Poly(A) Tail Recognition by a Viral RNA Element Through Assembly of a Triple Helix

Author:

Mitton-Fry Rachel M.1,DeGregorio Suzanne J.1,Wang Jimin2,Steitz Thomas A.234,Steitz Joan A.1

Affiliation:

1. Department of Molecular Biophysics and Biochemistry (MB&B), Howard Hughes Medical Institute (HHMI), Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536–9812, USA.

2. Department of MB&B, Yale University, Bass Center for Molecular and Structural Biology, 266 Whitney Avenue, New Haven, CT 06520–8114, USA.

3. Department of Chemistry, Yale University, New Haven, CT 06520–8107, USA.

4. HHMI, Yale University, Bass Center for Molecular and Structural Biology, 266 Whitney Avenue, New Haven, CT 06520–8114, USA.

Abstract

Self-Protection Mechanism Kaposi's sarcoma–associated herpesvirus (KSHV) causes an AIDS-associated cancer. During its lytic phase, the virus produces a noncoding polyadenylated nuclear RNA that accumulates to high levels in infected cells. This occurs because a helix-loop-helix element, called ENE within the RNA, that contains a uridine-rich internal loop, sequesters the poly(A) tail, preventing the initiation of RNA decay. Mitton-Fry et al. (p. 1244 ) have determined the 2.5 angstrom structure of the ENE core bound to the RNA. Instead of just binding to the uridine-rich loop, as was expected, the poly(A) tail interacts with the loop and lower stem to form a triple helix to prevent decay. Similar mechanisms may protect other noncoding RNAs from rapid turnover.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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