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.

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-
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-
occurred by two different mechanisms.
The levels of the shorter cyc1-512 transcripts were
enhanced in the cbc1-
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-
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.
Present address: Division of Biology, California Institute of
Technology, Pasadena, CA 91125.
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