| Aspect | Key finding | Evidence type | Experimental details/conditions | Quantitative data | Source (first author year journal) | DOI/URL |
|---|---|---|---|---|---|---|
| Identity | ORF SPCC1919.01, previously named **Ppk34**, was identified as a second **CaMKK-family** kinase in *S. pombe* and renamed **Ckk2**; it is most similar to mammalian CaMKK2 and also related to Ssp1. (pqac-00000011, pqac-00000019, pqac-00000025) | Sequence comparison, genetic | BLAST/sequence comparison in Ca2+-signaling study; compared with human CaMKK1/2 and Ssp1. (pqac-00000025) | Ckk2 similarity: **34% identity** to human CaMKK2, **32%** to Ssp1, **28%** to human CaMKK1; coverages **86%**, **63%**, **52%**, respectively. (pqac-00000025) | Cisneros-Barroso 2014 *Nucleic Acids Research* | https://doi.org/10.1093/nar/gku684 |
| Molecular function | Ppk34/Ckk2 functions as an upstream **serine/threonine kinase** in a CaMKK-like role, activating downstream kinases in stress signaling rather than being merely an uncharacterized kinase. (pqac-00000006, pqac-00000019) | Genetic, biochemical inference | Ca2+ response assays and pathway analysis place Ckk2 upstream of Cmk1; nitrogen-stress assays place Ppk34 upstream of AMPK/Ssp2 activation. (pqac-00000003, pqac-00000019) | No direct catalytic constants reported for Ppk34/Ckk2 itself in retrieved sources. (pqac-00000003, pqac-00000019) | Cisneros-Barroso 2014 *Nucleic Acids Research*; Davie 2015 *Current Biology* | https://doi.org/10.1093/nar/gku684; https://doi.org/10.1016/j.cub.2014.12.034 |
| Substrates | In the **Ca2+ pathway**, Ckk2/Ppk34 is required for **Cmk1 phosphorylation/activation**; in the **nitrogen-stress pathway**, Ppk34 is required for the increase in **AMPKα/Ssp2 Thr189 phosphorylation**. (pqac-00000019, pqac-00000021) | Biochemical, genetic | For Cmk1: CaCl2 treatment and mobility-shift assays in wt vs Δckk2. For Ssp2: glutamate→proline shift, western blot with anti-phospho-AMPK antibody in wt vs ppk34Δ. (pqac-00000021, pqac-00000025) | AMPK/Ssp2 Thr189 phosphorylation increased **~2.5-fold after 30 min** nitrogen stress in wt; this increase was absent in **ppk34Δ**. (pqac-00000021) | Davie 2015 *Current Biology*; Cisneros-Barroso 2014 *Nucleic Acids Research* | https://doi.org/10.1016/j.cub.2014.12.034; https://doi.org/10.1093/nar/gku684 |
| Pathways | Ppk34/Ckk2 participates in at least **two distinct signaling modules**: **Ckk2→Cmk1→Prz1/Cdc25** in Ca2+ signaling and **Ppk34→Ssp2/AMPK→TORC1 inhibition** during nitrogen stress. (pqac-00000005, pqac-00000006, pqac-00000019) | Genetic, biochemical, review | Ca2+ stress: 100 mM CaCl2 time courses and mutant analysis. Nitrogen stress: shift from glutamate to proline and TORC1 readouts/Maf1 phosphorylation/rapamycin rescue. Review literature summarizes this axis in yeast physiology. (pqac-00000020, pqac-00000021, pqac-00000027) | Nitrogen stress activates Ssp2 and inhibits TORC1; rapamycin rescues the ppk34Δ mitotic-entry defect. (pqac-00000021) | Davie 2015 *Current Biology*; Cisneros-Barroso 2014 *Nucleic Acids Research*; Alao 2023 *Cells* | https://doi.org/10.1016/j.cub.2014.12.034; https://doi.org/10.1093/nar/gku684; https://doi.org/10.3390/cells12040519 |
| Localization | Retrieved primary papers support **cytosolic signaling function** for the Ckk2/Cmk1/Prz1 module but do **not provide a direct subcellular localization experiment for Ppk34/Ckk2 itself**. (pqac-00000006, pqac-00000025) | Inference from pathway model | Model places calcineurin, Ckk2, and Cmk1 as Ca2+-responsive cytosolic cascades acting on Prz1 nuclear shuttling; no direct GFP-localization of Ckk2 reported in retrieved excerpts. (pqac-00000006, pqac-00000025) | No direct localization percentages or compartment-enrichment values reported. (pqac-00000006, pqac-00000025) | Cisneros-Barroso 2014 *Nucleic Acids Research* | https://doi.org/10.1093/nar/gku684 |
| Phenotypes | **ppk34Δ/ckk2Δ is viable** and was initially unassigned functionally in the systematic kinase-deletion set, but later screens and mechanistic work linked it to polarity and stress signaling. (pqac-00000000, pqac-00000001, pqac-00000019) | Deletion screen, genetic | Genome-wide kinase deletion study; NETO/polarity screen; Ca2+ sensitivity and nitrogen-stress mitotic-entry assays. (pqac-00000000, pqac-00000001, pqac-00000021) | Among 106 kinases analyzed, **17 essential** and **89 dispensable**; Ppk34 was among viable deletions. (pqac-00000000) | Bimbó 2005 *Eukaryotic Cell*; Koyano 2010 *Bioscience, Biotechnology, and Biochemistry*; Cisneros-Barroso 2014 *Nucleic Acids Research* | https://doi.org/10.1128/ec.4.4.799-813.2005; https://doi.org/10.1271/bbb.100223; https://doi.org/10.1093/nar/gku684 |
| Phenotypes | In a growth-polarity screen, **ppk34 deletion increased bipolar growth**, identifying Ppk34 as a putative **negative regulator of NETO**. (pqac-00000001, pqac-00000026) | Genetic screen | Quantified monopolar/bipolar/septated cells at 25°C and 36°C in kinase-deletion strains. (pqac-00000001, pqac-00000026) | **25°C:** 39.8% monopolar, 47.1% bipolar, 13.1% septated; **36°C:** 31.9% monopolar, 55.9% bipolar, 12.2% septated. (pqac-00000001) | Koyano 2010 *Bioscience, Biotechnology, and Biochemistry* | https://doi.org/10.1271/bbb.100223 |
| Phenotypes | In **Ca2+ stress**, **Δckk2** and **Δcmk1 Δckk2** are **Ca2+-resistant**, similar to **Δcmk1**, supporting that Ckk2 and Cmk1 act in the same pathway. (pqac-00000019, pqac-00000025) | Genetic | Spot assays on YES plates containing CaCl2; comparison of wt, Δcmk1, Δckk2, and double mutant. (pqac-00000025) | Resistance phenotype observed on plates with **50–75 mM CaCl2** and with **100 mM CaCl2** in signaling assays. (pqac-00000024, pqac-00000025) | Cisneros-Barroso 2014 *Nucleic Acids Research* | https://doi.org/10.1093/nar/gku684 |
| Phenotypes | In **nitrogen stress**, **ppk34Δ** fails to **accelerate mitosis** and does not reduce cell size at division to the same extent as wild type; **rapamycin rescues** this defect, placing Ppk34 upstream of TORC1. (pqac-00000003, pqac-00000021) | Genetic, pharmacological | Early exponential cultures shifted from glutamate to proline; mutants analyzed for mitotic-entry timing and response to rapamycin. (pqac-00000021) | Qualitative rescue by rapamycin reported; no exact rescue percentage given in retrieved excerpt. (pqac-00000021) | Davie 2015 *Current Biology* | https://doi.org/10.1016/j.cub.2014.12.034 |
| Quantitative stats | Ppk34 specifically controls **stress-induced** AMPK activation, whereas **Ssp1** is required for **basal** Ssp2 Thr189 phosphorylation; thus the two CaMKK-like kinases show **nonredundant specificity**. (pqac-00000021, pqac-00000027) | Biochemical, genetic, review | wt, ssp1Δ, and ppk34Δ compared under steady-state and nitrogen-stress conditions; phospho-specific westerns and Phos-tag gels used. (pqac-00000021) | **ppk34Δ:** basal Thr189 phosphorylation retained, but no stress-induced increase; **ssp1Δ:** Thr189 phosphorylation absent even basally. (pqac-00000021) | Davie 2015 *Current Biology*; Alao 2023 *Cells* | https://doi.org/10.1016/j.cub.2014.12.034; https://doi.org/10.3390/cells12040519 |
| Quantitative stats | AMPK activation by nitrogen stress in *S. pombe* can occur **without the AMPK β and γ subunits**, highlighting an unusual activation mode in which Ppk34 contributes to α-subunit activation. (pqac-00000005, pqac-00000020, pqac-00000027) | Biochemical, genetic, review | amk2Δ, cbs2Δ, and double mutants assayed after glutamate→proline shift; Ssp2 T189 phosphorylation and mitotic response monitored. (pqac-00000020, pqac-00000027) | β/γ subunits not essential for mitotic advancement under nitrogen stress; wt Ssp2 T189 phosphorylation rises **~2.5-fold** after 30 min. (pqac-00000021) | Davie 2015 *Current Biology*; Alao 2023 *Cells* | https://doi.org/10.1016/j.cub.2014.12.034; https://doi.org/10.3390/cells12040519 |
| Current understanding / gap | Recent authoritative review literature continues to place S. pombe Ppk34/Ckk2 within the **AMPK–TOR stress-response network**, but **2023–2024 primary literature specifically focused on Ppk34/Ckk2 is sparse** in the retrieved corpus. (pqac-00000027) | Review / literature-gap assessment | 2023 review summarizes Ssp1/Ssp2/TOR cross-talk and cites earlier work showing ppk34-related nitrogen-stress signaling. (pqac-00000027) | No new 2023–2024 Ppk34-specific quantitative primary dataset identified in retrieved sources. (pqac-00000027) | Alao 2023 *Cells* | https://doi.org/10.3390/cells12040519 |


*Table: This table compiles the main experimentally supported findings for *S. pombe* Ppk34/Ckk2 (Q9UU87/SPCC1919.01), including identity, pathway placement, phenotypes, and quantitative results. It highlights where direct evidence exists and where current knowledge remains inferential or limited.*