ArticleGenetics2009
Mcm10 mediates the interaction between DNA replication and silencing machineries.
Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed.
- Maturation-Dependent Constraints in the Ability of Human Monocytes to Initiate Trained Immunity.MedComm · 2026Article
- The tumor suppressor menin is a key scaffold mediator for homologous recombination repair.Nucleic acids research · 2026Article
- Multifaceted role of the DNA replication protein MCM10 in maintaining genome stability and its implication in human diseases.Cancer metastasis reviews · 2024Review
- Modulation of Gene Silencing by Cdc7p via H4 K16 Acetylation and Phosphorylation of Chromatin Assembly Factor CAF-1 inGenetics · 2019Article
- Novel roles of HP1a and Mcm10 in DNA replication, genome maintenance and photoreceptor cell differentiation.Nucleic acids research · 2017Article
- Establishment of expression-state boundaries by Rif1 and Taz1 in fission yeast.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Review
- Xenopus Mcm10 is a CDK-substrate required for replication fork stability.Cell cycle (Georgetown, Tex.) · 2016Article
- Mcm10 is required for oogenesis and early embryogenesis in Drosophila.Mechanisms of development · 2015Article
- Switch on the engine: how the eukaryotic replicative helicase MCM2-7 becomes activated.Chromosoma · 2015Review
- MCM10: one tool for all-Integrity, maintenance and damage control.Seminars in cell & developmental biology · 2014Review
- Drosophila Mcm10 is required for DNA replication and differentiation in the compound eye.PloS one · 2014Article
- Epigenetics in Saccharomyces cerevisiae.Cold Spring Harbor perspectives in biology · 2013Review
- Human SIRT1 regulates DNA binding and stability of the Mcm10 DNA replication factor via deacetylation.Nucleic acids research · 2013Article
- Enigmatic roles of Mcm10 in DNA replication.Trends in biochemical sciences · 2013Review
- Mcm10 associates with the loaded DNA helicase at replication origins and defines a novel step in its activation.The EMBO journal · 2012Article
- Structural biology of replication initiation factor Mcm10.Sub-cellular biochemistry · 2012Review
- Linking DNA replication to heterochromatin silencing and epigenetic inheritance.Acta biochimica et biophysica Sinica · 2012Review
- Multiple functions for Drosophila Mcm10 suggested through analysis of two Mcm10 mutant alleles.Genetics · 2010Article
- Novel DNA binding properties of the Mcm10 protein from Saccharomyces cerevisiae.The Journal of biological chemistry · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The connection between DNA replication and heterochromatic silencing in yeast has been a topic of investigation for >20 years. While early studies showed that silencing requires passage through S phase and implicated several DNA replication factors in silencing, later works showed that silent chromatin could form without DNA replication. In this study we show that members of the replicative helicase (Mcm3 and Mcm7) play a role in silencing and physically interact with the essential silencing factor, Sir2, even in the absence of DNA replication. Another replication factor, Mcm10, mediates the interaction between these replication and silencing proteins via a short C-terminal domain. Mutations in this region of Mcm10 disrupt the interaction between Sir2 and several of the Mcm2-7 proteins. While such mutations caused silencing defects, they did not cause DNA replication defects or affect the association of Sir2 with chromatin. Our findings suggest that Mcm10 is required for the coupling of the replication and silencing machineries to silence chromatin in a context outside of DNA replication beyond the recruitment and spreading of Sir2 on chromatin.
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.