To anyone who has ever bothered participating in life with a scientific temper, it is no news how illusions can veil the truth, and presumption can overtake reality.
The most notable assumption that was most recently quaked and dismissed concerns the size of the human genome. For decades since this obvious curiosity first began plaguing the sharpest of our minds, we had comfortable declared ourselves to be the most ‘complex’ and ‘evolved’ organisms on the face of the planet.
It was not until 2003 that some of us were coerced to rethink the conceptual basis of evolution. With the becoming of April of this year, it was first published for everyone to see how the human genome was not a 100,000 gene controversy.
14 years later and 6 re-iterations through, we now know we are less than half as ‘complex’ as we consider ourselves to be, at least numerically. There are of course two ways to approach this realisation, the latter amongst which includes redefining our criteria for categorisation into complexity. Some scientists have come up to justify our superior stature by presenting an acceptable basal logic that speaks about how a limited set of genes can ultimately translate to several different sets of proteins.
Secondarily, genome sequencing of phyla has revealed that amphibians have a larger genome than humans by several hundred times.
So where do we stand on ‘evolution’ – and how do we determine its proportionality with ‘complexity’?
If this question does not already appear stressful to you, allow me to introduce you to another nitty-gritty that has been unfolded not before 5 years ago. Safe to declare, it is a foetal havoc that has not fallen too far from the fatheromics.
Epigenomics has taken the world of precision medicine and genomics by storm. It has struck the grave of Lamarck and Darwin with herculean gravity, presenting an evident resurrection of the golden debate.
As a result, chromatin fibres in the nucleus are now considered to be carriers of not only genetic but also epigenetic information.
Epigenetics is conceptually divergent from the usual omics that are concerned with the central dogma of life. It has been developed to resolve the question of difference between cells with identical genetic material in terms of both amount and nature but different functions. It talks not about the detectable changes in nucleotide base pair sequences but in the interaction between the base pairs and the phenotypes produced.
Purely concerning modification of gene expression, it is dismissed very conveniently by some scientists for its lack of physicality in contrast with genomics. However, it has without doubt raised very critical questions in the field of genomics, proteomics, and metabolomics each, proposing a wave of change in the way we look at genetic inheritance, population growth patterns and precision medicine.
With the discovery of this branch of omics, DNA sequencing alone has proved unfruitful since the science has shown how we inherit not only the genetic codes from our parents, but also the signatures of ancestral and present lifetime experiences that get incorporated into the genome via ‘epigenetic modifications’ of the original genetic code.
An example used to display the vitality of epigenetics in the world around us speaks about the bee community. While the queen bee is capable of reproduction, foraging and nurse bees arising from the same set of genes are infertile. The reason for which has now been derived from the epigenetic modulators found in royal jelly – the food of the bees. The amount of food consumed by each bee determines the degree of methylation of genetic code, thereby causing changes in fertility.
Another plot more intimately concerning us, the human community speaks about the body shapes and nutrition linking it with patterns in hereditary while establishing how the environment is capable of inflicting modifications on our genetic code, causing an imprint of a set of epigenetic modifications that are passed on through generations. Science has always known and shown that obese fathers contribute to the birth of unhealthy daughters. This was very concisely captured by an experiment varying availability of food for a group of lab rats. These lab rats were starved for 50+ generations before they were fed high calorie (not necessarily nutritious) food. The next generation produced post the change of diet however, was obese. Genetically the insulin gene was observed to have been regulated internally post the alteration in diet. Now ideally, availability of food is an external environmental factor that accounts as a life experience. However, this experiment sharply validated the fact that the environment is capable of shaping susceptibility to modification in genomes. Therefore, even as the nucleotide base pair sequence remains the same between the progeny and the parental generation, the environment dictates which gene product is to be silenced or amplified, reversibly or irreversibly. And this change is inherited in the form of modified gene expression within the gametes which ultimately changes phenotypes and as observed in the global scenario, accounts for diseases.
These alterations in gene expression may not necessarily be of the same kind. They maybe via methylation, histone modification etc. and are attributed to the kind of change in the environment. The body can inherit and propagate stress or the lack of it, for instance. Therefore, these epigenetic changes are dynamic through the lifetime of an individual but remain stable through inheritance, provided they are irreversible.
So as it pans out, we truly are what we eat.
Author: Aastha Munjal Date of Publishing: 10th Jun 2017 Artwork: Lund University