genetic interactions of maf1 identify a role for med20 in transcriptional repression of ribosomal protein genes遗传相互作用med20 maf1识别作用的核糖体蛋白基因的转录镇压.pdfVIP

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genetic interactions of maf1 identify a role for med20 in transcriptional repression of ribosomal protein genes遗传相互作用med20 maf1识别作用的核糖体蛋白基因的转录镇压.pdf

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genetic interactions of maf1 identify a role for med20 in transcriptional repression of ribosomal protein genes遗传相互作用med20 maf1识别作用的核糖体蛋白基因的转录镇压

Genetic Interactions of MAF1 Identify a Role for Med20 in Transcriptional Repression of Ribosomal Protein Genes 1 2¤a 2¤b 2 2 2 Ian M. Willis *, Gordon Chua , Amy H. Tong , Renee L. Brost , Timothy R. Hughes , Charles Boone , Robyn D. Moir1 1 Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York, United States of America, 2 Banting and Best Department of Medical Research, University of Toronto, Toronto, Ontario, Canada Abstract Transcriptional repression of ribosomal components and tRNAs is coordinately regulated in response to a wide variety of environmental stresses. Part of this response involves the convergence of different nutritional and stress signaling pathways on Maf1, a protein that is essential for repressing transcription by RNA polymerase (pol) III in Saccharomyces cerevisiae. Here we identify the functions buffering yeast cells that are unable to down-regulate transcription by RNA pol III. MAF1 genetic interactions identified in screens of non-essential gene-deletions and conditionally expressed essential genes reveal a highly interconnected network of 64 genes involved in ribosome biogenesis, RNA pol II transcription, tRNA modification, ubiquitin- dependent proteolysis and other processes. A survey of non-essential MAF1 synthetic sick/lethal (SSL) genes identified six gene-deletions that are defective in transcriptional repression of ribosomal protein (RP) genes following rapamycin treatment. This subset of MAF1 SSL genes included MED20 which encodes a head module subunit of the RNA pol II Mediator complex. Genetic interactions between MAF1 and subunits in each structural module of Mediator were investigate