Yeast Genetics and Molecular Biology 2000
University of Washington
Seattle, Washington USA
July 2000


Name: Cox, Kathleen
Mailing Address: Microbiology and Immunology, University of Tennessee, 858 Madison Ave., Memphis, TN 38163, U.S.A.
Email Address: kcox@utmem.edu
Phone & FAX numbers: (901) 448-4662 & (901) 448-8462

#091

S. cerevisiae GATA sequences function as TATA elements during nitrogen catabolite repression because Gln3p is excluded from the nucleus.
Kathleen Cox, Rajendra Rai, Makenzie Distler, Jon Daugherty, Jonathan Coffman, Terrance Cooper
Microbiology and Immunology, University of Tennessee, 858 Madison Ave., Memphis, TN 38163, U.S.A.

S. cerevisiae selectively uses good nitrogen sources (GLN) in preference to poor ones (PRO) by repressing GATA-factor-dependent transcription of the genes needed to transport and catabolize poor nitrogen sources, a physiological process designated nitrogen catabolite repression (NCR). We show that some NCR-sensitive genes produce two transcripts of slightly different sizes. Synthesis of the shorter transcript is NCR-sensitive, while that of the longer one is not. The longer transcript also predominates in gln3 deletion mutants irrespective of the nitrogen source provided. The longer mRNA species arises through the use of an alternative transcription start site generated by the Gln3p binding sites (GATAAs) acting as surrogate TATA elements. The ability of GATAAs to serve as surrogate TATAs, i.e., when synthesis of the shorter, NCR-sensitive transcript is inhibited, correlates with sequestration of EGFP-Gln3p in the cytoplasm in a way that is indistinguishable from that seen with EGFP-Ure2p. However, when the shorter, NCR-sensitive transcript predominates, EGFP-Gln3p is nuclear. From these data and a previous report, suggesting existence of a Ure2p-Gln3p complex, we conclude that formation of a cytoplasmic Gln3p-Ure2p complex results in Gln3p being excluded from the nucleus. This in turn prevents Gln3p from reaching its GATAA binding sites upstream of NCR-sensitive genes and activating their transcription. Supported by NIH grant GM-35642.


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