| Claim/annotation | Evidence type | Key experimental details (strain/condition/assay) | Quantitative/statistical data | Primary source (authors year journal) | DOI URL |
|---|---|---|---|---|---|
| Phd1 is a transcription factor and a master regulator of filamentous differentiation in *S. cerevisiae* | Genetics; regulatory analysis | Primary study summarized Phd1 as regulating expression of most other differentiation TFs; overproduction induced filamentation; evidence integrated with nitrogen-starvation differentiation assays (pqac-00000001, pqac-00000004) | Overexpression sufficient to induce filamentation; no exact fold reported in gathered evidence (pqac-00000001, pqac-00000004) | Raithatha et al. 2012, *Molecular and Cellular Biology* (pqac-00000001, pqac-00000004) | https://doi.org/10.1128/MCB.05420-11 |
| Primary molecular function is transcriptional regulation of pseudohyphal/invasive growth programs rather than enzymatic catalysis | Genetics; phenotype suppression | Overexpression of **PHD1** strongly promoted pseudohyphal growth even on nitrogen-rich medium and could suppress pseudohyphal defects of **tpk2** and **ste12** mutants (pqac-00000006) | Strong pseudohyphal growth on rich medium upon overexpression; **phd1/phd1** mutants alone showed no obvious pseudohyphal defect in that assay (pqac-00000006) | Pan & Heitman 2000, *Molecular and Cellular Biology* (pqac-00000006) | https://doi.org/10.1128/MCB.20.22.8364-8372.2000 |
| Phd1 positively regulates **FLO11/MUC1**, a key cell-surface flocculin required for filamentation/invasion | Genetics; transcriptional cascade | Genome-array/Northern analyses in **sok2/sok2** hyperfilamentous mutants placed **PHD1** in a cascade with Ash1 controlling **FLO11** expression and cell-cell adhesion (pqac-00000006); review synthesis places Phd1 in Sok2→Phd1/Ash1/Swi5→FLO11 regulation (pqac-00000007) | In **sok2** background, Phd1 and Ash1 were largely required for filamentation; exact expression fold not given in gathered excerpts (pqac-00000006, pqac-00000007) | Pan & Heitman 2000, *MCB*; Kumar 2021, *Annual Review of Genetics* (pqac-00000006, pqac-00000007) | https://doi.org/10.1128/MCB.20.22.8364-8372.2000; https://doi.org/10.1146/annurev-genet-071719-020249 |
| Phd1 functions in pseudohyphal growth and haploid invasive growth pathways | Genetics; phenotypic analysis | Ste12 and **PHD1** were required for haploid invasive growth; PHD1 induction/stabilization tracked with nitrogen starvation, a canonical pseudohyphal trigger (pqac-00000000, pqac-00000001) | Nitrogen starvation increased PHD1 mRNA and stabilized protein; invasive-growth requirement shown genetically but without exact percentages in gathered text (pqac-00000000, pqac-00000001) | Raithatha et al. 2012, *MCB* (pqac-00000000, pqac-00000001) | https://doi.org/10.1128/MCB.05420-11 |
| Upstream pathway context includes Ras2/cAMP-PKA, MAPK/Kss1, and Snf1; Phd1 acts within or alongside this network | Review synthesis; genetics | Filamentous differentiation broadly regulated by MAPK (Kss1), Ras-cAMP-PKA, and Snf1-AMPK; Sok2 is thought to act downstream of cAMP/PKA, while the Sok2→Phd1/Ash1/Swi5 cascade can regulate **FLO11** independently of direct PKA/MAPK control (pqac-00000001, pqac-00000006, pqac-00000007) | Pathway placement is qualitative in gathered evidence; no direct kinetic constants reported (pqac-00000001, pqac-00000006, pqac-00000007) | Raithatha et al. 2012, *MCB*; Pan & Heitman 2000, *MCB*; Kumar 2021, *Annu Rev Genet* (pqac-00000001, pqac-00000006, pqac-00000007) | https://doi.org/10.1128/MCB.05420-11; https://doi.org/10.1128/MCB.20.22.8364-8372.2000; https://doi.org/10.1146/annurev-genet-071719-020249 |
| PHD1 is directly repressed by Sok2 in rich medium | Genetics; transcriptional regulation | In rich medium, Sok2 acted as a negative regulator of filamentation and directly/indirectly repressed the transcription-factor cascade including **PHD1**; **PHD1** was induced in **sok2/sok2** hyperfilamentous mutants (pqac-00000000, pqac-00000006) | **PHD1** induction observed in **sok2/sok2** mutants; exact fold change not given in gathered excerpts (pqac-00000000, pqac-00000006) | Pan & Heitman 2000, *MCB*; Raithatha et al. 2012, *MCB* (pqac-00000000, pqac-00000006) | https://doi.org/10.1128/MCB.20.22.8364-8372.2000; https://doi.org/10.1128/MCB.05420-11 |
| PHD1 expression is partially dependent on Ste12, and Ste12 binds the PHD1 promoter in vitro | Promoter binding; genetics | DNase I footprinting/promoter analysis showed Ste12 binds sites on the **PHD1** promoter in vitro; in vivo promoter occupancy also implicated Tec1, Flo8, Sok2, and Phd1 itself (pqac-00000000, pqac-00000003, pqac-00000005) | Qualitative promoter-binding evidence; no occupancy percentages in gathered excerpts (pqac-00000000, pqac-00000003, pqac-00000005) | Raithatha et al. 2012, *MCB* (pqac-00000000, pqac-00000003, pqac-00000005) | https://doi.org/10.1128/MCB.05420-11 |
| Phd1 positively autoregulates its own expression under nitrogen limitation | Promoter binding; regulatory model | Promoter occupancy and regulatory model indicate Phd1 can bind/activate its own promoter, forming a positive-feedback loop during differentiation (pqac-00000000, pqac-00000003) | Positive feedback described qualitatively; no exact fold increase reported in gathered excerpts (pqac-00000000, pqac-00000003) | Raithatha et al. 2012, *MCB* (pqac-00000000, pqac-00000003) | https://doi.org/10.1128/MCB.05420-11 |
| Cdk8 negatively regulates Phd1 by phosphorylation-dependent destabilization | Protein stability assay; in vitro kinase/phosphopeptide analysis | Cycloheximide-chase, 32Pi metabolic labeling, immunoprecipitation, in vitro kinase assays, and phosphopeptide analysis showed Cdk8-dependent phosphorylation promotes Phd1 degradation (pqac-00000001, pqac-00000004, pqac-00000005) | Phd1 half-life was reported as ~10–15 min in wild type/rich medium and >45 min in **cdk8Δ** cells (pqac-00000001, pqac-00000003, pqac-00000005) | Raithatha et al. 2012, *MCB* (pqac-00000001, pqac-00000003, pqac-00000005) | https://doi.org/10.1128/MCB.05420-11 |
| Natural polymorphism at the Cdk8 phosphosite stabilizes Phd1 and enhances filamentation | Protein stability assay; allele comparison | Comparison of PHD1 alleles (S92 versus S92F) showed that the 1278b strain carries S92F, removing a Cdk8 phosphorylation site and stabilizing Phd1 (pqac-00000001, pqac-00000003, pqac-00000004) | Wild-type S92 Phd1 half-life ~15 min in rich medium; stabilized variant and/or **cdk8Δ** backgrounds showed >45 min stability (pqac-00000003, pqac-00000004) | Raithatha et al. 2012, *MCB* (pqac-00000001, pqac-00000003, pqac-00000004) | https://doi.org/10.1128/MCB.05420-11 |
| Nitrogen starvation stabilizes Phd1 protein and increases PHD1 transcript, promoting differentiation | Protein stability assay; transcript analysis | Cells shifted to SLAD/nitrogen-limiting medium showed increased **PHD1** mRNA and marked stabilization of Phd1 protein; model proposes loss of Cdk8 activity under these conditions (pqac-00000000, pqac-00000001, pqac-00000003, pqac-00000009) | Half-life increased from ~15 min in SD to ~40 min after 2 h in SLAD and >45 min after 4 h in SLAD (pqac-00000003, pqac-00000009) | Raithatha et al. 2012, *MCB* (pqac-00000000, pqac-00000001, pqac-00000003, pqac-00000009) | https://doi.org/10.1128/MCB.05420-11 |
| Forced expression of PHD1 is sufficient to induce pseudohyphal growth synthetically, even in rich media and in haploids | Synthetic induction | Synthetic gene-regulation circuits controlling native **PHD1** and **FLO8** expression triggered pseudohyphal growth in diploid and haploid cells in rich media; used as an engineered, externally inducible differentiation system (pqac-00000002) | Phenotype induction in both diploid and haploid strains under non-starvation conditions; exact percentages not given in gathered excerpt (pqac-00000002) | Pothoulakis & Ellis 2018, *Communications Biology* (pqac-00000002) | https://doi.org/10.1038/s42003-017-0008-0 |
| Recent 2024 colony-morphology data support association of PHD1 expression with structured colony regions, but deletion may be background-dependent and nonessential in F13 | RNA-seq/cluster; deletion phenotype | In structured-colony strain F13, **PHD1/YKL043W** clustered with genes whose expression correlated positively with colony structure (cluster I9); however, **phd1Δ** retained central smooth plus outer structured zones at day 5, unlike **flo11Δ** or **msb2Δ** (pqac-00000008) | **phd1Δ** had little effect on F13 morphology, whereas **flo11Δ** and **msb2Δ** remained fully smooth at day 5 (pqac-00000008) | Cromie et al. 2024, *PLOS ONE* (pqac-00000008) | https://doi.org/10.1371/journal.pone.0311061 |
| Subcellular localization is expected to be nuclear for a transcription factor, but no direct Phd1 localization evidence was identified in the gathered sources | Evidence gap / inference | Gathered primary and review sources discuss Phd1 as a transcription factor regulating promoters and differentiation programs, but none of the retrieved evidence IDs reported direct GFP/immunolocalization for Phd1 (pqac-00000000, pqac-00000006) | No direct localization measurement available in gathered evidence (pqac-00000000, pqac-00000006) | Evidence gap within retrieved literature (pqac-00000000, pqac-00000006) | N/A |


*Table: This table summarizes experimentally supported functional annotations for Saccharomyces cerevisiae PHD1/Phd1 using only the gathered evidence contexts. It highlights molecular function, pathway placement, regulatory inputs, phenotypes, and the current evidence gap for direct localization data.*