Yeast Genetics and Molecular Biology 2002
University of Wisconsin
Madison, Wisconsin USA
July 30 - August 4, 2002


Name: Willis, Ian
Mailing Address: Department of Biochemistry, Albert Einstein Col. Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
Email Address: willis@aecom.yu.edu
Phone & FAX numbers: 718-430-2839 & 718-430-8565
URL: http://www.bioc.aecom.yu.edu/labs/willislab/homepage.htm

Abstract #28


Session Title: Control Gene Regulators
Session Time: Thursday, August 1 -- 9:00AM - 10:30AM
Presentation: Platform
Topic: Gene Expression

A unique role for G1 cyclins in transcription by RNA polymerase III.
Neelam Desai, Ian Willis
Department of Biochemistry, Albert Einstein Col. Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA

Pol I and pol III gene transcription in metazoans is repressed in mitosis, increases in early G1 phase but only becomes maximally activated after the cells are committed to a round of division. In Saccharomyces cerevisiae, there is no global repression of transcription during mitosis and changes in transcription by pols I or pol III at other stages in the cell cycle have not been reported. In this work, we have examined tRNA gene transcription in yeast cells synchronized using different regimes and find that the levels of short-lived precursor tRNAs fluctuate in a manner consistent with the need to reassemble preinitiation complexes after DNA replication. During these studies we found that high levels of pol III transcription in G1 phase are dependent on G1 cyclins (Clns). G1 cyclin deprivation, leading to cell cycle arrest at START, produced a sharp drop in tRNA and 5S rRNA synthesis that was not seen following treatment with alpha factor, in conditional cdc28 strains or in cells arrested in mitosis with nocodazole. The functional link between G1 cyclins and pol III transcription was shown to be independent of Cdc28 kinase activity and did not appear to require a physical association between the Clns and Cdc28. We propose that the elevation of G1 cyclin levels at START serves to activate pol III gene transcription to ensure continued cell growth during the division cycle.


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