A new study has concluded that some of that ‘junk DNA’ we inherited from our ancestors could be guiding some brain’s activity.
The human genome contains all the instructions needed to build and maintain our bodies — however half of it appears to be ‘junk’ that doesn’t code for any proteins.
Much of this ‘junk DNA’ comes in the form of something called transposon which are also known as ‘jumping genes’. These are genes that can change their position within a genome, sometimes creating or reversing mutations and altering the cell’s genetic identity and genome size. It is thought that transposons originated from ancient viruses and can today be harmful if they ‘jump’ into a gene causing disruption to cellular processes.
At Oxford’s Centre for Neural Circuits and Behaviour, researchers have been investigating transposon activity in the brains of fruit flies using single cell sequencing.
Their findings showed that transposons are not active across the whole fly brain, but instead operate in certain areas only, forming distinct patterns of expression.
The patterns they form appear to be linked to the genes located near the transposons, meaning they might have something to do with how the gene is expressed.
Molecular biologist Christoph Treiber and his colleges investigated this further using software tools they developed to explore how transposons are expressed.
They found that transposons segments are often part of the messenger RNA sent from neural genes in the cell nucleus out to the cytoplasm where proteins are made.
They suggest this means that transposons may be used to alter neural function — and act on genes that have roles in such brain activities as the formation of memories and the sleep-wake cycle.
‘We know that animal genomes are selfish and changes that are not beneficial often don’t prevail,’ said Dr Treiber.
‘Since transposons are parts of hundreds of genes in every fly strain that we looked at, we think these physical links likely represent an advantage for the fly.’
‘We now want to understand the impact of these new alleles on the behaviour of individual animals.’
‘Transposons might broaden the range of neuronal function in a fly population, which in turn could enable a few individuals to react more creatively in challenging situations,’ he added.
‘Also, our preliminary analyses show that transposons might play a similar role in our brain,’ said Dr Treiber.
‘Since every person has a unique transposon “fingerprint”, our findings could be relevant to the need to personalise pharmacological treatments for patients with neurological conditions.’
