The revolutionary gene-editing technique known as Crispr-Cas has been embroiled in a patent dispute between two leading US research institutions. In one corner, the University of California at Berkeley, where Jennifer Doudna discovered it in collaboration with Emanuelle Charpentier, and in the other, MIT’s Broad Institute, where Feng Zhang’s group first demonstrated its use in living cells.
Now the two institutions are competing against each other again, as both recently demonstrated the usefulness of a different Crispr system for the detection of pathogens. Doudna’s and Zhang’s groups had shown in 2016 that a Crispr-type enzyme called C2c2, now renamed Cas13, targets single stranded RNA, unlike the ones used in gene editing, such as Cas9, which edit double-stranded DNA. Moreover, it doesn’t stop cutting once it has destroyed its target. It goes on to cleave thousands of other RNA molecules that happen to be nearby. This collateral damage provides a useful amplification step enabling the sensitive detection of the original target RNA, whose recognition can be programmed just as in the gene-editing method.
Aiming to turn this into a clinically usable sensor, Zhang teamed up with Jim Collins, also at MIT, who was involved in the race to develop practical methods for rapid detection of the Zika virus.
Read all about it in my latest news story in Chemistry World which is out now (free access if you haven't read any other CW stories this week, they have a free quota):
Crispr enables rapid disease detection