See allHide authors and affiliations

Science  19 Dec 2008:
Vol. 322, Issue 5909, pp. 1753
DOI: 10.1126/science.322.5909.1753m

Clustered, regularly interspaced short palindromic repeat (CRISPR) loci, found in many bacteria, confer immunity against bacteriophage infection by a mechanism that relies on identity between CRISPR repeats and phage target sequences. Marraffini and Sontheimer (p. 1843) find CRISPR repeats in Staphylococcus epidermidis that match the nickase gene present in all staphylococcal conjugative plasmids. These repeats block the transfer of these plasmids, both by conjugation and transformation, into S. epidermidis. CRISPR prevents S. epidermidis acting as a recipient, and the small CRISPR (cr)RNAs are identical to, rather than complementary to, messenger RNA (mRNA) target sequences, suggesting that the target for crRNA is DNA [unlike small interfering (si)- or micro (mi)RNAs, where RNA is the target]. Evidence supporting this view comes from a self-splicing group I intron that disrupts DNA but not mRNA recognition.

Navigate This Article