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A flaky boyfriend who won't meet the parents, difficult friendship break-ups and skincare regimes - this week's Dear Fifi. Using state-of-the-art DNA sequencing techniques, the researchers analysed and compared their genomes, and identified no less than 10 different mutations that cause congenital insensitivity to pain, all within a gene called PRDM12 , located on the long arm of chromosome 9.
Individuals carrying two defective copies of this gene produce a non-functional PRDM12 protein, and as a result of this have been unable to feel any kind of physical pain, or to distinguish between painfully hot and cold temperatures, from birth. Most of them have experienced numerous, painless injuries. As infants and young children, they bit their fingers, toes, and lips so often that they are severely mutilated, and hurt themselves many times and in many other ways.
The worst affected have suffered repeated infections while growing up, injuries that scarred their skin and deformed their bones. PRDM12 is the third human gene to be associated with congenital insensitivity to pain. SCN9A was the first such gene to be discovered, and we now know of at least 13 different mutations in it, all of which cause congenital insensitivity to pain.
In , another research team reported that they had identified a mutation in a related gene, called SCN11A , which also causes the condition.
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Mutations in SCN9A produce a non-functional sodium channel, so that pain fibres can still detect painful stimuli but are unable to send signals about them to the brain. The PRDM12 mutations cause pain insensitivity another way. When Woods and his colleagues examined biopsies from several of the affected people they studied, they found that the skin in their legs contains no nerve endings whatsoever, and that one of the sensory nerves in their legs contains about half the normal number of pain-sensing fibres.
This led them to speculate that PRDM12 plays an important role in the development of pain-sensing neurons and their fibres. Exploring further, they examined the distribution of PRDM12 in developing mouse embryos, and in pain neurons generated from human stem cells.
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This revealed that the protein is synthesized at the exact time when pain neurons are forming, and in exactly the right places — in the region where immature pain neurons are first created, along the migration route they take before maturing, and in the dorsal root ganglia and superficial layers of the spinal cord, where their cell bodies and fibres end up, respectively.
The researchers then reduced the amount of PRDM12 protein synthesized by developing frog embryos, and found that this significantly altered the distribution of pain nerves. Woods and his colleagues performed one final set of experiments which suggest that it does so by means of epigenetic modifications that switch these genes on or off by altering chromosome structure. These results confirm that PDRM12 is essential for the development of pain-sensing neurons, and neatly explain why it causes pain insensitivity when mutated.