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And that is, certain genes can evolve progressively over a long period of time, because they don't encode vital functions, or they may even be sequences between genes that don't encode phenotype at all. Imagine, for example, we have a situation were here we have a gene which encodes a vital function, like the eye, here's another gene that encodes another function, oh I don't know, a leg. And here we have intergenic sequences. After all, as you have learned by now, more than 96% of the DNA in our genome, doesn't encode proteins, and probably isn't even responsible for regulating genes. So these sequences, right in here, can mutate freely during the course of evolution, without having a deleterious effect on the phenotype of the organism. There's no evolutionary pressure to constrain the evolution of these genes

And many of these neutral mutations, which have no effect on organismic fitness, but are simply evolutionary neutral, are sometimes called polymorphisms. The term polymorphism, -morph is once again morphology, derives from the fact that species tend to be polymorphic, we don't all have blond hair, we don't all have brown eyes.

If you look at two chimpanzees living on opposite sides of the same hill in West Africa, they are genetically far more distantly related to one another, than any one of us, by a factor of 10 to 15. Two chimpanzees, they look exactly the same, they have the same peculiar habits, but they're genetically far more distantly-related than we are to one-another, than I am to any one of you, or than any one of you is to one another. And what does that mean? It means that, roughly speaking, the species of chimpanzees is, at least, 10 or 15 times older than our species are. We're a young species, chimpanzees probably first speciated three or four million years ago, if the paleontological record is, is accurate. Paleontology is the study of old, dusty bones, so you can begin to imagine when chimpanzee bones become recognizable in the earth.

And what you see already, in such small populations, is that for example, this male here has two girls, and right away, to the extent he had an interesting Y chromosome, that Y chromosome was lost from the gene pool. This girl, here, had an interesting mitochondrial DNA, but right away that's lost, because she has, she has just two boys. And what you see, in very rapid order, in small populations, there's a homogenization of the genetic compliment, just because the alleles are lost within what's called, genetic drif

And if you ask that question, the answer is that we all had a common ancestress who lived about 150,000 years ago. All of us trace our mitochondrial DNA to her. Does that mean that there was only one woman alive there, she's called, Mitochondrial-Eve, again, we don't know her name. Does that mean there was only one woman alive, well it doesn't mean that at all because of what I just told you, in small populations the proto-human population.

How much are all of our mitochondrial DNA are related to one another, how distantly related are they to one another, given the rate of evolution of mitochondrial DNA sequences?

So where do we all come from, all of us human beings? How closely related are we to one another? Here's, here's a measurement of the distances between different mitochondrial DNA's from different branches of humanity. And what you see is something really quite extraordinary and stunning. Here, you'll see that the people, the non-African lineages here and here, are actually relatively closely related to one another.

And by the way, all the genes that are present here, the alleles that are present here, can also be found in Africa, but in relatively small proportions in Africa

So, what happens there, that's a testimonial to the tragic fate of the Indians, where the conquistadors from Spain came in, killed all the men, and took all the women, to be their brides. How else can you explain the fact that there's no Indian Y chromosomes, there's all, there is instead only European Y chromosomes.

When you do genetic counseling of family these days, one of the strictures is, that you never tell the family if the children have genetic polymorphisms that don't match that of the person whom they think is their father. They don't look like their, the person whom they regard as father, but that's always assumed to be a role of the genetic dice.

Here's a fun story I like to tell each year, and it's about the Cohen and Y chromosome, and you'll see what an amusing story this is, just from genetics. Now the name Cohen, in Hebrew means, a high priest, and you've heard people named Cohen, it's not such an uncommon name among the Jews. And it says, in the Bible, in Genesis and Exodus, that all the high priests in the Bible are the descendants of Aaron, the brother of Moses.

hen it should be the case that all male Cohen's should have the same Y chromosome, right?

Because keep in mind, any single affair with the milkman or the mailman, over 3,000 years, would've broke this chain of inheritance, any single incidence of non-paternity. It's a really astounding story, and it's hard, there can be no artifact to it, there's no bias in it, there's no other way to explain it.

And what they found was that all members of the, almost all members of the ruling cast among the Lembas, had the same Y chromosome, and the Y chromosome had exactly the same polymorphisms of the Cohen Y chromosome

What I'm telling you is that these two genes are totally interchangeable, that they are effectively indistinguishable from one another, functionally they have some sequence relatedness, but in terms of the way they program development, they are effectively equivalent. And what this means is that the progenitor of these two genes must've already existed at the time that the flies and we diverged, which six or seven-hundred million years ago, and in the intervening six or seven-hundred million years, these genes have been totally unchanged.

once the gene was developed, evolution could not tinker with it, and begin to change it in different ways, ostensibly because such tinkering would render these genes dysfunctional, and thereby would inactivate them, thereby depriving the organism of a critical sensory organ.

Boycotts and sit-ins and nonviolent confrontations—which were the weapons of choice for the civil-rights movement—are high-risk strategies. They leave little room for conflict and error. The moment even one protester deviates from the script and responds to provocation, the moral legitimacy of the entire protest is compromised.

A networked, weak-tie world is good at things like helping Wall Streeters get phones back from teen-age girls.

These events in the early sixties became a civil-rights war that engulfed the South for the rest of the decade—and it happened without e-mail, texting, Facebook, or Twitter.

The cadre of prominent bloggers, like Andrew Sullivan, who championed the role of social media in Iran, Esfandiari continued, misunderstood the situation. “Western journalists who couldn’t reach—or didn’t bother reaching?—people on the ground in Iran simply scrolled through the English-language tweets post with tag #iranelection,” she wrote. “Through it all, no one seemed to wonder why people trying to coordinate protests in Iran would be writing in any language other than Farsi.”

“It is time to get Twitter’s role in the events in Iran right,” Golnaz Esfandiari wrote, this past summer, in Foreign Policy. “Simply put: There was no Twitter Revolution inside Iran.”

What mattered more was an applicant’s degree of personal connection to the civil-rights movement.