We Are What Our Grandparents Ate??

Written by Mary Lor 41214752

It has always been said; “we are what we eat” this is true of course, as what we eat affects our health and performance for the rest of our lives. But what if, what our grandparents ate and experienced during their lifetimes, affect how we are as well?

Interestingly, scientists now believe that this might in fact, be true. Studies have shown that pregnant mothers living under harsh starvation conditions gave birth to relatively small babies. When they grew up and had children, they were also unexpectedly small, which indicates that poor nutrition can be inherited from generation to generation. But how is this possible? Nutrition cannot be genetically inherited. Scientists believe that this can be explained by the phenomenon: epigenetics, which describes that there are ‘hidden influences’ on phenotypes such as nutritional health, that doesn’t affect or alter the genome that is inherited.

Somehow, our genes have ‘memories’ imprinted on them, which our progeny inherits and then pass through generations. Scientists believe that these ‘memories’ can include anything from what we eat to our life experiences of diseases and disorders. Although this does explain all the mysterious reasons why we are what we are and why we are more susceptible to some diseases than others, how do we know if there are really ‘hidden influences’ that affect us?

Scientists are still struggling to uncover the truth on this mysterious phenomenon of epigenetics.

Primary Reference:
C. Dennis, ‘Epigenetics and disease: Altered states’, Nature 421, 686 – 688 (2003)

Secondary Reference:
J. M. Levenson, J. D. Sweatt, ‘Epigenetic mechanism in memory formation’ Nature Reviews Neuroscience 6, 108-118 (2005)

Could a single protein buffer genetic variation?

Heat-shock proteins (Hsps) have long been known to perform the vital role of protecting other proteins during periods of stress (i.e. environmental change). In light of recent evidence, however, a specific protein, Hsp90, has been found to help organisms in another, unexpected way: buffering them against genetic change. It does this by masking the effects of new genetic variations. Resistance of organisms to genetic and environmental change has been speculated since the 1940’s and has been termed ‘canalisation’. It was not until experiments involving Drosophila melanogaster and Arabidopsis thaliana that the specific role of Hsp90 in this process was uncovered.

A more recent study questions whether Hsp90 is the sole capacitor responsible for protecting organisms against genetic perturbations. It specifically looked at fruit flies’ bristles and wing sizes. These are complex quantitative traits, which had not been tested in previous studies. The study analysed the effects of inhibiting Hsp90 on these traits. The results proved surprising. It was found that genetic canalisation did not solely depend on Hsp90. This raises the possibility that the involvement of Hsp90 in protecting organisms against genetic change is only contributory. Clearly more extensive research is required in order to further elucidate the exact role of Hsp90 in buffering genetic variation.

Picture: A schematic diagram of Hsp90.

References

Milton, C. C., Huynh, B., Batterham, P., Rutherford, S. L. and Hoffmann, A. A. (2003) Proceedings of the National Academy of Sciences 100, 13396-13401.

Pigliucci, M. (2002) Nature, 417, 598-599.

Queitsch, C., Sangster, T. A. and Lindquist, S. (2002) Nature, 417, 618-624.

Rutherford, S. L. and Lindquist, S. (1998) Nature, 396, 336-342.

Stearns, S. C. (2002) Proceedings of the National Academy of Sciences 99, 10229-10230.

Sangster, T. A., Lindquist, S. and Queitsch, C. (2004) BioEssays, 26, 348-362.

Posted by: s41187089

Topic: Directed Mutation (heat-shock proteins)