ArticleMolecular and cellular biology1999
A genetic screen for ribosomal DNA silencing defects identifies multiple DNA replication and chromatin-modulating factors.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
124 citing papers in PubMed, 225 citations in OpenAlex.
- The histone chaperone CAF-1 prevents homologous recombination-mediated instability of the budding yeast ribosomal DNA during replication-coupled DNA double-strand break repair.Nucleic acids research · 2025Article
- Interpreting the Origins and Functions of Noncoding RNAs From the Ribosomal Genes.Journal of cellular physiology · 2025Review
- Psoralen Crosslinking-Chromatin Endogenous Cleavage Assay to Examine Histone DNA Interactions of Active and Inactive rRNA Genes.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Heterochromatin in plant meiosis.Nucleus (Austin, Tex.) · 2024Review
- Acidic growth conditions stabilize the ribosomal RNA gene cluster and extend lifespan through noncoding transcription repression.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Chromatin assembly factor-1 preserves genome stability inCell stress · 2023Article
- Diverse and dynamic forms of gene regulation by the S. cerevisiae histone methyltransferase Set1.Current genetics · 2023Review
- Fob1-dependent condensin recruitment and loop extrusion on yeast chromosome III.PLoS genetics · 2023Article
- DNA polymerase epsilon interacts with SUVH2/9 to repress the expression of genes associated with meiotic DSB hotspot inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Rpd3 regulates single-copy origins independently of the rDNA array by opposing Fkh1-mediated origin stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Analysis of the long-read sequencing data using computational tools confirms the presence of 5-methylcytosine in theAccess microbiology · 2022Article
- Global genomic instability caused by reduced expression of DNA polymerase ε in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Smc5/6 in the rDNA modulates lifespan independently of Fob1.Aging cell · 2021Article
- Increased numbers of nucleoli in a genome-wide RNAi screen reveal proteins that link the cell cycle to RNA polymerase I transcription.Molecular biology of the cell · 2021Article
- Saccharomyces cerevisiae rDNA as super-hub: the region where replication, transcription and recombination meet.Cellular and molecular life sciences : CMLS · 2020Review
- 53BP1 Supports Immunoglobulin Class Switch Recombination Independently of Its DNA Double-Strand Break End Protection Function.Cell reports · 2019Article
- Analyses of rRNA gene chromatin in cell cycle arrestedData in brief · 2019Article
- Depletion of Limiting rDNA Structural Complexes Triggers Chromosomal Instability and Replicative Aging ofGenetics · 2019Article
- Ribosomal DNA instability and genome adaptability.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019Review
- Rif1 promotes a repressive chromatin state to safeguard against endogenous retrovirus activation.Nucleic acids research · 2017Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Transcriptional silencing in Saccharomyces cerevisiae occurs at several genetic loci, including the ribosomal DNA (rDNA). Silencing at telomeres (telomere position effect [TPE]) and the cryptic mating-type loci (HML and HMR) depends on the silent information regulator genes, SIR1, SIR2, SIR3, and SIR4. However, silencing of polymerase II-transcribed reporter genes integrated within the rDNA locus (rDNA silencing) requires only SIR2. The mechanism of rDNA silencing is therefore distinct from TPE and HM silencing. Few genes other than SIR2 have so far been linked to the rDNA silencing process. To identify additional non-Sir factors that affect rDNA silencing, we performed a genetic screen designed to isolate mutations which alter the expression of reporter genes integrated within the rDNA. We isolated two classes of mutants: those with a loss of rDNA silencing (lrs) phenotype and those with an increased rDNA silencing (irs) phenotype. Using transposon mutagenesis, lrs mutants were found in 11 different genes, and irs mutants were found in 22 different genes. Surprisingly, we did not isolate any genes involved in rRNA transcription. Instead, multiple genes associated with DNA replication and modulation of chromatin structure were isolated. We describe these two gene classes, and two previously uncharacterized genes, LRS4 and IRS4. Further characterization of the lrs and irs mutants revealed that many had alterations in rDNA chromatin structure. Several lrs mutants, including those in the cdc17 and rfc1 genes, caused lengthened telomeres, consistent with the hypothesis that telomere length modulates rDNA silencing. Mutations in the HDB (RPD3) histone deacetylase complex paradoxically increased rDNA silencing by a SIR2-dependent, SIR3-independent mechanism. Mutations in rpd3 also restored mating competence selectively to sir3Delta MATalpha strains, suggesting restoration of silencing at HMR in a sir3 mutant background.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.