If Our DNA Doesn’t Make Humans Different From Chimps — What Does?

human vs. chimp

When we imagine the course of human evolution — the roughly three-million-year period from the moment when Lucy began to walk upright through grasses of the Awash River Valley to modern times, it’s hard to determine the moment at which we became human, or at least as human as we might recognize ourselves. After all, there’s only a one percent difference in protein-coding genomes between ourselves and our closest living ancestor, the chimpanzees — even less distinction between our two species than there is between mice and rats. You might be quick to think that the moment we became human was the moment when we grew larger brains that allowed us to explore beyond the trees — endowing us with the ability to create and speak languages that would set us apart from our fellow primates — but how did it happen?

Pursuing an answer to this question, researchers at the SIB Swiss Institute of Bioinformatics collaborated with a team from the University of Lausanne to look for human-specific genetic changes in the brain. Their results, published by Science Advances, offer some new insights into human evolution and developmental biology as well as neuroscience.

Think Expression — Not Sequences

That one percent statistic seems hard for us to process as fact, but it’s not so much about the DNA sequence, or genetic ingredients, as it is the “regulation” of genes that set us apart from our ape relatives — in other words, when, where, and how strongly the genes are expressed in a living organism that play a key role. Although the sequences have been known for some time, specifically, determining and mapping out the regulatory agents that adjust the genes like light switches, has been a difficult task that continues to elude researchers.

Dr. Marc Robinson-Rechavi who served as the group leader at SIB and co-authored the study, suggests that the key is to determine what parts of the genome are influenced by positive selection, the evolutionary mechanism through which favorable traits occur in a population. A classic example proposed by Darwin was the shape of beaks from finches on the Galapagos Island changing in each generation due to the nature of the food supply — a continuity of wet seasons forced the finches to eat larger seeds during the dry season and generations of birds were born with larger beaks equipped for taking on the larger seeds. Surprisingly, with the brain — a great deal of its regulatory elements — those in charge of maintaining the body systems — have been positively selected throughout our history — more so compared to the evolution of critical organs like the human heart or stomach.

Rechavi and his research partner, Dr. Jialin Liu, a researcher who served as the study’s lead author came to their conclusions using a combination of machine learning models and experimental data — creating a model that showed how the proteins used to signal genetic regulation binded in various tissues and then looked at evolutionary differences between humans, chimpanzees, and another fairly close cousin on the family tree: gorillas.

“We now know which are the positively selected regions controlling gene expression in the human brain. And the more we learn about the genes they are controlling, the more complete our understanding of cognition and evolution, and the more scope there will be to act on that understanding,” says Robinson-Rechavi.

Mutations With A Purpose

We tend to think of the word “mutation” in a negative sense — but the reality is that the overwhelming majority of mutations simply happen without us noticing — they take place over a span of time and aren’t necessarily good or bad. They build up at a predictable rate in the amount of time two living species diverge from their common ancestor.

An acceleration, in the rate of mutation however, for a certain part of the genome, can bring with it a positive selection for a mutation that gives one population of species a survival advantage, allowing them to reproduce and pass their mutation on to another generation. The regulatory elements of genes are typically a few nucleotides long, which can make estimating the rate of acceleration exceptionally difficult.

A Matter Of Recognition

The nature of gene expression in the brain and how it impacts social behaviors has been recently studied in other species as well — honey bees were examined in a study reported in the journal eLife this month, where it was shown that just a single error in transcription as mutations occur can affect the way dozens of other genes are expressed — either activating or deactivating an array of them all at once.

“If the queen in a colony dies and the workers fail to rear a replacement queen, some worker bees activate their ovaries and begin to lay eggs,” said Dr. Beryl Jones, a researcher at the University of Illinois Urbana-Champaign who conducted the study alongside her colleague, the entomology professor Dr. Gene Robinson and Dr. Sriram Chandrasekaran, who is a professor of biomedical engineering at the University of Michigan.

“This is an example of ‘behavioral plasticity,’ the ability to change behavior in response to the environment,” Jones said. “We know that behavioral plasticity is influenced by the activity of genes in the brain, but we do not know how genes in the brain work together to regulate these behavioral differences.”

Jones’ study looked at bee colonies run without a queen — and studied the insects’ collective egg-laying and foraging behaviors since they are generally performed for the benefit of the colony, but if done selfishly could become detrimental to that colony. A hive with a queen is maintained as the queen lays eggs and her workers provide food to produce honey — a distinction that comes about because the queens are fed and nurtured apart from the workers as they mature. In a queenless colony, Jones and her colleagues could analyze the worker bees objectively, using bar codes and computer vision. Computer algorithms by the researchers tracked thousands of individual bees and revealed patterns of genetic activity in their brains as it happened from day to day.

A noticeable difference that caught Jones’ eye was the recurring differences between the bees who began foraging in the absence of the queen, compared to their counterparts who began to focus on the task of egg-laying within the hive. The patterns were in fact so consistent that the researchers were able to use the algorithms to accurately predict if one of the tagged bees was a worker or an egg-layer. They also recognized a third group of bees that dabbled in both tasks and also had their own unique gene-expression.

“We identified 15 transcription factors that best explained the behavioral differences in the bees,” says Jones. The findings suggest that changes in the activity of a small number of influential transcription factors can lead to strikingly different behavior.”

“Some of the transcription factors we identified as important for honey bee behavior were previously identified as influencing the evolution of social behavior in other species,” Robinson concluded, indicating that his findings could show how the concept of society with its hierarchies came about in other species — and we may not be far away from knowing the specifics of how shaping each others’ brains became a group effort.

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1 Comment

  1. There is an obvious humungous hole in the simplicity with which that proposal is put forth. The variations in gene expression can only come from one of two places: the genome or the environment (where environment could be either the physical environment or the behavioral treatment by other individuals).

    If they come from the genome, then once again, all ultimate development (and any differences in development between species, such as humans and chimpanzees) has its causal origin in the genome — undermining the claim that the small percentage of genetic difference is insufficient to account for such development and developmental differences. It just means the minor genetic differences measurable at the level of base pair variation govern not only direct transcription but also regulatory patterns. And since regulatory patterns are one step removed from direct transcription, it isn’t too surprising that they could have multiplicative effects across the whole system, such that minuscule genetic changes could yield tremendous developmental changes. And it gets exponentially more powerful if you consider a regulatory effect UPON OTHER regulatory effects. And so on. In this way, a single base pair mutation could conceivably produce sweeping differences across the developed organism. At the least, we can’t rule out the notion that minor genetic variations between humans and chimps could fully account for the phenotypic differences that ultimately arise.

    Alternatively, the authors indicate bees as a classic example of individuals (not species, mind you, but clones within a colony) who development radically different phenotypes from an identical underlying genome on the basis of environment (namely, how members of the colony feed and otherwise raise one another).

    There are two problems with passing the ownership of developmental variation off to the environment. First, it still comes down the genome once you dig deep enough. The CAUSAL REASON bees raise various sisters differently, leading some toward workers, some toward queens, etc. is all wrapped up in their genetically motivated behavior in the first place. It’s still genes in the end, if you just pull the causal thread far enough.

    Now, one could conceive of a multi-generational genome/phenotype/external-environmental system that is a single conglomerated whole, stretching across generations, across populations, and across the interactive physical environment. In this way, the reason bees behave the way they do might not be entirely FOUND within the genome, but also be because the only environment bees ever live in, for thousands of generations stretching across millennia of time, is the highly constrained environment of the inside of a beehive. This is, to a minor extent, Dawkins’ extended phenotype (although I think he was implying the effect of other genomes on a given phenotype). BUT, the only reason bees live in beehives is that their long evolutionary history has genetically pigeon-holed them into continuously living in beehives. So the causal explanation is still essentially genetic. It’s just that some of that genetic cause has gotten muddled up in the extended timeline stretching back through the evolutionary history of bees.

    Furthermore, the argument the authors are making by using a bee analogy is that if you raise a chimp baby a certain way (not just how you behave toward it, but the aggressive ways difference with which bees feed a varying diet, alter the temperature, etc., which would yield gene regulatory changes), it would grow up into a human, and that you could raise a human baby to grow up into a chimpanzee just by feeding it certain foods or putting it in a certain kind of crib or something. We aren’t just talking about minor neurological developmental changes, such as raising a chimp to learn a few words or raising a human to never stand up, or only knuckle walk at best (after all, neurological differences don’t imply any genetic difference whatsoever; that’s what learning is for heaven’s sake). I’m saying you should be able to TURN A HUMAN INTO A CHIMP and A CHIMP INTO A HUMAN according to the proposed theory. Obviously, that is patent nonsense and no one would dispute it. The reason that makes no sense, and yet bees can develop incredible phenotypic diversity from IDENTICAL CLONES is that in the case of the bees, the variation is the highly constrained behavioral environment of their siblings, which itself is ultimately an extended phenotype of the bee genome anyway, thereby alleviating the need for genetic differences between individuals, while humans and chimps with their substantially MORE different genomes fail to develop into another by mere differences in treatment because the genome was of critical importance all along.

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