Tuskless Female Elephants: Epigenetics for Beginners

During the 20-year Mozambican civil war, due to heavy poaching the African elephant populations in Gorongosa National Park declined by 90%. As the population recovered after the war, a relatively large proportion of females were born tuskless. Tusklessness has not been observed in male elephants in the same region. Now scientists have identified the genes responsible for female elephants born without tusks. At present, it has proven hard to pin down exactly what’s happening genetically in these populations. This brings us to genetics and Charles Darwin.

In On the Origin of Species (1859), Darwin advanced his theory of natural selection and survival of the fittest. He wrote that characteristics developed through environmental influences will not be passed on to future generations; only traits passed by genes will be inherited, and genes take millennia to change.

A 1988 paper published by John Cairns in Nature launched a tectonic shift in genetics. The paper described an experiment in which a particular strain of bacteria, E. Coli, that could not metabolize lactose (a sugar found in dairy products), was placed on a lactose medium (scientific jargon for food on which bacteria grow, usually in a Petri dish). Instead of starving, the bacteria very quickly underwent genetic changes, which allowed them to digest lactose and thus survive. Cairns reported that at least in some cases, selective pressures could specifically direct mutations.

Goodbye, Darwinist orthodoxy. Cairns, some critics said, “brazenly,” raised the specter of possible Lamarckian hereditary mechanisms—one could not have been more heretic than that in 1988. In the same issue of Nature, Franklin Stahl, Emeritus Professor of Biology at the University of Oregon, endorsed Cairns’ conclusions and presented his own model of how “directed mutations” may take place.

A decade after the publication of Cairns’ paper, Indiana University biology professor P.L. Foster wrote, “Much subsequent research has shown that mutation rates can vary and that they increase during certain stresses such as nutritional deprivation. The phenomenon has come to be called “adaptive mutation.” Today, adaptive mutation has been transformed into epigenetics. And suddenly, every university lab is studying it.

While Darwin’s work defined evolution as a process of incidental, random mutation between generations and survival of the fittest, the new science of epigenetics is much closer to the much-maligned theory of French biologist Jean-Baptiste Lamarck, who suggested that an organism can pass to its offspring characteristics acquired during its lifetime.

Epigenetics is the study of changes in gene activity that do not alter the genes themselves but still get passed down to at least one successive generation. These patterns of gene expression are governed by the cellular material—the epigenome—that sits on top of the genome, just outside it (hence the prefix epi-, which means above). A key component of epigenetics is methylation, in which a chemical group (methyl) attaches to parts of the DNA—a process that acts like a dimmer on gene function in response to physical and psychosocial factors. Epigenetic “switches” turn genes on or off, and all points in between.

Methylation is a dynamic process, and levels of methylation can change from moment to moment and over the course of a person’s lifetime depending on the person’s experiences whether these be external or internal. The opposite process to methylation is acetylation. Methylation turns down or totally silences the function of a gene while acetylation turns the gene on partially or totally.

One of the primary objectives of epigenetics is to study data transfer from one generation to the next by biological rather than psychological means. Biological inheritance speaks to the idea that the germ cells (sperm and eggs) are affected by significant environmental events, and that these changes in the genome are then passed on to descendants. I suggest that it is this phenomenon that led to the births of tuskless elephants in response to the threat of annihilation.

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The field of epigenetics gained momentum when several decades ago, scientists studied the children born to women who were pregnant during a period of famine toward the end of World War II in Holland. They found that these children carried a particular chemical mark, or epigenetic signature, on one of their genes. The researchers linked that finding to differences in the children’s health later in life. The children grew smaller than the Dutch average and had higher-than-average body mass. Their children were also smaller and more susceptible to diabetes, obesity, and cardiovascular disease. These changes were detectable over three generations.

At about the same time as Cairns was performing his experiments, Lars Olov Bygren of the University of Umea, Sweden, wondered, “Could parents’ experiences early in their lives somehow change the traits they passed to their offspring?” Bygren and many other scientists have now amassed a great deal of historical evidence suggesting that powerful environmental conditions (near death from starvation, for instance) can leave an imprint on the genetic material in eggs and sperm. These genetic imprints can short-circuit evolution and pass along new traits in a single generation.

But it is not just stressful or traumatic incidents that can change gene expression (activity). David Clayton, a neurobiologist at the University of Illinois, found that if a male zebra finch heard another male zebra finch sing nearby, a particular gene in the bird’s forebrain would be stimulated and it would do so differently depending on whether the other finch was strange and threatening, or familiar and safe. Songbirds demonstrated massive, widespread changes in gene expression in just 15 minutes.

We are learning that brain responses to social stimuli can be massive, involving hundreds, sometimes thousands of genes. Even as recently as 20 years ago, no self-respecting geneticist or neuroscientist would have thought in their wildest dreams that social experiences lead to changes in brain gene expression and behavior.

Complex diseases such as cancer, diabetes, obesity, autism, and birth defects are increasing in prevalence at rates that cannot be explained by classical genetics alone. Studies in humans and animals strongly suggest that epigenetic mechanisms may be responsible.

Compelling scientific data show that our social lives, our interactions with others and ourselves can change our gene expression with a rapidity, breadth, and depth previously unknown. Genes don’t make us who we are. Gene expression does. And gene expression varies depending on the life we live. In other words, the food we eat, the water we drink, the air we breathe, our interpersonal relationships, and our relationship to ourselves—all affect us on a deep biological level which in turn affects our minds.

Do genes matter? Absolutely. But so does the physical, psychological and social environment, not only from birth on but extending back to the nine months of womb life, conception and, in many ways, several generations further back. The advance of epigenetics has shattered the old Darwinian paradigm of genetics.

More on this in The Embodied Mind (2021).