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


Name: Hopper, Anita K
Mailing Address: Biochemistry/ Molecular Biol., Penn. State Univ. Coll. Med., H171, 500 Univ. Dr., Hershey, PA 17033, USA
Email Address: ahopper@psu.edu
Phone & FAX numbers: 717-531-6008 & 717-531-7072

#054

The yeast Trm1p ADEPT specifying inner nuclear membrane location.
Shing-Fen Kao (1), Gang Peng (1), David R Stanford (1), Nancy C. Martin (2), Anita K. Hopper (1)
(1) Biochemistry/ Molecular Biol., Penn. State Univ. Coll. Med., H171, 500 Univ. Dr., Hershey, PA 17033, USA; (2) Dept. Biochem., U. Louisville Sch. Med., Louisville, KY 40202

Sorting isozymes are encoded by single genes, but are distributed to multiple subcellular compartments. We compared genes for 5 eukaryotic sorting isozymes with the archaeal/eubacterial counterparts and found that eukaryotic genes possess extra sequences. Those additions that have been studied serve subcellular targeting roles and, thus, we term the additions 'ADEPTs' -additional domains for eukaryotic protein targeting (Stanford et al. 2000). Trm1p is a sorting isozyme. Nuclear Trm1p is peripherally associated with the inner nuclear membrane (INM; Rose et al. 1995). We employed the ADEPT concept to predict the Trm1p motif responsible for its INM location. Trm1p contains 4 'extra' sequences. The N-terminal addition is a mitochondrial targeting sequence; addition 2 (aa 91-136) includes the NLS. Deletion of the 3rd addition (aa 346-367) causes Trm1-GFP to be nucleoplasmic. Thus, ADEPT 3 appears to be necessary for INM location. Addition of sequences including ADEPT 3 to a nucleoplasmic reporter causes the reporter to locate at the INM. So, ADEPT 3 appears to be sufficient for INM location. We are mapping the aa that specify INM location and we are searching for trans-acting mutations that mislocate Trm1-GFP. So far, we identified mutants in which Trm1p is located at an ER-like structure or at 1-2 nuclear membrane spots. We are testing the hypothesis that the mutants define an ER to INM pathway for nuclear proteins. (Funded by NIH and NSF grants to AKH and NCM).


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