Bacteria and archaea play diverse and critical roles in human life - from deadly human pathogens to essential residents of our bodies and of the earth's ecosystems.  We also make use of prokaryotes extensively in biotechnology, food production, and industrial processes.  Importantly, all of these organisms are constantly attacked by viruses and phage.  The Terns Lab in the Department of Biochemistry and Molecular Biology at the University of Georgia is breaking new ground in understanding how bacteria and archaea defend themselves against virus infection.  Their studies are delineating a series of newly-identified RNA-mediated immune systems that protect prokaryotes from viruses and other invaders - the CRISPR-Cas systems.  They have found that CRISPR RNAs (like the antibodies of the human immune system) guide an immune response that destroys viral nucleic acid.  The CRISPR RNAs arise from a collection of short invader sequences acquired by the prokaryote within its CRISPR locus.  This exciting research is leading to new ways to strengthen beneficial microorganisms that produce food, pharmaceuticals and biofuels, combat disease-causing bacteria, and prevent the spread of antibiotic resistance.

 

For more information:

cov150h-1.gifIn a study highlighted on the cover of Cell and in many news and review articles, the Terns Lab describes the discovery of the RNA targeting branch of the CRISPR-Cas system.  Click on the link below to read the Cell article, or read a science news article describing the findings here.
RNA-Guided RNA Cleavage by a CRISPR RNA-Cas Protein Complex. Hale et al. (2009) Cell, 139(5):945-56.

 

The Terns Lab has begun to capitalize on their understanding of CRISPR-Cas systems by redirecting the system to target a gene that provides bacteria with antibiotic resistance.  Click on the link below to read the Molecular Cell article, or read a science news article describing this advance here.
Essential features and rational design of CRISPR RNAs that function with the Cas RAMP module complex to cleave RNAs. Hale et al. (2012) Molecular Cell, 45(3):292-302.