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That’s exactly what Jun Jiang from the University of Massachusetts Medical School has done: she used XIST to shut down chromosome 21.
So far, the team have only done this in Down’s syndrome cells, grown in a laboratory, so the technique is a very long way from any clinical use. Lawrence has spent years studying XIST, and has always thought about applying this work to Down’s syndrome. For a start, XIST is huge—far larger than any other gene that has been deliberately inserted into a genome before. In this study, Jiang ensured that XIST only shut down one of the three chromosomes by tweaking its concentration. Even if that worked, it would be very challenging to use the XIST technique in people—you’d need to get the giant gene into the right cells at the right stage.  “I doubt that XIST by itself has the potential to become a therapeutic agent in patients,” says Stylianos Antonarakis from the University of Geneva. The study also has more immediate benefits: “It’s a way of getting at the biology that underlies the different aspects of Down’s,” says Lawrence. Jiang’s work also confirms something important about XIST—it evolved to shut down the X chromosome, but it works on all of them.
Indeed, Lawrence suspects that her work on XIST and Down’s might eventually tell us more about how the genome is organised. Lawrence’s team have moved beyond this debate, and are one of the first to actually use a lncRNA to target and silence a set of genes. I read this story first on the BBC website, then came to your blog in the hopes that you had a more in depth piece. I don’t understand the field enough to make more than fuzzy speculation, but it seems to me that this research could have huge implications. This is the most encouraging news that I have ever heard regarding the cause and possible solution for the disabilities caused by Down syndrome. When wounded, poisonous nightshade can be sweet, a revelation that has scientists reconsidering the evolution of nectar. Top picks You can sign up for The Ed’s Up—a weekly newsletter of my writing plus some of the best stuff from around the Internet. Sign up for my weekly newsletter - The Ed's Up - to find out about my writing and other activities. DisclaimerThe views expressed are those of the writer and are not necessarily those of the National Geographic Society. The artista€™s reconstruction of the man, who has been named a€?Inuka€?, is based on screening for single nucleotide polymorphisms (SNPs). The views expressed in the contents above are those of our users and do not necessarily reflect the views of MailOnline. In the last decade, scientists have made tremendous strides in correcting these faults through “gene therapy”—using viruses to sneak in working versions of the affected genes.

Down’s syndrome, for example, happens when people are born with three copies of the 21st chromosome, rather than the usual two.
This double dose of X-linked genes might cause problems, so women inactivate one copy of X in each cell. It produces a large piece of RNA (a molecule closely related to DNA) that coats one of the two X chromosomes and condenses it into a dense, inaccessible bundle. After all, she used to provide counselling for parents whose babies are born with disabilities, and she regularly talks to families who are affected by Down’s, some of whom talk at the genetics course she runs. If the team got it into the right place, would it actually silence chromosome 21 without killing the cell? Jiang used enzymes called zinc finger nucleases, which cut DNA at very specific points, to smuggle the giant XIST gene into a pre-defined spot on the 21st chromosome. In the future, the team might target it to sequences found in only one of the three copies. Jiang saw some promising signs.  For example, after XIST, the Down’s cells grew more quickly, produced larger colonies, and were far better at dividing into neuron-making cells. It’s somewhat surprising that it took so long for someone to apply this to chromosome 21, but the group had to overcome some very significant technical challenges,” says Roger Reeves from Johns Hopkins University. For example, many children with Down’s develop myoproliferative disease, where they produce too many blood cells and run a high risk of leukaemia.  If doctors saw kids with this condition, it might be possible to activate XIST in their blood stem cells, to prevent them from developing cancer. The syndrome includes dozens of symptoms across many different organs, including intellectual disabilities, heart problems, leukaemia and Alzheimer’s at an early age. Scientists could activate XIST in one of two groups of identical cells, and watch what happens to the rest of their genes. XIST is one of several pieces of RNA that are transcribed from the genome, but never used to make proteins. Apologies for being a pedant, but I think this article has the potential to be widely viewed by lots of mums, and I want them to be able to trust you as I know they can. As someone that had a brother with Down’s Syndrome, this article was particularly appealing to me. Perhaps, one day DS could be shut down at the first sign of it–nearly eliminating its physical and cognitive effects. I have this weekly journal club with my group and tomorrow in fact we’ll be discussing about this paper.
His work has appeared in Wired, the New York Times, Nature, the BBC, New Scientist, Scientific American, the Guardian, the Times, and more. Phenomena is hosted by National Geographic magazine, which invites you to join the conversation.
It is comparable in quality to a modern human genome.a€?We can see the man had brown eyes, brown hair and a tendency to baldness.

This condition, called trisomy, leads to hundreds of abnormally active genes rather than just one. But while using XIST to inactivate chromosome 21 was an obvious strategy, it was also a risky one. She did this in cells from a boy with Down’s syndrome, which had been reprogrammed into a stem cell-like state. This supports the idea that people with Down’s syndrome can’t make enough cells (and neurons, in particular) as they grow up. They could do this in neurons, heart cells, or any of the other tissues that are affected in Down’s syndrome.
She thinks it might recognise repetitive bits of DNA that are found throughout our genome, but have no obvious purpose. Because of its large size, it’s classified as a “long, non-coding RNA” or lncRNA—a group that includes tens of thousands of members. It also seems that this could be an extremely helpful tool for genomicists–possibly allowing them to shut off other chromosomes in order to learn more completely what those chromosomes do. We as scientists have a moral obligation towards the society to convey a CANDID message and utility of our research in the long run ! The clump of hair we found suggests he probably died quite young.a€?We can also see he had A-plus blood type.
XIST did its thing, “painting” one of the three chromosome-21s, and condensing it into a tight bundle.
A minority of these, like XIST, clearly help to control how other genes are used, but there’s a lot of debate about what the rest do, if anything (see Carl Zimmer’s post for more). But it should be able to shut down other chromosomes too, if we could just insert it into the right place. And, as Antonarakis says, scientists could do this not just for Down’s syndrome, but for the many other disorders that are caused by unusual number of chromosomes. These changes, or mutations, in our DNA can have important consequences for how the gene gets physically expressed. So there are several possible combinations, some of which are more heavily associated with, for example, blue eyes, than with brown eyes.

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