Dr Nick Burton
- Next Generation Fellow (2017)
- Assistant Professor Van Andel Institute (VAI)
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About
Nick Burton is an assistant professor in Van Andel Institute's Department of Epigenetics. Prior to joining the Institute, he was an independent Next Generation Fellow at University of Cambridge’s Loke Centre for Trophoblast Research.
“In the last decade, it has become increasingly clear that an individual’s environment and their epigenetics play a major role in determining whether or not they will go on to develop many different pathologies ranging from diabetes to autism,” Burton said. “We are now beginning to understand the mechanisms underlying many of these observations. At Van Andel Institute, I look forward to working alongside many world-class researchers looking to solve these mechanisms and find new ways to improve human health.”
Burton’s research explores how a person’s environmental exposures can impact the health of their children and subsequent generations. These factors, called intergenerational effects, influence physiological development and may help offspring adapt to the environment into which they are about to be born. However, many of these adaptations can also have negative consequences in mismatched environments and may even predispose individuals to certain diseases. He is particularly interested in how microbes and the microbiome — the complex population of bacteria and other microorganisms that call the human body home — can contribute to and interact with these processes.
Burton hopes to reveal the mechanisms that govern intergenerational effects and leverage his findings to improve health and combat disease.
“Dr. Burton’s cutting-edge research has major implications for revealing new insights into how the experiences and exposures of one generation may predispose the next generation to health or disease,” said J. Andrew Pospisilik, Ph.D., chair of VAI’s Department of Epigenetics.
Key publications:
Burton NO#, Willis A, Fisher K, Braukmann F, Price J, Stevens L, Baugh LR, Reinke AW, and Miska EA. Intergenerational adaptations to stress are evolutionarily conserved, stress specific, and have deleterious trade-offs. eLife 2021;10:e73425 doi: 10.7554/eLife.73425
#Corresponding author
Burton NO & Greer, E. L. Multigenerational epigenetic inheritance: Transmitting information across generations. Seminars in Cell & Developmental Biology (2021) doi:10.1016/j.semcdb.2021.08.006.
Chandrasekaran V*, Desai N*, Burton NO*, Yang H, Price, J, Miska EA#, Ramakrishnan V#. Visualising formation of the ribosomal active site in mitochondria. eLife 2021;10:e68806 doi: 10.7554/eLife.68806
*Equal contribution
Burton NO#, Riccio C, Dallaire A, Price J, Jenkins B, Koulmann A, Miska EA. Cysteine synthases CYSL-1 and CYSL-2 mediate C. elegans heritable adaptation to P. vranovensis infection. Nature Communications. 2020 Apr 8; 11 1741
#Corresponding author
Escribano APG, Bono-Yague J, Roca M, Panadero J, Sequedo MD, Saini R, Knoelker HJ, Blanca JM, Burguera JA, Lahoz A, Canizares J, Millan JM, Burton NO, Vazquez-Manrique R. Multiple hormonal signalling pathways function cell-nonautonomously to control protein homeostasis in Caenorhabditis elegans. 2019 Submitted. Manuscript available at – bioRxiv - https://www.biorxiv.org/content/10.1101/551580v1.article-info
Burton NO#, Dwivedi VK, Burkhart KB, Kaplan REW, Baugh LR, and Horvitz HR#. Neurohormonal signalling via a cytosolic sulfotransferase controls insulin sensitivity of C. elegans. Nature Communications. 2018 Dec 4; 9(1) 5152
#Co-Corresponding author
Burton NO, Futura T, Webster AK, Kaplan REW, Baugh LR, Arur S, and Horvitz HR. Insulin-like signalling to the maternal germline controls progeny response to osmotic stress. Nature Cell Biology. 2017 Feb 6; 19 252-257
Burton NO, Burkhart KB, and Kennedy S. Nuclear RNAi Maintains Heritable Gene Silencing in C. elegans. Proc Natl Acad Sci USA. 2011 Dec 6;108(49):19683-8
Guang S, Bochner AF, Burkhart KB, Burton N, Pavelec DM, Kennedy S. Small Regulatory RNAs inhibit RNA Polymerase II during the elongation phase of transcription. Nature. 2010 Jun 24;465(7301):1097-101
Cortesio CL, Chan KT, Perrin BJ, Burton NO, Zhang S, Zhang ZY, Huttenlocher A. Calpain 2 and PTP1B function in a Novel Pathway with Src to regulate invadapodia dynamics and breast cancer cell invasion J Cell Biol. 2008 Mar 10;180(5):957-71
Research
A mother's exposure to environmental stress can program her offspring's development and physiology in diverse organisms ranging from silk moths to red squirrels. For example, in pea aphids the exposure of mothers to environmental stress can program their offspring to develop wings, which enhances offspring survival by allowing them to fly away from unfavorable conditions. However, the development of wings comes at a reproductive cost. This type of maternal bet hedging (where a mother programs her offspring to adapt to one environmental stress at the expense of another) has been observed in a variety of organisms. However, the mechanisms by which a mother's environment can so dramatically alter offspring physiology remain unknown.
More recently, a mother's exposure to environmental stress has been observed to modify fetal development and physiology in humans. Specifically, epidemiological studies from populations around the world found that maternal exposure to environmental stress during pregnancy correlates with low birth weight. This slowing of fetal growth rate has been proposed to be an adaptive response to the environmental stress experienced by the mother.
Consistent with observations of maternal bet hedging in other organisms, low birth weight also correlates with long-lasting changes in offspring physiology including enhanced offspring susceptibility to metabolic disorders, such as type 2 diabetes. These observations suggest that fetal responses to maternal exposure to environmental stress, such as slowing growth rate, might be an evolutionarily conserved process to adapt to acute environmental stresses at the expense of long-term health and ability to respond to other stresses.
We have developed a model system to study how a mother's environment can program offspring physiology in the nematode C. elegans. We observed that maternal exposure to mild osmotic stress protects their offspring from future exposure to osmotic stress at the expense of the offspring's ability to respond to other stresses such as anoxia and starvation. We found that this programming is controlled by insulin-like signalling to oocytes. Using this model we are now investigating the mechanism(s) by which information about insulin-like signalling to oocytes can be transmitted across a generation and program offspring physiology.