| Quantitative data point | Value | Experimental context | Citation |
|---|---:|---|---|
| Telomere cluster number in untreated cells | ~3–5 foci | Rap1-GFP live-cell imaging of 32 telomeres in haploid cells; baseline telomere clustering at the nuclear periphery | (pqac-00000016, pqac-00000018) |
| Telomere cluster number after edelfosine | ~6–7 foci | Nuclear-envelope lipid perturbation disperses Sir4-associated telomere clusters without abolishing anchoring | (pqac-00000016) |
| Differentially expressed genes after edelfosine | 224 total | RNA-seq after NE deformation by edelfosine | (pqac-00000017) |
| Upregulated vs downregulated genes after edelfosine | 119 up, 105 down | Same RNA-seq dataset; stringent cutoff > ln(2)-fold and FDR p < 0.01 | (pqac-00000017) |
| Subtelomeric fraction among strongly upregulated genes | 12.6% | Genes upregulated >2-fold after edelfosine were enriched in subtelomeric regions | (pqac-00000017) |
| Genome-wide subtelomeric baseline | 4.2% | Background fraction of yeast genes in the same subtelomeric interval | (pqac-00000017) |
| Subtelomeric enrichment significance | p = 0.0001 | Fisher’s exact test for enrichment of subtelomeric genes among edelfosine-upregulated targets | (pqac-00000017) |
| Upregulated genes in the 0–10 kb subtelomeric zone | 29 of 120 genes | Sir2/Sir4-regulated subtelomeric interval queried after edelfosine treatment | (pqac-00000017) |
| PAU-family induction after edelfosine | 2.5 ± 0.49 ln-fold | qPCR validation of known Sir-regulated subtelomeric targets | (pqac-00000017) |
| COS-family induction after edelfosine | 1.5 ± 0.82 ln-fold | qPCR validation of known Sir-regulated subtelomeric targets | (pqac-00000017) |
| Sir4 level drop during prolonged G1 arrest | ~4–5-fold decrease after 5 h | Cell-cycle regulation of Sir4 abundance; de novo heterochromatin establishment studies | (pqac-00000024) |
| Time for Sir4 level recovery after G1 arrest | 2 cell cycles | Recovery of Sir4 protein abundance after release from arrest | (pqac-00000024) |
| De novo silencing assembly time | 1–2 divisions | Full silent chromatin formation/repression requires more than one cell cycle | (pqac-00000023) |
| Silencing weakened by reduced SIR4 dosage | ~2–3-fold reduction in SIR4 dosage | Quantitative buffering analysis identifies Sir4 as the limiting SIR component | (pqac-00000025) |
| Acetyl-mimic threshold for loss of silencing | 50–75% of nucleosomes | H4K16 acetyl-mimic threshold measured for stability of silent chromatin | (pqac-00000025) |
| Acetylation threshold to lose silencing in updated review model | ~75% of nucleosomes | Review synthesis of hysteresis in silent-domain switching | (pqac-00000010, pqac-00000013) |
| Deacetylation threshold to re-establish silencing | >75% unacetylated nucleosomes | Hysteresis model for transition from active to silent state | (pqac-00000010, pqac-00000013) |
| HML silencing loss frequency | ~1 in 1000 cells | Wild-type stability of HM-locus silencing | (pqac-00000010, pqac-00000013) |
| Modeled/observed silencing loss rate at HMR | ~1% | Bistability model with dynamic chromatin compaction and Sir feedback | (pqac-00000019) |
| Drop in establishment rate with larger locus size | ~20-fold decrease | HMR establishment falls as locus expands from 6 to 16 nucleosomes | (pqac-00000019) |
| Silencer-binding nonlinearity threshold | >50% of E-silencer binding loss when nucleosome Sir binding <20% of WT | Cooperative link between nucleosome-bound Sir complex and silencer occupancy | (pqac-00000019, pqac-00000030) |
| Sir4 titration concentration window | ~0–0.4 µM | PNAS 2024 modeling/fit of Sir4 concentration versus bistability coefficient | (pqac-00000029) |
| Scaling factor between estradiol-induced and native Sir4 promoter regimes | ~2-fold | Model–experiment normalization for Sir4 titration/switching analyses | (pqac-00000030) |
| Sir4 H-BRCT affinity for Esc1/Ubp10 phosphopeptides | ~0.07 µM KD | MST measurements of phosphopeptide binding by Sir4 H-BRCT | (pqac-00000026) |
| Alternate reported Sir4 H-BRCT affinity value | 2.96 µM KD | Figure-reported Ubp10-related binding value in Deshpande et al. | (pqac-00000026) |
| Sir4 H-BRCT affinity for Ty5 phosphopeptide | 5.57 µM KD | Weaker phosphopeptide interaction than Esc1/Ubp10 | (pqac-00000026) |
| Sir4 H-BRCT crystal structure resolution | 1.1 Å | Structural definition of the Sir4 phosphopeptide-binding module | (pqac-00000027) |
| Wild-type Sir4 nuclear foci | 4–6 foci per nucleus | Sir4-GFP localization with intact H-BRCT phosphobinding | (pqac-00000026) |
| sir4 RKR mutant nuclear foci | 1–3 foci per nucleus | H-BRCT phosphobinding-defective mutant reduces Sir4 clustering | (pqac-00000026) |
| Nuclear Sir4-GFP reduction in sir4 RKR | ~30% lower | Total nuclear Sir4 signal reduced by H-BRCT phosphobinding mutation | (pqac-00000026) |
| Reduction in Sir4-containing telomere clusters upon isolated H-BRCT overexpression | ~40% reduction | Dominant competition for phospho-interactors disrupts clustering and silencing | (pqac-00000026) |
| Rap1 occupancy density at telomeres | ~1 Rap1 every ~20 bp | Recruitment platform for Sir4 at telomeric repeats | (pqac-00000020) |
| Rap1 molecules per telomere | ~15–20 | Estimated telomere-bound Rap1 copy number supporting Sir4 recruitment | (pqac-00000020) |
| Fraction of total cellular Rap1 at telomeres | ~10% | Indicates strong enrichment of Rap1 at telomeres relative to rest of genome | (pqac-00000020) |
| SIR complex stoichiometry on nucleosomes | 1:1:1 Sir2:Sir3:Sir4 | Telomeric SIR complex composition | (pqac-00000020, pqac-00000021) |
| In vitro SIR:nucleosome stoichiometry in spreading model | 2:1 | Biochemical model for SIR complex engagement with nucleosomes | (pqac-00000022) |
| Distance of SIR spreading from nucleation sites | 3–20 kb | Extent of telomeric heterochromatin spreading | (pqac-00000012, pqac-00000022) |


*Table: This table compiles the main numerical findings relevant to S. cerevisiae Sir4 across localization, silencing, structural binding, and transcriptomic studies. It is useful as a compact evidence map for comparing Sir4 dosage effects, telomere organization, and recent 2023–2024 mechanistic results.*