Coupling of RNA polymerase III assembly to cell cycle progression in Saccharomyces cerevisiae
| Autor: | Marta Płonka, Małgorzata Cieśla, Magdalena Boguta, Donata Wawrzycka, Robert W. Wysocki |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cytoplasm Cell cycle checkpoint Saccharomyces cerevisiae Proteins Transcription Genetic Mutant Saccharomyces cerevisiae Cell Cycle Proteins RNA polymerase III 03 medical and health sciences 0302 clinical medicine RNA Transfer Gene Expression Regulation Fungal Molecular Biology biology RNA Polymerase III assembly Wild type G1 Phase RNA RNA Polymerase III Cell Biology Cell cycle biology.organism_classification Cell biology 030104 developmental biology 030220 oncology & carcinogenesis Mutation Developmental Biology Research Paper Transcription Factors |
| Popis: | Assembly of the RNA polymerases in both yeast and humans is proposed to occur in the cytoplasm prior to their nuclear import. Our previous studies identified a cold-sensitive mutation, rpc128-1007, in the yeast gene encoding the second largest Pol III subunit, Rpc128. rpc128-1007 is associated with defective assembly of Pol III complex and, in consequence, decreased level of tRNA synthesis. Here, we show that rpc128-1007 mutant cells remain largely unbudded and larger than wild type cells. Flow cytometry revealed that most rpc128-1007 mutant cells have G1 DNA content, suggesting that this mutation causes pronounced cell cycle delay in the G1 phase. Increased expression of gene encoding Rbs1, the Pol III assembly/import factor, could counteract G1 arrest observed in the rpc128-1007 mutant and restore wild type morphology of mutant cells. Concomitantly, cells lacking Rbs1 show a mild delay in G1 phase exit, indicating that Rbs1 is required for timely cell cycle progression. Using the double rpc128-1007 maf1Δ mutant in which tRNA synthesis is recovered, we confirmed that the Pol III assembly defect associated with rpc128-1007 is a primary cause of cell cycle arrest. Together our results indicate that impairment of Pol III complex assembly is coupled to cell cycle inhibition in the G1 phase. |
| Databáze: | OpenAIRE |
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