The human genome contains many "molecular fossils" or dead genes, also known as pseudogenes, which were once functional but are no longer active. One such example is the GULOP gene, which allowed our ancestors to produce vitamin C. This gene became inactive around 61 million years ago, and since then, humans have had to obtain vitamin C from their diet. Another example is the UoX gene, which coded for an enzyme that broke down uric acid. The loss of this gene may have given our ancestors an evolutionary advantage by allowing them to store fat more efficiently.
Research has shown that many pseudogenes are linked to changes in diet and nutrition. For example, some carnivores have lost the ability to taste sweetness, while humans have a relatively well-rounded set of taste receptors. However, we have also lost some bitter taste receptors, which may have become less important as our diets changed and we learned to cook with fire.
The study of pseudogenes and their evolution can provide valuable insights into our evolutionary history and the pressures that have shaped our genomes. By analyzing these "molecular fossils," scientists can learn more about the history of life on Earth and the adaptations that have allowed humans and other organisms to survive and thrive.
Here are the key facts extracted from the text:
1. Geneticist Susumu Ohno wrote about the concept of molecular fossils in a 1972 paper.
2. Our genome contains bits of DNA that are no longer functional, known as molecular fossils.
3. One of these molecular fossils is the GULOP gene, located on the 8th chromosome.
4. GULOP used to give our early primate ancestors the ability to make their own vitamin C.
5. The GULOP gene became a pseudogene around 61 million years ago.
6. Our more distant primate cousins, like lemurs, can still make their own vitamin C.
7. The loss of the GULOP gene meant that our side of the primate family tree had to get vitamin C from food.
8. Without vitamin C in our diets, we risk suffering from diseases like scurvy.
9. There are thousands of dead genes in our genome, and we've only just begun to unravel their stories.
10. Over 90% of our genome doesn't actually code for anything.
11. We've found around 20,000 pseudogenes in our genome, which rivals the number of active genes.
12. Pseudogenes can be the result of ancient gene duplication events or unitary pseudogenes.
13. Mutations can occur randomly in our DNA and can lead to gene death.
14. Gene death isn't necessarily bad and can create opportunities for evolution.
15. The loss of the UoX gene, which coded for the uricase enzyme, occurred around 17 million years ago.
16. The uricase enzyme helps break down uric acid, a waste product of metabolism.
17. Humans and other living apes have high uric acid levels in their blood, which can lead to diseases like gout.
18. Researchers have resurrected ancient uricase proteins in the lab to study their function.
19. The loss of the UoX gene may have given our ancestors an evolutionary advantage in storing fat during times of abundance.
20. Our taste receptors have evolved to respond to different tastes, and some have become pseudogenes over time.
21. We have 25 working bitter taste receptor genes and 11 dead ones.
22. Two of the dead bitter taste receptor genes died relatively recently in our evolution, after our last common ancestor with chimpanzees and bonobos.
23. Our cultural knowledge of food sources and the ability to cook with fire may have made some taste receptors less important over time.
24. Evolutionary genomics is a young science, and our understanding of dead genes will continue to grow with time.
25. The genome is not just a recipe book for building an organism, but also a historical record of our evolutionary legacy.