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Maternal signalling to oocytes and programming of offspring development and physiology

Maternal signalling to oocytes and programming of offspring development and physiology

 

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 offspring to develop wings, which enhances offspring survival by allowing them to fly away from unfavorable conditions. Similarly dramatic changes in offspring physiology that are controlled by a mother's environment have been observed in many 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 offspring physiology in humans1. Specifically, epidemiological studies from populations around the world found that maternal exposure to environmental stress during pregnancy correlates with low birth weight, long-lasting changes in offspring physiology, and enhanced offspring susceptibility to metabolic disorders, including type 2 diabetes1. These observations suggest that the programming of offspring physiology by a mother's environment might be an evolutionarily conserved process and that abnormal programming or a mismatch between a mother's environment and her offspring's environment might underlie certain human pathologies including cardiovascular disease and diabetes.

 

We have developed a model of 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 stress3. We found that this programming is controlled by insulin-like signalling to oocytes3. Using this model we now want to determine the mechanism by which information about insulin-like signalling to oocytes can be transmitted across a generation.

 

The successful candidate will use RNA-seq to profile gene expression in embryos from mothers with abnormal insulin-like signalling, LC/MS to profile metabolism in embryos from mothers with abnormal insulin-like signalling, and mutagenesis screening to identify new genes that function in mothers to regulate offspring physiology.

 

For further information please contact Dr. Nick Burton. email: nob20@cam.ac.uk

 

References

1. Hales, C.N., and Barker, D.J. (2001). The thrifty phenotype hypothesis. British Medical Bulletin 60, 5–20.

2. Burton, N.O., Furuta, T., Webster, A.K., Kaplan, R.E.W., Baugh, L.R., Arur, S., and Horvitz, H.R. (2017). Insulin-like signalling to the maternal germline controls progeny response to osmotic stress. Nat Cell Biol 19, 252–257.