a, Science & Technology

When Mendel meets Darwin

First there was Darwin, who published the revolutionary On the Origin of Species in 1859, introducing the world to the theory of natural selection. According to this theory, genetic variations arise as adaptions to differential environments, where any profitable traits that incur a survival advantage are selected for and preserved through inheritance. In other words, if a long nose gave you the upper hand over other members of your species, the population would evolve to favour large snouts.

creationrevolution.com
creationrevolution.com

Enter Gregor Mendel and the re-discovery of his pea experiment. Mendel cross-bred different combinations of peas in order to illustrate patterned inheritance of genes from one generation to the next. A contemporary of Darwin, the scientific community did not accept the significance of Mendel’s work until the 20th century, when DNA was identified as the molecule that was passed down from parents to their offspring.

After this recognition, Mendelian genetics could be combined with natural selection, placing a new emphasis on reproductive success. In the modern evolutionary view of natural selection, it is imperative that an organism survives until the age of sexual maturity in order to pass on their genes. ‘Mutation proposes and nature disposes,’ with regards to new genetic traits.

Interestingly, throughout this evolutionary discourse, it was assumed that natural selection exerts its pressures only on the organism. But what about our cells? Our bodies are made up of trillions of cells—would they not be exposed to the same selective pressures?

Scientists asked these questions too, adopting an accepted model of cellular and genetic integrity. According to this model, while there are different types of cells with different functions, each cell contains the same genetic profile. Whether DNA is extracted from our blood or our hair, the sequence should theoretically be the same—the only notable exception is the distinctive mutations observed in cancer cells.

Recently, with the advancements made in biotechnology, this model came into question. For the first time in history, we have the tools to readily sequence different tissues at will. As a result, some evidence shows that we are not composed of a single genetic sequence, but rather, a mosaic of many genetic sequences specific to different tissues.

How does this genetic diversity arise? McGill professor of the Department of Human Genetics Dr. Bruce Gottlieb explains:

“Studies have shown that early on in fetal development, you can get the DNA repair mechanism turned off in certain tissue, and you acquire variant [gene sequences].”

This variation leads to a kind of cellular ‘survival of the fittest,’ where the cells with the evolutionary upper hand prosper, compared to others who fail.

“Selection then takes place, and you only select the wild type (the trait that prevails in normal conditions) [of the gene]; however, the others are still there,” says Gottlieb. “The idea is that, you are getting a panoply of variants, and they are there to protect the tissue. If you get a change in environment, they can respond to it.”

bp.blogspot.com
bp.blogspot.com

Based on this new theory, our bodies should be thought of as a composite of microenvironments to which our cells must adapt. Therefore, genetic diversity would be advantageous to an organism. Having the ability to adapt would provide cells with a better chance at survival in many different situations, such as if a virus killed off a certain cell lineage, but left another one unaffected. In order to survive, this remaining cell lineage would require genetic variation, in order to make up for the other lineage being killed off.

This theory is gaining momentum among cancer researchers, as it helps to explain our failure to identify carcinogens. For instance, cigarette smoke is believed to be a cause of lung cancer. However, when you expose cells to smoke, they are not mutagenized, compared to what occurs when you are, for example, exposed to UV rays. An alternative explanation may be that it is this smoke that is selecting for a lung cancer causing mutation, since those cancer cells thrive in the conditions. Based on this new theory, cigarette smoke does not cause a mutation; rather, the mutation was always there. The smoke selects the mutant out of our diverse gene bank.

While it is necessary that more research be conducted before drawing conclusions, it appears that the theory of natural selection should be applied to our cells. At the end of the day, why should they be treated any differently?

Share this:

Leave a Comment

Your email address will not be published.

*

Read the latest issue

Read the latest issue