ScienceDaily (Nov. 28, 2009) — Bacteria don't have easy lives. In addition to mammalian immune systems that besiege the bugs, they have natural enemies called bacteriophages, viruses that kill half the bacteria on Earth every two days.
Still, bacteria and another class of microorganisms called archaea (first discovered in extreme environments such as deep-sea volcanic vents) manage just fine, thank you, in part because they have a built-in defense system that helps protect them from many viruses and other invaders.
Bacteria and archaea (first discovered in extreme environments such as deep-sea volcanic vents, such as the one shown above) manage to survive thanks in part to a built-in defense system that helps protect them from many viruses and other invaders. (Credit: OAR/National Undersea Research Program (NURP); NOAA)
A team of scientists led by researchers at the University of Georgia has now discovered how this bacterial defense system works, and it could lead to new classes of targeted antibiotics, new tools to study gene function in microorganisms and more stable bacterial cultures used by food and biotechnology industries to make products such as yogurt and cheese.
The research was published November 26 in the journal Cell.
"Understanding how bacteria defend themselves gives us important information that can be used to weaken bacteria that are harmful and strengthen bacteria that are helpful," said Michael Terns, a professor of biochemistry and molecular biology in UGA's Franklin College of Arts and Sciences. "We also hope to exploit this knowledge to develop new tools to speed research on microorganisms."
Other authors on the Cell paper include Rebecca Terns, a senior research scientist in biochemistry and molecular biology at UGA; Caryn Hale, a graduate student in the Terns lab at UGA; Lance Wells, an assistant professor of biochemistry and molecular biology and Georgia Cancer Coalition Scholar at UGA and his graduate student Peng Zhao; and research associate Sara Olson, assistant professor Michael Duff and associate professor Brenton Graveley of the University of Connecticut Health Center.
The system, whose mechanism of action was uncovered in the Terns lab (Michael and Rebecca Terns are a husband-wife team), involves a "dynamic duo" made up of a bacterial RNA that recognizes and physically attaches itself to a viral target molecule, and partner proteins that cut up the target, thereby "silencing" the would-be cell killer.
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Cell
Volume 139, Issue 5, 25 November 2009, Pages 945-956
RNA-Guided RNA Cleavage by a CRISPR RNA-Cas Protein Complex
Caryn R. Hale1, Peng Zhao1, Sara Olson3, Michael O. Duff3, Brenton R. Graveley3, Lance Wells1, Rebecca M. Terns1, , and Michael P. Terns1, 2, ,
1Departments of Biochemistry and Molecular Biology, University of Georgia, Athens, GA 30602, USA
2Department of Genetics, University of Georgia, Athens, GA 30602, USA
3Department of Genetics and Developmental Biology, University of Connecticut Stem Cell Institute, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030, USA
Received 15 October 2008; revised 13 April 2009; accepted 17 July 2009. Published: November 25, 2009. Available online 26 November 2009.
Summary
Compelling evidence indicates that the CRISPR-Cas system protects prokaryotes from viruses and other potential genome invaders. This adaptive prokaryotic immune system arises from the clustered regularly interspaced short palindromic repeats (CRISPRs) found in prokaryotic genomes, which harbor short invader-derived sequences, and the CRISPR-associated (Cas) protein-coding genes. Here, we have identified a CRISPR-Cas effector complex that is comprised of small invader-targeting RNAs from the CRISPR loci (termed prokaryotic silencing (psi)RNAs) and the RAMP module (or Cmr) Cas proteins. The psiRNA-Cmr protein complexes cleave complementary target RNAs at a fixed distance from the 3′ end of the integral psiRNAs. In Pyrococcus furiosus, psiRNAs occur in two size forms that share a common 5′ sequence tag but have distinct 3′ ends that direct cleavage of a given target RNA at two distinct sites. Our results indicate that prokaryotes possess a unique RNA silencing system that functions by homology-dependent cleavage of invader RNAs.
Author Keywords: RNA; MICROBIO
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