Jamie Kramer, PhD
What is memory and how are memories formed at the cellular and molecular levels? Decades of research have yet to pinpoint definitive answers to these questions, however, recent studies in the field of epigenetics suggest that modifications to chromatin structure may play an important role. Epigenetics was first discussed in the context of developmental biology and was proposed to be the mechanism that allows for cellular differentiation by determining and maintaining the "correct" gene expression profile for a given cell type. The biochemical changes that mediate epigenetic regulation include chromatin modifications, such as DNA methylation, histone modification, and ATP-dependent nucleosome remodeling. In addition to their role in cell type determination and stable maintenance of genes expression patterns, chromatin modifications also play a role in the dynamic regulation of gene expression in post mitotic cells. Several studies have shown that DNA methylation and histone modifications are dynamically regulated in neurons in response to external cues. This type of environmentally induced epigenetic plasticity has been implicated in complex neuronal processes like learning and memory. These post-mitotic neuro-epigenetic mechanisms may provide a resolution for the dichotomy of "Nature vs. Nurture" since we now know that the environment (Nurture) can directly affect gene activity (Nature) in our brains.
There are hundreds of evolutionarily conserved proteins involved in the regulation of chromatin structure. My lab takes a systems-biology approach to understand the role of these proteins in the brain. To do this we use the fantastic and highly efficient model organism, Drosophila melanogaster, to analysis genomic and epigenomic processes underlying learning and memory. We also aim to understand more about the contribution of epigenetic regulators to human cognitive disorders, like Intellectual Disability (ID).
We are currently seeking highly motivated graduate and undergraduate students.
Degrees and Institutions
- BSc - University of Guelph, 2000
- PhD - Memorial University of Newfoundland, 2006
- Postdoc - Radboud University Medical Center, Netherlands, 2006-2014
- Kochinke K., Zweier C., Nijhof B., Fenckova M., Cizek P., Honti F., Keerthikumar S., Oortveld M.A.W., Kleefstra T., Kramer J.M., Webber C., Huynen M., Schenck A. 2016. Systematic phenomics analysis deconvolutes intellectual disability genes into biologically coherent modules. American Journal of Human Genetics, 98(1):149-64.
- Kramer J.M. 2016. Regulation of cell differentiation and function by the euchromatin histone methyltranserfases G9a and GLP. Biochemistry and Cell Biology, 94(1): 26-32.
- Merkling S., Bronkhorst A.W., Kramer J.M., Overheul G.J., Schenck A., van Rij R.P. 2015. The epigenetic regulator G9a mediates tolerance to RNA virus infection in Drosophila. PLoS Pathogens, 11: e1004692.
- Berube, N.G. and Kramer, J.M. Epigenetics in Intellectual Disability. 2014. In Epigenetics in Psychiatry, ed. Jacob Peedicayil, Dimitri Avramopoulos, and Dennis R. Grayson. Elsevier.
- Gupta V.K., Scheunemann L., Eisenberg T., Mertel S., Bhukel A., Koemans T.S., Kramer J.M., Liu K.S., Schroeder S., Stunnenberg H.G., Sinner F., Magnes C., Pieber T.R., Dipt S., Fiala A., Schenck A., Schwaerzel M., Madeo F., and Sigrist S.J. 2013. Restoration of polyamines protects from age-induced memory impairment in an autophagy-dependent manner. Nature Neuroscience, 16(10):1453-60.
- Kleefstra, T.*, Kramer, J.M.*, Neveling, K., Willemsen, M.H., Koemans, T., Vissers, L.E., Wissink-Lindhout, W., van den Akker, W., Kasri, N.N., Nillesen, W.M., Prescott, T., Clark, R.D., Devriendt, K., van Reeuwijk, J., de Brouwer, A.P.M., Gilissen, C., Zhou, H., Veltman, J.A., Schenck, A., van Bokhoven, H. 2012. Disruption of an EHMT1-associated chromatin modification module causes intellectual disability. American Journal of Human Genetics, 91(1): 73-82. *equal contribution
- Koolen, D.A.*, Kramer, J.M.*, Neveling, K.*, Nillessen, W.M., Moore-Barton, H., Elmslie, F.V., Toutain, A., Amiel, J., Tsai, A.C., Cheung, S.W., Gillissen, C., Verwiel, E., Martens, S., Feuth, T., Bongers, E., de Vries, P., Scheffers, H., Vissers, L.E., de Brouwer, A.P.M., Brunner, H.G., Schenck, A., Veltman, J.A., Yntema, H., de Vries, B.A.B. 2012. Mutations in the chromatin modifier gene KANSL1 cause the 17q21.31 microdeletion syndrome. Nature Genetics, 44(6): 639-41. *equal contribution
- Kramer, J.M., Kochinke, K., Oortveld, M.A.W., Marks, H., Kramer, D., de Jong, E.K., Asztalos, Z., Westwood, J.T., Stunnenberg, H.G., Sokolowski, M.B., Keleman, K., Zhou, H., van Bokhoven, H., and Schenck, A. 2011. Epigenetic regulation of learning & memory by Drosophila EHMT/G9a. PLoS Biology, 9(1): e1000569.