Towards a unified model of transcription terminationDr. David Bentley (University of Colorado School of Medicine) and colleagues have developed a new, unified model for transcription termination by RNA Poymerase II. Over the years, research into the mechanism of poly(A) site-dependent transcription termination has generated two different models: the allosteric and the torpedo models. The allosteric, or antiterminator, model proposes that transcription of the poly(A) site triggers conformational changes that destabilize the elongating RNA polymerase, resulting in termination. The torpedo model proposes that an exonuclease degrades the nascent RNA, and eventually catches up to the elongation complex, causing its termination. Using a novel experimental system to study the function of the exonuclease Rat1 in yeast, Dr. Bentley's team now shows that while the exonucleases Rat1 and Xrn1 do degrade the nascent RNA transcript, this degradation is not sufficient to cause polymerase termination. Rather, Rat1 helps recruit cleavage and polyadenylation factors that are necessary for termination. "As is often the case with competing hypotheses like the torpedo and allosteric models for transcription termination, neither one can explain the whole story, but aspects of both are correct, and these form the basis for a unified model," explains Dr. Bentley.
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