Abstract
The adjustment of transcription and translation rates to the changing needs of cells is of utmost importance for their fitness and survival. We have previously shown that the global transcription rate for RNA polymerase II in budding yeast Saccharomyces cerevisiae is regulated in relation to cell volume. Total mRNA concentration is constant with cell volume since global RNApol II-dependent nascent transcription rate (nTR) also keeps constant but mRNA stability increases with cell size. In this paper, we focus on the case of rRNA and RNA polymerase I. Contrarily to that found for RNA pol II, we detected that RNA polymerase I nTR increases proportionally to genome copies and cell size in polyploid cells. In haploid mutant cells with larger cell sizes, the rDNA repeat copy number rises. By combining mathematical modeling and experimental work with the large-size cln3 strain, we observed that the increasing repeat copy number is based on a feedback mechanism in which Sir2 histone deacetylase homeostatically controls the amplification of rDNA repeats in a volume-dependent manner. This amplification is paralleled with an increase in rRNA nTR, which indicates a control of the RNA pol I synthesis rate by cell volume.
Highlights
Eukaryotic cells have distributed the transcription work in its nuclei among three different RNA polymerases (RNA pol)
We previously found that cells with asymmetric division, such as budding yeasts, use a compensatory change in the global RNA polymerase II synthesis rate and mRNA decay rate to maintain mRNA homeostasis
We address the same issue for the RNA polymerase that makes rRNAs, which are essential components of ribosomes and the most
Summary
Eukaryotic cells have distributed the transcription work in its nuclei among three different RNA polymerases (RNA pol). It would appear that the high SR required for the rRNA synthesis needed during active cell growth and proliferation [7] cannot be achieved only by using RNA pol I at its maximum capacity, and the multiplication of the rDNA gene is necessary This is a slow SR regulation system because the change in the rDNA copy number can be done only during genome replication using an unequal homologous recombination between sister chromatids [6,8,9]. Apart from regulating the rDNA copy number, regulating rRNA synthesis is possible by acting on RNA pol I transcription initiation [14] or elongation (see [15] for a recent review), and by controlling the proportion of active rDNA repeats [16] This last option is feasible because repeats can exist as either silenced chromatin covered by regularly packaged nucleosomal arrays or a transcriptionally active and nucleosome-depleted copy [7,17]. This mechanism is likely to be slow as the change between chromatin states requires the passage of the replication fork through rRNA genes to reset nucleosome assembly [18]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
