Princeton University (jointly supervised by Peter Andolfatto and Gil Rosenthal), finishing in February 2016.[6][7]
After her PhD, Schumer worked as a postdoctoral researcher at Columbia University with Molly Przeworski before joining the Harvard Society of Fellows in July 2016, where she worked in the lab of David Reich.[8][7] She became a Hanna H. Grey Fellow at HHMI in 2017, and was hired for her current assistant professorship at Stanford University in 2019.[3]
Research
Schumer's lab investigates biological hybrids and population genetics. Model organisms used in the lab are primarily fish and include the Gila topminnow, Xiphophorus (swordtail), and Julidochromis.[9]
Key Publications
Schumer has authored or co-authored multiple publications that have been cited 100 or more times.[10] As of January 2021, these include:
- "How common is homoploid hybrid speciation?" Evolution.[11]
- "Parallel molecular evolution in an herbivore community," Science.[12]
- "Phylogenomics reveals extensive reticulate evolution in Xiphophorus fishes," Evolution.[13]
- "Natural selection interacts with recombination to shape the evolution of hybrid genomes," Science.[14]
- "A serine cluster mediates BMAL1-dependent CLOCK phosphorylation and degradation," Cell Cycle.[15]
