igo1 curation notes

2026-09-27 Initial review (P79058, SPAC10F6.16, igo1 / mug134)

Inputs

Gene identity

Holistic picture

  1. Core function: Ppk18-phosphorylated PP2A-B55 (Pab1) inhibitor that couples
    nitrogen status to G2/M size control.     [PMID:26776736 "Here we show that the
    greatwall-endosulfine (Ppk18-Igo1 in fission yeast) pathway couples the
    nutritional environment to the cell-cycle machinery by regulating the
    activity of PP2A·B55."; "When nutrients are limiting, TORC1 activity falls
    off, and the activation of greatwall (Ppk18) leads to the phosphorylation of
    endosulfine (Igo1) and inhibition of PP2A·B55, which in turn allows full
    activation of Cdk1·CyclinB and entry into mitosis with a smaller cell size."].
    Falcon adds the Ser64 site, the elevated PP2A-B55 activity in igo1Δ and the
    pab1 epistasis [file:igo1-deep-research-falcon.md "Loss of igo1 causes
    abnormally high PP2A-B55 activity under nitrogen-poor or nitrogen-free
    conditions, while genetically reducing PP2A-B55 can rescue multiple igo1Δ
    phenotypes."]. Ser64 phosphorylation is detected in vivo with a P-ENSA
    antibody on nitrogen starvation or tor2-51 inactivation (Martin 2017, Fig S4;
    online full text). GO:0004865 IDA, GO:1905287 IMP and GO:0035556 IMP all
    ACCEPT; GO:0004864 IBA ACCEPT (igo1 in its own WITH/FROM is expected).
  2. Nutrient relay to differentiation (Laboucarie 2017, online full text).
    "Therefore, starvation induces the phosphorylation of Igo1‐Ser64, most likely
    through the Ppk18 kinase, and this pathway is required to promote
    differentiation"; ste11+/mei2+ induction and differentiated-cell counts are
    reduced in ppk18Δ, igo1Δ and igo1-S64A; "gcn5 Δ and pab1 Δ mutants suppress the
    sterility of ppk18 Δ and igo1‐S64A mutants (Appendix Fig S8)"; "Taf12
    phosphorylation is reduced in starved ppk18 Δ, igo1 Δ, and igo1‐S64A mutants";
    "the absence of PP2A‐Pab1 rescues the inability of igo1‐S64A mutants to
    induce Taf12 phosphorylation". Cached abstract only gives the framework
    PMID:29079657. Martin 2017
    (online): igo1Δ blocks Gad8 Ser546 phosphorylation and mei2 induction on
    tor2-51 TORC1 inactivation; constitutively active ryh1QL (TORC2 activator)
    rescues mei2 expression in tor2-51 igo1Δ. GO:0031139 IGI (with pab1,
    SPAC227.07c) ACCEPT and made the second core function, as for ppk18.
  3. Quiescence entry / translation (del Dedo 2024, online full text; Falcon).
    "elevated PP2A/B55 phosphatase activity, resulting from the deletion of
    Endosulfine (igo1∆), impairs the translation efficiency of mRNAs enriched in
    AAA codons during entry into quiescence"; igo1Δ loses Rap1, Sgo2, Clr2/Clr3,
    telomere attachment and subtelomeric silencing after nitrogen removal, all
    rescued by repressing pab1; reduced mcm5s2U34 and t6A37 tRNA modification;
    paromomycin sensitivity; partial rescue by gsk3Δ [file:igo1-deep-research-
    falcon.md "In igo1Δ cells, polysome-to-monosome ratios were 78% of wild
    type in nitrogen-rich medium     and only 27% after four hours of
    starvation    ."]. Autophagy: [file:igo1-deep-research-falcon.md "Igo1 loss
    also reduces autophagic flux, and deletion of the PP2A catalytic subunit gene
    ppa2 rescues this defect."]. None of this is in GOA. Not proposed as NEW:
    the work of translation/tRNA modification is done by Elongator, Ctu1, Trm112
    and TORC2-Gad8 downstream; Igo1's contribution is entirely through PP2A-B55
    inhibition, which is already captured. Folded into the narrative of core
    function 2.
  4. Sds23 genetic interaction (full text cached). PMID:31553675; double
    mutants more bent and larger at division, but for division symmetry "the
    double mutants were not significantly different from sds23∆ alone despite
    this trend (Figure 5E)". GO:1902472 IGI -> MARK_AS_OVER_ANNOTATED, same
    grading as the ppk18 review.
  5. Localisation. Only direct datum: ORFeome YFP screen (rich medium),
    cytosol + nucleus PMID:16823372;
    UniProt "SUBCELLULAR LOCATION: Nucleus {ECO:0000269|PubMed:16823372}.
    Cytoplasm". Falcon says it found no direct localisation
    [file:igo1-deep-research-falcon.md "not direct Igo1 microscopy or
    fractionation"] - a retrieval gap, not a contradiction. Laboucarie 2017 used
    Igo1-MYC only for Phos-tag westerns. All four CC rows ACCEPT.
  6. Other phosphosites (Falcon, from the Garcia Blanco 2021 thesis). Cdk1
    sites Ser31/Ser89/Ser102 in vitro and by MS; PKA-consensus Ser76/Ser115;
    Igo1-4A has nutrient-dependent size phenotypes [file:igo1-deep-research-
    falcon.md "Cdk1–Cyclin B phosphorylates Igo1 in vitro."]. Raised as a
    suggested question, not annotated.

NEW-term consideration

Decisions summary

Open items