Meredith A. Sommars, Ph.D.

I have been in the Biological and Health Sciences (BHS) department since January 2022. After earning my B.S. in Biology from Duke University, I earned my Ph.D. in Molecular Biology from Northwestern University, where I also completed a Master of Public Health (MPH) degree. Broadly, I am interested in understanding how cells control expression of metabolic gene programs in health and disease. As a scientist, it is an honor to wonder at and worship God through the study of His creation. I particularly enjoy getting to do this alongside my students. Outside of the classroom and the research lab, I can be found hanging with my husband and two kids.

Northwestern University
Ph.D., Molecular Biology

Northwestern University
M.P.H., Focus in Epidemiology

Duke University
B.S., Biology, with Distinction

• BIOL 241. Organization of Life:  Genetics and Cell Biology
• BIOL 326. Advanced Cell and Molecular Biology
• BIOL 342. Introduction to Bioinformatics
• BIOL 356. Genetics
• BHS 494. The Integrated Biological and Health Scientist
  

• Genetics and genomics
  
• Gene expression regulation
  
• Molecular biology
• Bioinformatics
  
• Liver metabolism
  
• Pancreatic alpha cell
• Public Health
  

Ever since my days as an undergraduate at Duke University, I have been fascinated by understanding how cells finely tune and control which genes are expressed and by how much. One of the great surprises of the Human Genome Project (HGP) was that less than 2% of the human genome encodes for proteins. In the early days following the HGP, the remaining 98% of the human genome was called genetic “junk.” Scientists have spent the last several decades demystifying this “junk” DNA and have since recognized the significant role that non-protein coding DNA plays in controlling how genes are expressed. 

This surprising discovery from the HGP propelled me into the exciting field of human genetics and genomics, as I wanted to be a part of understanding the purpose of the remaining 98% of our genomes. During my PhD program at Northwestern University, I studied the role of a transcription factor called BCL6 in regulating gene programs controlling hepatic lipid metabolism and glucose homeostasis. Transcription factors play critical roles in interacting with non-protein coding DNA sequences to precisely control gene expression in a spatially and temporally dependent manner.

In my lab at Wheaton College, we are broadly interested in understanding how transcription factors control metabolic gene programs. More specifically, I am interested in understanding mechanisms by which extracellular signals control glucagon regulation and secretion in the pancreatic alpha cell. Our studies aim to understand inter-organ signaling mechanisms that control dynamic glucagon regulation, as well as the impact of external exposures such as microplastics on alpha cell glucagon control. Additionally, I study transcriptional control of gene expression in the liver, both during homeostasis and disease. I am particularly interested in understanding how sex-specific gene expression programs contribute to differential metabolic activities and susceptibilities in the liver. I use a variety of cell culture, molecular biology, and bioinformatic approaches in my research.

Fruzyna, E., Sommars, M. A., Omura, Y., Yarnoff, K. M., Wang, J. C., Futtner, C. R., … Barish, G. D. (2025). Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk. Cellular and Molecular Gastroenterology and Hepatology. DOI: 10.1016/j.jcmgh.2025.101706

Ramachandran K, Futtner CR, Sommars MA, Quattrocelli M, Omura Y, Fruzyna E, Wang JC, Waldeck NJ, Senagolage MD, Telles CG, Demonbreun AR, Prendergast E, Lai N, Arango D, Bederman IR, McNally EM & Barish GD (2024), Transcriptional programming of translation by BCL6 controls skeletal muscle proteostasis. Nature Metabolism 6(2): 304- 322. DOI: 10.1038/s42255-024-00983-3

Kriegermeier A, Hyon A, Sommars MA, Hubchak S, LeCuyer B, Liu X, Barish G and Green RM (2021), Hepatic X-Box Binding Protein 1 and Unfolded Protein Response Is Impaired in Weanling Mice With Resultant Hepatic Injury. Hepatology. DOI: 10.1002/hep.32031

Levine, D.C., Kuo, HY., Hong, HK. et al. NADH inhibition of SIRT1 links energy state to transcription during time-restricted feeding. Nat Metab 3, 1621–1632 (2021). https://doi.org/10.1038/s42255-021-00498-1

Ramachandran K, Senagolage MD, Sommars MA, Futtner CR, Omura Y, Allred AL, et al. (2019) Dynamic enhancers control skeletal muscle identity and reprogramming. PLoS Biol 17(10): e3000467. https://doi.org/10.1371/journal.pbio.3000467

Sommars MA, Ramachandran K, Senagolage MD, Futtner CR, Germain DM, Allred AL, Omura Y, Bederman IR, Barish GD. Dynamic repression by BCL6 controls the genome-wide liver response to fasting and steatosis. eLife 2019; 8. doi: 10.7554/eLife.43922. DOI: 10.7554/eLife.43922

Senagolage MD, Sommars MA, Ramachandran K, Futtner CR, Omura Y, Allred AL, Wang J, Yang C, Procissi D, Evans RM, Han X, Bederman IR, Barish GD. Loss of transcriptional repression by BCL6 confers insulin sensitivity in the setting of obesity. Cell Rep 2018; 25(12):3283-3298.e6. doi: 10.1016/j.celrep.2018.11.074. DOI: 10.1016/j.celrep.2018.11.074

Alleyne D, Witonsky DB, Mapes B, Nakagome S, Sommars MA, Hong E, Muckala KA, Di Rienzo A, Kupfer SS. Colonic transcriptional response to 1α,25(OH)2 vitamin D3 in African- and European-Americans. J Steroid Biochem Mol Biol. 2017 Apr;168:49-59. doi: 10.1016/j.jsbmb.2017.02.001. Epub 2017 Feb 3. PMID: 28163244; PMCID: PMC5642973. DOI: 10.1016/j.jsbmb.2017.02.001

Mapes B, Sommars (née Chase) MA, Hong E, Ludvik A, Ceryes K, Huang Y, Kupfer SS. Ex vivo culture of primary human colonic tissue for studying transcriptional responses to 1α,25(OH)2 and 25(OH) vitamin D. Physiol Genomics. 2014 Apr 15;46(8):302-8. doi: 10.1152/physiolgenomics.00194.2013. Epub 2014 Feb 18. PMID: 24550213; PMCID: PMC4035659.

Maranville JC, Baxter SS, Witonsky DB, Sommars (née Chase) MA, Di Rienzo A. Genetic mapping with multiple levels of phenotypic information reveals determinants of lymphocyte glucocorticoid sensitivity. Am J Hum Genet. 2013;93(4):735-743... doi:10.1016/j.ajhg.2013.08.005