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Molecular and Cellular Biology, April 2000, p. 2827-2838, Vol. 20, No. 8
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

The Role of Nuclear Cap Binding Protein Cbc1p of Yeast in mRNA Termination and Degradation

Biswadip Das,1 Zijian Guo,1,dagger Patrick Russo,1,2 Pascal Chartrand,3 and Fred Sherman1,*

Department of Biochemistry and Biophysics, University of Rochester Medical School, Rochester, New York 146421; Institute for Molecular Medicine, Albert Einstein College of Medicine, Bronx, New York 104613; and Department of Plant Pathology, Cornell University, Ithaca, New York 148532

Received 16 September 1999/Returned for modification 20 November 1999/Accepted 16 January 2000

The cyc1-512 mutation in Saccharomyces cerevisiae causes a 90% reduction in the level of iso-1-cytochrome c because of the lack of a proper 3'-end-forming signal, resulting in low levels of eight aberrantly long cyc1-512 mRNAs which differ in length at their 3' termini. cyc1-512 can be suppressed by deletion of either of the nonessential genes CBC1 and CBC2, which encode the CBP80 and CBP20 subunits of the nuclear cap binding complex, respectively, or by deletion of the nonessential gene UPF1, which encodes a major component of the mRNA surveillance complex. The upf1-Delta deletion suppressed the cyc1-512 defect by diminishing degradation of the longer subset of cyc1-512 mRNAs, suggesting that downstream elements or structures occurred in the extended 3' region, similar to the downstream elements exposed by transcripts bearing premature nonsense mutations. On the other hand, suppression of cyc1-512 defects by cbc1-Delta occurred by two different mechanisms. The levels of the shorter cyc1-512 transcripts were enhanced in the cbc1-Delta mutants by promoting 3'-end formation at otherwise-weak sites, whereas the levels of the longer cyc1-512 transcripts, as well as of all mRNAs, were slightly enhanced by diminishing degradation. Furthermore, cbc1-Delta greatly suppressed the degradation of mRNAs and other phenotypes of a rat7-1 strain which is defective in mRNA export. We suggest that Cbc1p defines a novel degradation pathway that acts on mRNAs partially retained in nuclei.

* Corresponding author. Mailing address: Department of Biochemistry and Biophysics, Box 712, University of Rochester Medical School, Rochester, NY 14642. Phone: (716) 275-6647. Fax: (716) 275-6007. E-mail: Fred_Sherman{at}urmc.rochester.edu.

dagger Present address: Division of Biology, California Institute of Technology, Pasadena, CA 91125.

Molecular and Cellular Biology, April 2000, p. 2827-2838, Vol. 20, No. 8
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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