Abstract
Sub1 and Maf1 exert an opposite effect on RNA polymerase III transcription interfering with different steps of the transcription cycle. In this study, we present evidence that Sub1 and Maf1 also exhibit an opposite role on yeast chronological life span. First, cells lacking Sub1 need more time than wild type to exit from resting and this lag in re-proliferation is correlated with a delay in transcriptional reactivation. Second, our data show that the capacity of the cells to properly establish a quiescent state is impaired in the absence of Sub1 resulting in a premature death that is dependent on the Ras/PKA and Tor1/Sch9 signalling pathways. On the other hand, we show that maf1Δ cells are long-lived mutant suggesting a connection between Pol III transcription and yeast longevity.
Highlights
In its natural environment, the budding yeast Saccharomyces cerevisiae spends most of its life in a quiescent state where it can maintain both viability and the capacity to re-enter the proliferation cycle upon the addition of a carbon source
During the course of our experiments on the regulation of Pol III transcription, we reproducibly observed that cells deprived of Sub1 needed more time than wild type to regrow when inoculated into fresh liquid medium
Since a delay in exiting quiescence could be due to a loss of cell viability, the proportion of living cells was measured over time using trypan blue staining of cells grown to stationary phase in nutrient-rich yeast extract/peptone/dextrose medium (YPD) medium, in synthetic complete (SC) medium or in SD medium supplemented 4X with the appropriate doi:10.1371/journal.pone.0114587.g001
Summary
The budding yeast Saccharomyces cerevisiae spends most of its life in a quiescent state where it can maintain both viability and the capacity to re-enter the proliferation cycle upon the addition of a carbon source. Yeast CLS provides a fruitful model for aging research and many progress have been made to understand the mechanisms regulating the cell quiescence cycle, including the entry into quiescence, the maintenance of viability and the capacity to re-proliferate. A massive reprogramming of gene expression occurs with a down regulation of most of the genes transcribed by all three RNA polymerases. These changes are under the control of the Ras/PKA and Tor1/Sch signalling pathways that integrate nutrient availability to regulate cell proliferation. To repress transcription by RNA polymerase (Pol) III, these pathways converge to Maf1 [3, 4]. Maf is dephosphorylated and accumulates in the nucleus where it interacts directly with the Pol III transcription machinery, leading to transcriptional repression [5]
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