A team of researchers from the Institute of Biotechnology at the Life Sciences Center of Vilnius University has made a breakthrough in understanding the mechanism of bacterial defense systems, particularly CRISPR-Cas10. This system acts as a sensor that detects viral infections and triggers a response to protect the bacterium.
When a virus attacks, it sends a “message” by synthesizing unique signal molecules called cyclic oligoadenylates. These signaling molecules are recognized by effectors, which enhance the bacterial defense against viruses. The researchers studied the tripartite CalpL-CalpT-CalpS effector, which is activated by CRISPR-Cas10 signaling molecules.
The complex system works as follows: CalpL acts as a signal-recognizing protein scissors that forms a polymeric filament when it binds to a signaling molecule. The filament structure allows the CalpT-CalpS heterodimer to attach, positioning the active center of the scissors near the inhibitor CalpS. This enables CalpL to cleave CalpT, releasing CalpS and allowing it to regulate gene expression.
The activity of the CRISPR-Cas protein scissors is tightly regulated in time, with an internal timer mechanism activated upon binding of signaling molecules and filament formation. This unique mechanism sets the system apart from other signal-sensing effector proteins.
The discovery of this bacterial defense system has sparked significant scientific interest and provides a breakthrough in understanding signaling pathways. The study’s results have been published in Molecular Cell, paving the way for further research into the practical application of regulated CRISPR-Cas protein scissors as a molecular indicator of infection.
Source: https://phys.org/news/2024-10-filament-crispr-cas-protein-scissors.html