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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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General repression of RNA polymerase III transcription is triggered by protein phosphatase type 2A- mediated dephosphorylation of Maf1.

We report genome-wide analyses that establish Maf1 as a general and direct repressor of yeast RNA polymerase ( Pol) III transcription. Chromatin immunoprecipitation (ChIP) coupled to microarray hybridization experiments showed an increased association of Maf1 to Pol III-transcribed genes under repressing condition (rapamycin treatment) correlated with a dissociation of Brf1 and Pol III. Maf1 can exist in various phosphorylation states and interacts with Pol III in a dephosphorylated state. The largest subunit of Pol III, C160, was identified as a target of Maf1. Under repressing conditions, Maf1 is dephosphorylated and accumulates in the nucleus, and Pol III-Maf1 interaction increases. Mutations in protein phosphatase type 2A (PP2A) catalytic subunit- encoding genes prevented rapamycin- induced Maf1 dephosphorylation, its nuclear accumulation, and repression of Pol III transcription. The results indicate that Pol III transcription can be globally and rapidly downregulated via dephosphorylation and relocation of a general negative cofactor.[1]

References

  1. General repression of RNA polymerase III transcription is triggered by protein phosphatase type 2A-mediated dephosphorylation of Maf1. Oficjalska-Pham, D., Harismendy, O., Smagowicz, W.J., Gonzalez de Peredo, A., Boguta, M., Sentenac, A., Lefebvre, O. Mol. Cell (2006) [Pubmed]
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