What makes us the same




















Recognizing this value should change the way we approach a person with whom we disagree. It should lead us to civility. And neither am I. Most of the time, we are incredibly forgiving of ourselves for our imperfections; however, we also tend to be incredibly forgetful that others are just as imperfect as we are.

We give ourselves loads of grace for making a hasty comment, a rude interjection, or angry response. But if someone does that to us, watch out! Finding common ground means giving the same grace we give ourselves to others. It means recognizing we will make mistakes, and others will make mistakes with us. We are more alike, my friends, than we are different. Remembering what unites us will lead us to common ground, which will allow for us to have great conversations, hear stories, gain perspective, and grow.

Join the Discussion. Your email address will not be published. Perhaps taking the time to get to know others better— others that we may have assumed were different— and discovering the things we have in common will help us to see ourselves more clearly. Certainly, we all have something in common, we are all the same in our humanity. Your email address will not be published. Close Menu Home. Considering Consciousness. My Books. Book Coaching.

Memoir Writing. Ask a Question. Ishani Gupta. Ishani Gupta "We are all different that's what makes us the same. Ishani Gupta We are all different. T hat's what makes us the same. Substitute another word for "different", and you can get something like these, none of which is mysterious or mind-boggling in any way: We are all human.

I think it's supposed to be amusing. These six major groups encompass more than 1, different families of RNA genes, each one distinguished by the structure and function of the encoded RNA in the cell.

HAR1 is also the first documented example of an RNA-encoding sequence that appears to have undergone positive selection. It might seem surprising that no one paid attention to these amazing bases of the human genome earlier. But in the absence of technology for readily comparing whole genomes, researchers had no way of knowing that HAR1 was more than just another piece of junk DNA. Whole-genome comparisons in other species have also provided another crucial insight into why humans and chimps can be so different despite being much alike in their genomes.

In the past decade the genomes of thousands of species mostly microbes have been sequenced. It turns out that where DNA substitutions occur in the genome—rather than how many changes arise overall—can matter a great deal. In other words, you do not need to change very much of the genome to make a new species.

The way to evolve a human from a chimp-human ancestor is not to speed the ticking of the molecular clock as a whole. Rather the secret is to have rapid change occur in sites where those changes make an important difference in an organism's functioning. HAR1 is certainly such a place. So, too, is the FOXP2 gene, which contains another of the fast-changing sequences I identified and is known to be involved in speech. Its role in speech was discovered by researchers at the University of Oxford, who reported in that people with mutations in the gene are unable to make certain subtle, high-speed facial movements needed for normal human speech, even though they possess the cognitive ability to process language.

The typical human sequence displays several differences from the chimp's: two base substitutions that altered its protein product and many other substitutions that may have led to shifts affecting how, when and where the protein is used in the human body.

One finding has shed some light on when the speech-enabling version of FOXP2 appeared in hominids: in scientists at the Max Planck Institute for Evolutionary Anthropology in Leipzig sequenced FOXP2 extracted from a Neandertal fossil and found that these extinct humans had the modern human version of the gene, perhaps permitting them to enunciate as we do.

Current estimates for when the Neandertal and modern human lineages split suggest that the new form of FOXP2 must have emerged at least half a million years ago.

Most of what distinguishes human language from vocal communication in other species, however, comes not from physical means but cognitive ability, which is often correlated with brain size.

Primates generally have a larger brain than would be expected from their body size. But human brain volume has more than tripled since the chimp-human ancestor—a growth spurt that genetics researchers have only begun to unravel. One of the best-studied examples of a gene linked to brain size in humans and other animals is ASPM.

Genetic studies of people with a condition known as microcephaly, in which the brain is reduced by up to 70 percent, uncovered the role of ASPM and another gene— CDK5RAP2 —in controlling brain size. More recently, researchers at the University of Chicago, the University of Michigan and the University of Cambridge have shown that ASPM experienced several bursts of change over the course of primate evolution, a pattern indicative of positive selection.

At least one of these bursts occurred in the human lineage since it diverged from that of chimps and thus was potentially instrumental in the evolution of our large brains. Other parts of the genome may have influenced the metamorphosis of the human brain less directly. The computer scan that identified HAR1 also found other human accelerated regions, most of which do not encode proteins or even RNA.

Instead they appear to be regulatory sequences that tell nearby genes when to turn on and off. Amazingly, more than half of the genes located near HARs are involved in brain development and function. And, as is true of FOXP2 , the products of many of these genes go on to regulate other genes. Thus, even though HARs make up a minute portion of the genome, changes in these regions could have profoundly altered the human brain by influencing the activity of whole networks of genes.

Although much genetic research has focused on elucidating the evolution of our sophisticated brain, investigators have also been piecing together how other unique aspects of the human body came to be.

HAR2, a gene regulatory region and the second most accelerated site on my list, is a case in point. In researchers at Lawrence Berkeley National Laboratory showed that specific base differences in the human version of HAR2 also known as HACNS1 , relative to the version in nonhuman primates, allow this DNA sequence to drive gene activity in the wrist and thumb during fetal development, whereas the ancestral version in other primates cannot.

This finding is particularly provocative because it could underpin morphological changes in the human hand that permitted the dexterity needed to manufacture and use complex tools. Aside from undergoing changes in form, our ancestors also underwent behavioral and physiological shifts that helped them adapt to altered circumstances and migrate into new environments.



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