For those who put the want it explained, if you really want to know:
CRISPR is a method that some bacteria use to combat viral infections. It's sort of like how our bodies can remember viral particles from our vaccines to protect against infection. The bacteria that have this system will cut viral DNA (if they survive the infection) and add some of it to their genome. Making a sort of hybrid. This addition to their genome is a sort of a "FBI's Most Wanted List". Next time the same virus infects the bacterium, the viral DNA will be cut with a molecular switch-blade,
and left to bleed out like a bitch and the viral DNA will be destroyed. That molecular switch-blade is called
Cas9. If you provide Cas9 a small (20 nucleotide) segment of RNA (b/c
transcription), it will search the genome until it finds a match, and then it will make a cut within that match. If you give Cas9 two RNAs (or a
bunch), and it will make two cuts, and the DNA between the cuts can get degraded and the two cut ends will get glued back together (by the
cell's machinery). This has now created a deletion in the genome. This deletion in the genome will now be passed down to the next generation of cells; unless the deletion is detrimental to the cell's health.
So, now to what I do. I look at mutations (natural mutations not cool Xmen ones) that are a
ssociated with disease. Specifically, I study mutations that are in non-coding regions (outside of genes, sort of). In the past, Science called this DNA "junk DNA" b/c they didn't know what it did. It turns out the non-coding part of the genome regulates the coding part. Meaning, the DNA around genes are responsible for turning the gene on and off.
These non-coding associated mutations might be associated with diabetes, but we don't know which gene they are turning on or off. We can guess b/c if the mutation is associated with diabetes, then we can look at the known biology of the closest genes to the mutation. That's just a guess. I deleted a couple of those mutations associated with high cholesterol and cardiac disease traits, and measured the gene expression of then nearby genes and found the ones that were affected by the deletion. It proved which genes are affected by the mutations and thus, gives a genetic molecular mechanism by which the mutations causes the association with the disease/trait.
