Scientists do not yet know how most of the DNA that is uniquely ours affects gene function. But they can conduct whole-genome analyses—with intriguing results. For example, comparing the 33 percent of our genome that codes for proteins with our relatives' genomes reveals that although the sum total of our genetic differences is small, the individual differences pervade the genome, affecting each of our chromosomes in numerous ways.
More in this article: A Monkey's Blueprint. This article was originally published with the title "The 1 Percent Difference" in Scientific American , 3, September Kate Wong is a senior editor for evolution and ecology at Scientific American. Already a subscriber? Sign in. Unlike many human children, though, a baby gorilla usually nurses from the mother for up to four years to obtain important nutrients!
All moms can use a babysitter every now and then. So, what kind of characteristics lie within that 1. Well, remember the opposable thumbs we both have on our hands? Gorillas also have opposable toes! Often, you can see 2-year-old Floyd dragging some hay or wood wool behind him with his toes to play with later.
Having opposable digits on all their hands and feet helps them to be great climbers! Both inside and outside the gorilla building, our guys have plenty of props to climb around on and hang from. While gorillas and humans do have the same dentition or teeth structure, gorillas have a much stronger bite force. Even though our babies are costly, we can produce more of them than our living Great Ape relatives. And when humans are done making babies, they actually survive for a long time.
Our societies, long before medicine, the Industrial Age, or the farming age, allowed for grandmothers and grandfathers. Interestingly, in evolutionary biology it is pretty much accepted that toward the end of the reproductive period, there is a minimal force of selection.
But if you allow for cultural transmission, post-reproductive individuals can actually facilitate the survival of related, younger individuals, which opens up later stages in life to the action of natural selection. With regard to forming the next generation, what is striking is that to find strict monogamy in nonhuman primates, you need to look at the lesser apes, the Gibbons. They live only in the forests in Southeast Asia. For humans, what is striking is that even though humans live in groups, pair bonding is a major phenomenon.
This allows humans to participate in reciprocal exogamy, which essentially means exchanging mates across social groups. It allows for linking multiple kin lineages. Now, if you combine the cognitive capacity of our slowly maturing children, the allomothering, and the input of the group into each child, a striking array of things becomes possible. It essentially allows for our social-cultural niche. We share symbols.
We have personal names. We have kinship terms, which allows for the formation of tribes. We have shared rituals, dance and music, sacred spaces, and group identity markers, and we can increase the capacity to cooperate with and compete against other groups.
I would like to provide you with an example or two of how a process may have led to the differentiation of humans from our closest relatives, and then talk about a cellular system that allows us to look at potential molecular and cellular differences that might have led to dissimilarities in who we are. What we know is that the brain has increased in size across species during evolution along the branch that leads to humans.
And we have come to the hypothesis that the growth of the brain is causally linked to what it is to be human. The correlation is placed there because as the brain became larger, we acquired features that seemed more unique to the complexity in behavior that humans can exhibit.
For example, when we think about what are the measures that allow us to examine how we may have evolved, we can use genetic information. Sometimes we obtain postmortem brain tissue from our closest ancestral relatives. We can measure the magnitude of gyrations in the cortex and explore specific ideas or hypotheses about how they may be important. In addition, we have fossil crania to study and, from those skulls, we can build casts or make CT scans to get an idea of how the brain size was changing, again building our theories based on these measurements and the correlations that exist.
Furthermore, we have cultural icons as well that give us an idea of how far a species had emerged, given its ability to build, plan, and generate art. In each case, we have material that we can work with: genetic material, tissues, organs, and cultural artifacts. What has been missing, however, is living tissue from some of our lost ancestors and from our closest relatives, like chimps and bonobos.
We have established a bank of cellular tissues from many of our closest relatives that allows us to look at distinctions between ourselves and our closest relatives. As Pascal mentioned, chimpanzees and bonobos are our closest relatives, with 95 percent of our genomes being similar; yet, there are vast differences in phenotype. How can we begin to understand the cellular and molecular mechanisms responsible for these differences? One of the things we can do is take somatic cells, such as blood cells or skin cells, from all of our closest relatives.
Through a process called reprogramming — by overexpression of certain genes in these cells — we can turn the skin or somatic cell into a primitive cell, called an induced pluripotent stem iPS cell. These primitive cells are in a proliferating, living state that can be differentiated to form, in a dish, any cell of the body, allowing us, for the first time, to form living neurons or living heart cells from all of our closest relatives and then compare them across species.
These iPS cells represent a primitive state of development prior to the germ cell. So any change detected in these iPS cells will be passed along to their progeny through the germ cell and into their living progeny. Now a little bit of a disclaimer for those of us who work in this field: these cells have limitations. They are cells in culture. We cannot really look at social experience, and their relevance to a living organism is oftentimes questionable.
But we can ask the question: are there differences that are detectable at a cellular and molecular level that help us understand the origin of humans? We have begun building a library with other collaborators around the world, and have reprogrammed somatic cells from many of these species into iPS cells. They retain common features of embryonic stem cells at the cellular level and they have the same genetic makeup as predicted based on the species. In our first attempt to see if we could identify differences in these primitive cells, we did what is called a complete transcriptional mRNA analysis.
If we compare the transcriptional genomes of chimpanzees and bonobos, there are very few differences. So we pooled all our animals together and compared that combined nonhuman primate group to the human group. In analyzing these genomes, we detected two very interesting genes.
Why are we interested in these two proteins? These two proteins are active suppressors of the activity of what we call mobile elements, which are genetic elements that exist in all of our genomes. In fact, 50 percent of the DNA in human genomes is made up of these mobile elements molecular parasites of the genome.
So what are mobile elements? They are elements that exist in specific locations in the genome and, through unique mechanisms, they can make copies of themselves and jump from one part of the genome to another. Barbara McClintock discovered these elements through her work on maize. Some of us study a specific form of mobile elements called a LINE-1 retrotransposon. They exist in thousands of copies in the genome, as a DNA that makes a strand of RNA and then makes proteins that binds back onto the RNA, helping the element copy itself.
This combination of mRNA and proteins then moves back into the nucleus where the DNA resides and pastes itself into the genome at a new location.
These LINE elements continue to be active in our genome, and they are particularly active in neural progenitor cells. Not only do humans make more of these proteins, but as an apparent consequence, the lower levels of these L1 suppressors in chimpanzees and bonobos means the L1 elements are much more active in chimpanzees and bonobos than in humans.
When searching the DNA libraries genomes that have been sequenced for chimps, bonobos, and humans, there are many more L1 DNA elements in the genomes of chimps and bonobos relative to humans. This greater number of L1 elements in non-human primate genomes leads to an increase in DNA diversity and, thus, in the diversity of their offspring and potentially in their behavior.
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