For the first time, 29 genes have been simultaneously modified in different cell types of a live animal: the result is the first animal-mosaic that has greatly narrowed the causes of a generic disease that affects humans. The technique is based on Crispr, the molecular scissors of DNA, has been successfully tested in mice and promises to greatly accelerate biomedical research, especially for diseases caused by multiple genes. Obtained at ETH Zurich, the result is published in the journal Nature.
So far, the most common method of identifying the genetic causes of disease has been to delete a single gene in a laboratory animal and observe the consequences. The problem is that many diseases are triggered by more than one gene and this makes it extremely difficult to determine how much each gene is involved and in what aspect of the disease. To overcome this obstacle, researchers led by Antonio Santinha have developed a method that greatly simplifies and speeds up the search.
The authors of the study used harmless viruses to introduce into the organ of a live mouse, in this case the brain: each viral particle carries instructions to destroy a particular gene. The virus mixture was administered to the mice and each virual particle managed to reach different areas of the brain, deactivating the desired gene. As a result, a different gene was altered in each cell, in a sort of nolecular mosaic. Using this technique, the researchers obtained new clues about a rare genetic disorder in humans, known as '22q11.2 deletion syndrome': until now it was only known that the origin of the pathology is in a chromosomal region containing 106 genes, which the authors of the study managed to narrow down to just 3.
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