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Centre for Trophoblast 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.




Key publications: 

Burton NO, Dwivedi VK, Burkhart KB, Kaplan REW, Baugh LR, and Horvitz HR. Neurohormonal signalling controls insulin sensitivity and specificity in C. elegans. In preparation

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


2017 Next Generation Fellow
 Nick  Burton
Not available for consultancy