Christopher Gregg, Ph.D.

Assistant Professor of Neurobiology and Anatomy
Adjunct Assistant Professor of Human Genetics

(b. 1975); B.S. 1998, University of Lethbridge; Ph.D. 2006, University of Calgary; Post-Doctoral Fellow 2006-2011, Harvard University, Dept. of Molecular and Cellular Biology.

Department Phone: (801) 581-6128

Visit the Gregg Laboratory web site.


In many ways, adult health and behavior is a reflection of developmental processes and early life experiences. Uncovering the early life processes and mechanisms of inheritance that influence adult behavior and health is fundamental to our understanding and treatment of neurological and psychiatric diseases, as well as to broader social issues related to diet, parenting, education, and socioeconomic policies.

My laboratory is focused on understanding epigenetic and genetic pathways that influence feeding circuits and the neuroeconomic decision-making processes associated with foraging behavior (eg. assessing risk versus reward).  In particular, we are working to uncover heritable epigenetic regulatory pathways that communicate information from parents to offspring and that are able to influence gene expression in the brain and offspring behavior. Maternally and paternally inherited chromosomes are not functionally equivalent due to heritable epigenetic marks, called genomic imprints, which are formed at specific sites in the genome in the gametes of the parents.   Imprinted genes are unique, because they preferentially express either the maternally or the paternally inherited gene copy (allele), instead of expressing both parental alleles equally.  We have developed a genome-wide approach to study imprinting using next generation sequencing.  To date, our analyses have uncovered a vast array of complex parental effects and indicate the existence of distinct maternal and paternal gene expression programs in the brain (Gregg et al. Science 2010a, Gregg et al. Science 2010b).  We discovered that 60% of imprinted genes expressed in the developing brain preferentially express the maternally inherited allele.  However, in the adult brain, 70% of imprinted genes preferentially expressed the paternal allele.  Thus, mothers and fathers appear to differentially influence developmental processes versus adult brain functions in offspring.  Our work also suggests the X chromosome is the maternal nexus of genetic control over the adult brain, which may provide a clue for why the X chromosome evolved an enrichment for genes that influence cognition.  Currently, we are seeking to further understand the nature and functions of imprinted genes and maternal and paternal gene expression programs in the brain in the context of feeding and foraging behaviors.  Our work involves the use of both mouse and human tissue for study.  We utilize next generation sequencing technologies (genomics and epigenomics), bioinformatics, mouse genetics, molecular biology, histology and imaging technologies, as well as established and novel behavior assays to address a variety of questions:

  1. What is the nature and function of maternal and paternal gene expression programs in the brain?  How do they influence feeding and foraging behaviors?

  2. What are the regulatory mechanisms that govern maternal and paternal gene expression programs?

  3. Do environmental factors (eg. diet or drugs) influence the establishment and/or regulation of imprinted genes in the brain?  In what ways do environmental factors influence offspring brain function and behavior?

  4. How has imprinting evolved to regulate brain function and behavior in other species?  What is the nature of the human brain imprintome?  What is the relevance of imprinting to human diseases and disorders?

Our overall goal is to use new and highly creative approaches to uncover novel processes that impact brain evolution, development, function and animal behavior.  The lab’s methodologies, including genomics and bioinformatics, provide students and postdocs with valuable skills relevant to the future of biomedicine.   Our current exploration of parental effects influencing CNS gene expression is anticipated to lead to a new understanding of pathways that underlie a variety of neural processes and behaviors relevant to human health and disease.

Selected Publications

Search Pubmed for Christopher Gregg's lab publications

  • Christopher Gregg*, Jiangwen Zhang*, Brandon Weissbourd, Gary P. Schroth, David Haig, Catherine Dulac (2010) High-resolution analysis of parent-of-origin allelic expression in the mouse brain.  Science, 329(5992):643-8. *equal authors
  • Christopher Gregg, Jiangwen Zhang, James E. Butler, David Haig, Catherine Dulac (2010) Sex-specific parent-of-origin allelic expression in the mouse brain.  Science, 329(5992):682-5.
         - Highlighted in Science (2010) 329(5992):636-7, Nature (2010) 466(7308):823-4, and Neuron (2010) 67(3):359-62.
  • Christopher Gregg, Victor Shikar, Peter Larsen, Gloria Mak, Andrew Chojnacki, Voon Wee Yong, and Samuel Weiss (2007) White Matter Plasticity and Enhanced Remyelination in the Maternal Central Nervous System.  J Neurosci. 27(8): 1812-23
         -Highlighted in Nature Reviews Neuroscience (2007) 8(4): 245, Nature Medicine (2007) 13(4): 416, and The Journal of Neuroscience, 27(8).
  • Christopher Gregg and Samuel Weiss  (2005) CNTF/LIF/gp130 receptor complex signaling maintains a VZ precursor differentiation gradient in the developing ventral forebrain. Development. 132(3): 565-78.
  • Christopher Gregg and Samuel Weiss (2003) Generation of functional radial glial cells by embryonic and adult neural stem cells.  J Neurosci. 23(37): 11587-601.
  • Tetsuro Shingo, Christopher Gregg, Emeka Enwere, Hidiuki Fujikawa, Rozina Hassam, Colleen Geary, James C Cross, and Samuel Weiss. (2003) Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin.  Science.  299(5603): 117-20.