John Brookfield from the University Of Nottingham is July’s speaker at SciBar, talking about Jumping Genes in the Genome. We headed down to the Vat & Fiddle to hear from the gene genie.
Each of our cells contain 46 chromosomes arranged in 23 pairs with their nucleus. We get half from our mum and half from our dad and 22 of the pairs are the same across the sexes. The chromosomes are coded with base pairs called A, G, C and T and there are 6,000 million of these. The main function of DNA is to control the sequence of amino acids - the building blocks of protein. We have 25,000 genes in our chromosomes but only around 2% actually codes for protein. Whether a cell becomes a skin cell, a bone cell or anything else is determined by these proteins. Despite the huge advances in DNA sequencing over recent years, we only actually know what 10% of our DNA is doing.
We know that a chimpanzee’s DNA is only 1% different to ours. Comparing different animals actually sees a large degree of conservation in where the genes are on the chromosome, even if we compare humans to something really different such as a cow. The head genes, body genes, etc are all in a similar place.
Barbara McClintock looked at the mutation of maize back in the 1940s and 1950s, specifically kernels that were yellow with black spots. As an aside, all yellow corn is actually a mutant, it didn’t start that colour - thing about that next time you’re eating sweetcorn. McClintock won a Nobel prize in 1983 for her research. This was the first work done in gene transposition or jumping genes, which unlike the rest of our DNA can move around the chromosome. Now, DNA is the same in each of our cells, skin cells and bone cells have the same sequence. How then does one express bone protein and one express skin protein? It was thought that repeated DNA controls the expression of the genes next to them, almost like tags on genes showing where they should be expressed. This was disproved using experiments with fruit flies - they have different sequences repeated in different places. Genes don’t stay in the same place.
50% of our DNA is jumping genes, although the vast majority of it is now inactive but these genes used to move in the past. Every time they move they copy themselves and each time the sequences increase - these are parasites. In fact, they are very similar, in their base pairs, to retro viruses - it makes a DNA copy of itself and the cell creates lots of RNA copies. To put that 50% figure into some kind of perspective, due to our ancestors inter-breeding with Neanderthals, we have 4% Neanderthal DNA.
If you get a cold, there is a timescale for that - so, how long ago was the ancestor to these viruses? Looking at the mobile DNA in our chromosomes, we can tell how fast DNA sequences develop so we can calculate that the ancestor was 150million years ago. 150million years ago humans did not exist but the ancestor of all placental mammals did. Since then, this jumping DNA has evolved to help us - it’s become domesticated. We have anti-bodies that fight infections, the number of these that a person can make is in the millions. Rearrangement of the proteins in anti-bodies is done by the proteins that used to make DNA jump around.
How many more have evolved to help us? What we used to think was just junk DNA clearly isn’t. All of which leads to the next big question in researching the human genome - are mutation rates minimal or optimal?
SciBar returns to The Vat & Fiddle on the 29th of August at 7:30
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