ArticleMolecular biology of the cell2000
Role for the silencing protein Dot1 in meiotic checkpoint control.
Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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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.
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Who cites it
91 citing papers in PubMed, 177 citations in OpenAlex.
- Separable downmodulation of meiotic axis protein deposition and DNA break induction at chromosome ends.eLife · 2026Article
- Role of microRNAs in cisplatin response of cancer stem cells.Stem cell research & therapy · 2026Review
- Discovery of the first-in-class DOT1L PROTAC degrader.European journal of medicinal chemistry · 2025Article
- Transcriptional Reprogramming ofJournal of fungi (Basel, Switzerland) · 2023Article
- Exportin-mediated nucleocytoplasmic transport maintains Pch2 homeostasis during meiosis.PLoS genetics · 2023Article
- The DOT1L-MLLT10 complex regulates male fertility and promotes histone removal during spermiogenesis.Development (Cambridge, England) · 2023Article
- Histone methyltransferase DOT1L is essential for self-renewal of germline stem cells.Genes & development · 2022Article
- Article
- Ready, SET, Go: Post-translational regulation of the histone lysine methylation network in budding yeast.The Journal of biological chemistry · 2021Review
- Getting there: understanding the chromosomal recruitment of the AAA+ ATPase Pch2/TRIP13 during meiosis.Current genetics · 2021Review
- Pch2 orchestrates the meiotic recombination checkpoint from the cytoplasm.PLoS genetics · 2021Article
- SUMO is a pervasive regulator of meiosis.eLife · 2021Article
- Maternal DOT1L is dispensable for mouse development.Scientific reports · 2020Article
- DOT-1.1-dependent H3K79 methylation promotes normal meiotic progression and meiotic checkpoint function in C. elegans.PLoS genetics · 2020Article
- Active transcription and Orc1 drive chromatin association of the AAA+ ATPase Pch2 during meiotic G2/prophase.PLoS genetics · 2020Article
- Therapeutic strategies against hDOT1L as a potential drug target in MLL-rearranged leukemias.Clinical epigenetics · 2020Review
- The Role ofJBMR plus · 2020Article
- Distinct Functions in Regulation of Meiotic Crossovers for DNA Damage Response Clamp Loader Rad24(Rad17) and Mec1(ATR) Kinase.Genetics · 2019Article
- Characterization of Pch2 localization determinants reveals a nucleolar-independent role in the meiotic recombination checkpoint.Chromosoma · 2019Article
- Matrix Hyaluronan-CD44 Interaction Activates MicroRNA and LncRNA Signaling Associated With Chemoresistance, Invasion, and Tumor Progression.Frontiers in oncology · 2019Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
During the meiotic cell cycle, a surveillance mechanism called the "pachytene checkpoint" ensures proper chromosome segregation by preventing meiotic progression when recombination and chromosome synapsis are defective. The silencing protein Dot1 (also known as Pch1) is required for checkpoint-mediated pachytene arrest of the zip1 and dmc1 mutants of Saccharomyces cerevisiae. In the absence of DOT1, the zip1 and dmc1 mutants inappropriately progress through meiosis, generating inviable meiotic products. Other components of the pachytene checkpoint include the nucleolar protein Pch2 and the heterochromatin component Sir2. In dot1, disruption of the checkpoint correlates with the loss of concentration of Pch2 and Sir2 in the nucleolus. In addition to its checkpoint function, Dot1 blocks the repair of meiotic double-strand breaks by a Rad54-dependent pathway of recombination between sister chromatids. In vegetative cells, mutation of DOT1 results in delocalization of Sir3 from telomeres, accounting for the impaired telomeric silencing in dot1.
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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.