Evolution in our Genes

Somewhere in our genome is buried a very curious stretch of DNA. Located on the short arm of chromosome 8 is an unassuming group of 152 nucleotides.

If one compares this sequence to a mouse genome they find… it matches exon 10 of GULO gene with extremely high accuracy. This gene codes for the enzyme responsible for the final step tin vitamin C biosynthesis.

Well, this is curious since humans don’t have this protein. This is why if we don’t consume vitamin C we get scurvy.

Image

Why should this gene be there? These 152 nucleotides are part of a psuedogene, a completely nonfunctional piece of DNA. How do we know this DNA is nonfunctional (I can hear some of you asking without recalling 9th grade biology)?

Most of the exons (the DNA encoded into RNA, the translator between DNA and proteins, the building blocks of life) have been been deleted, but a few of this sequence remain.

The surviving sequence is riddled with mutations that would:

  • Change the amino acid sequence
  • Cause frame shifts
  • Add stop codons
  • Disrupt intron splice sites

No mRNA has been detected from this sequence.
No protein has ever been found.
(If any of the above sentences have been beyond your reading comprehension, don’t feel bad… you’re part of 97% of America, and you shouldn’t feel bad. Feel free to ask and and I’ll explain. However, there are a couple of people this is directed at who pretend to know this whole process and who should understand this whole process…)
Though the functionality of some of these genes may be debated, for all intensive purposes this DNA is abandoned real estate.

But why is it here? There are two scenarios:
1) It just appeared via spontaneous mutations.

Image

How far too many people interpret atheism.

2) It evolved from a previously functional gene.

Let’s humor the first possibility: the probability of having a particular stretch of DNA randomly having an 86.2% identical match is 1 / 1,800,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000.

Given the size and composition of our genome it is still unlikely: 1 / 100,000,000,000,000,000,000,000,000,000

But it gets more interesting. Other primates are also unable to make vitamin C. Yet they too have this sequence for matching exon 10 for GULO. The probability of four species (the number of primates sequenced for this gene thus far) having this same completely useless sequence at random is 1:100,000,000,000,000,000,000,000,000,000,000, 000,000,000,000,000,000,000,000,000,000,000,000,000.000, 000,000,000,000,000,000,000,000,000,000,000,000,000,000, 000,000,000,000,000,000,000,000,000. In other words, the odds of Pauly Shore winning an Oscar for best dramatic performance.

Intelligent Design / creationism give no explanation for this sequence’s existence. They make no testable predictions. Does this mean the designer is flawed? Or just fucking with us? Many creationists claim the sequence is functional, yet offer no data to the many scientific papers showing evidence to the contrary.

So what about the other possibility? Evolution is the only theory that can explain this seemingly impossible statistic. As any good scientific theory it goes further and makes testable predictions.

Prediction: If primates evolved from a common ancestor that lost function in this gene, closely related species should have more similar sequences than more distant species. Since this bit of DNA has no function, mutations have no affect on the organism’s fitness, and therefore the sequence can drift freely. However, species bound by a recent common ancestor will not have as much time to acquire diverging mutations as species joined by a more distant ancestor.

And this is exactly what we find. The human sequence is more similar to the chimp sequence than to the other primates.

Image

Reusing the most boring image I’ve ever used on the site because it’s once again relevant.

Similarity in GULO genes

  • Human – Chimp 97%
  • Human – Orangutan 94%
  • Human – Macaque 89

Let’s take this one step further. Another mammal has lost function in its GULO gene. The mighty guinea pig.

Image

Stare into the face of evil.

Phylogeny tells us that the primate pseudogene and the guinea pig pseudogene cannot be related, as there are many creatures in between the evolution of primates and guinea pigs that have functional vitamin C genes, including bats, flying lemurs, tree shrews, elephant shrews, and prosimians.

Evolution makes another prediction: Since guinea pigs are more closely related to rodents than to primates, the guinea pig sequence should be more similar to the rat and mouse sequence than it is to the primate sequence, despite the guinea pig and primate sequences having the same malfunction.

And it is.

Evolution is the only theory capable of explaining how this stretch of 152 nucleotides found its way into our genome: that it evolved from exon 10 of the GULO gene. Evolution not only gives us an explanation but goes further to make testable predictions which are confirmed by data.

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~ by kriskodisko on October 3, 2013.

One Response to “Evolution in our Genes”

  1. Oh, man, you went and said “intensive purposes”. And did it right after saying something about paying attention in ninth grade, too. Damn. That stuck in my head for the rest of the read.

    Still, thanks for hanging that all out there just the same.

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