| Paper | Publication date | Main Sir4-related finding | Quantitative data | URL / DOI | Evidence |
|---|---|---|---|---|---|
| Dhillon & Kamakaka 2024, *Epigenetics & Chromatin* | Sep 2024 | Updated review/model: Sir4 acts within multivalent Sir–nucleosome networks that stabilize silent domains despite flux; Sir-mediated silencing is probabilistic and domain-wide rather than a rigid static block. | Silent-state hysteresis at HM loci requires ~75% nucleosome acetylation to lose silencing and >75% unacetylated histones to re-establish it; HML silencing loss occurs in ~1/1000 cells in wild type. | https://doi.org/10.1186/s13072-024-00553-7 | (pqac-00000010, pqac-00000013) |
| Yuan & Moazed 2024, *PNAS* | Jan 2024 | Engineered epigenetic inheritance system leverages the native Sir3–Sir4/Sir2 interaction logic, highlighting how reduced-complexity silent chromatin can be built from positive-feedback design principles derived from the SIR system. | Study is conceptually quantitative but the retrieved excerpt mainly supports that Sir3 naturally interacts with Sir2-bound Sir4; no Sir4-specific numerical metric extracted in the available text. | https://doi.org/10.1073/pnas.2318455121 | (pqac-00000000) |
| Ponce et al. 2023, *Journal of Cell Biology* | Jan 2023 | Nuclear-envelope lipid perturbation by edelfosine disperses Sir4 from telomeres without abolishing telomere anchoring, linking membrane state to Sir4-dependent telomere silencing/clustering. | Rap1 telomere foci increased from ~3–5 to ~6–7 after edelfosine; Sir4 ChIP recovery decreased at three tested telomeres; 224 genes were differentially expressed (119 up, 105 down); 12.6% of >2-fold upregulated genes were subtelomeric vs 4.2% genome-wide; 29/120 genes in the 0–10 kb subtelomeric zone were upregulated; PAU and COS expression increased by 2.5 ± 0.49 and 1.5 ± 0.82 ln-fold, respectively. | https://doi.org/10.1101/2022.07.08.499406 | (pqac-00000016, pqac-00000017) |
| Bondra & Rine 2023, *PNAS* | Sep 2023 | Context-specific silencing analysis of Rap1 reinforces the importance of Rap1-dependent Sir4 recruitment in determining whether promoter-bound Rap1 behaves as an activator or a silencing factor. | No Sir4-specific numerical estimate retrieved from the available excerpts, but the paper narrows silencing to a step after activator recruitment and before productive transcription in Sir-silenced chromatin. | https://doi.org/10.1073/pnas.2304343120 | (pqac-00000002) |
| Miangolarra et al. 2023, *bioRxiv* | Aug 2023 | Modeling plus experiment support two-way cooperativity between silencer occupancy and Sir–nucleosome binding; Sir4 titration experiments support the idea that Sir4 dosage affects occupancy and bistable silencing behavior. | Silencing loss rates were ~1%; silencing establishment dropped ~20-fold when locus size increased from 6 to 16 nucleosomes; more than half of the drop in E-silencer binding occurred when nucleosomal Sir binding fell below 20% of wild type. | https://doi.org/10.1101/2023.08.12.552948 | (pqac-00000006, pqac-00000019) |
| Deshpande et al. 2020, *EMBO Journal* | Sep 2020 | Structural/mechanistic basis for a Sir4 phospho-interaction hub: the H-BRCT region in the PAD binds phosphorylated Esc1/Ubp10/Ty5 peptides and is required for proper Sir4 localization, telomere clustering, and repression. | Sir4 H-BRCT structure solved at 1.1 Å; Kd values included ~0.07 µM for Esc1/Ubp10 phosphopeptides and 5.57 µM for Ty5; sir4 RKR mutants showed 1–3 Sir4 foci per nucleus vs 4–6 in wild type and ~30% lower nuclear Sir4-GFP intensity; overexpressing isolated wt H-BRCT caused ~40% reduction in Sir4-containing telomere clusters and abolished URA3 silencing. | https://doi.org/10.15252/embj.2019101744 | (pqac-00000026, pqac-00000027) |
| Wu et al. 2021, *PNAS* | Dec 2021 | Quantitative buffering analysis identifies Sir4 as the limiting SIR component for silencing robustness, more sensitive to dosage reduction than Sir2 or Sir3. | Reducing SIR4 dosage by ~2–3-fold significantly weakened silencing, whereas similar reductions of Sir2 or Sir3 did not; loss of silencing required 50–75% acetyl-mimic histones. | https://doi.org/10.1073/pnas.2111841118 | (pqac-00000025) |
| Larin et al. 2015, *PLOS Genetics* | Nov 2015 | Sir4 abundance and availability regulate de novo heterochromatin assembly; telomeres compete with HM loci for a limiting Sir4 pool. | Sir4 levels decreased ~4–5-fold after 5 h of alpha-factor G1 arrest and recovered after two cell cycles; de novo silencing required 1–2 divisions; halving Sir4 slowed establishment whereas increased Sir4 accelerated establishment. | https://doi.org/10.1371/journal.pgen.1005425 | (pqac-00000023, pqac-00000024) |


*Table: This table compiles recent and foundational quantitative findings for budding yeast Sir4/SIR4, emphasizing 2023–2024 developments while retaining older landmark studies needed to interpret Sir4 dosage, localization, and silencing mechanisms.*