Sid2 is the NDR/LATS-family Ser/Thr protein kinase that is the most downstream
effector of the Septation Initiation Network (SIN) in S. pombe. With regulatory
subunit Mob1 it forms the Sid2-Mob1 complex, localizes to the SPB throughout the
cell cycle, and translocates transiently to the cell-division site/contractile
ring at the end of anaphase to trigger ring constriction and septum formation.
The source-aware wrapper refresh retained 48 review entries from 59 GOA rows and
backfilled 16 source-entity fields. All 22 cited publications were available through
just fetch-gene-pmids SCHPO sid2. The earlier claim that PMID:23087209 was uncached
is incorrect: its full text establishes Sid2 phosphorylation of Klp2 and associated
phenotypes. The original study reports slower spindle elongation in sid2-250 cells
and connects SIN inhibition of Klp2 to nuclear positioning when cytokinesis is delayed
PMID:23087209
PMID:23087209.
Klp2 S113/S123 phosphorylation inhibits its Mal3-dependent microtubule association;
postanaphase-array microtubules provide an additional positioning mechanism. The
nuclear-positioning dependence should not be generalized to every normal division.
Both formerly UNDECIDED process annotations are now ACCEPT.
Localization requires reporter and cell-cycle context. The original Sid2-GFP SPB
observations do not establish constitutive SPB residence of untagged Sid2:
PMID:22684255
PMID:22684255.
The core summary now includes the cytoplasmic G2 Sid2-Fin1 mechanism and the
Klp2 mechanism. The high-throughput localization study used YFP, not GFP.
The serine-kinase annotation now cites the substrate-specific original assay:
PMID:18951025.
The Mob1 and Pab1 IPI interactions remain biologically supported, but the Mob1
protein-binding row is removed as too generic and the Pab1 row is modified to
the more informative protein phosphatase 2A binding term. The broad
regulation-of-cell-cycle-process annotation is KEEP_AS_NON_CORE; its breadth
alone does not make it false, but more specific terms capture Sid2's core
outputs. For PMID:25501814, the abstract's SPB statement names Cdc7,
so it is no longer presented as a Sid2 imaging experiment; retain the curated Sid2
locations with independent localization evidence and explicit assay-level limits.
The associated PTHR24356 review now records five IBA assertions, removes donor-count
and UniProt-namespace arguments, and retains only the target-specific SIN/mitotic-exit
functional concern. The GO:0007096 ancestral assertion cites CGD:CAL0000197161, not a
verified S. cerevisiae Dbf2 source. Cached PAINT assertion identities were checked by
an independent reviewer; the tree/MSA placement was not independently reassessed.
Reproducible PAINT provenance: interpro/panther/PTHR24356/PTHR24356-paint.tsv
(IBD assertions/sources), PTHR24356-entries.csv in the same folder (Q09898
family/subfamily membership), and interpro/panther/panther.obo (official labels).
The independent reviewer checked the final gene/family diff and found no remaining
scientific blocker after clarifying the late-mitotic timing in the description.
The supported Falcon wrapper completed a 477-second literature refresh and saved
its report and one artifact. The report corroborates Sid2's SIN kinase,
Cdc11-feedback and Mid1/cytokinesis functions, but repeatedly misnames Sog2 as Sog1
(compare PMID:23394829). Its limited retrieval for Clp1, Klp2, Fin1 and Nak1 does
not supersede the available primary evidence. Fin1 activation occurs through a
cytoplasmic G2 Sid2-Mob1 pool independently of other known SIN components
(PMID:22684255); Klp2 phosphorylation supports anaphase spindle elongation and
nuclear positioning during delayed cytokinesis (PMID:23087209). The report's broad
mitotic-exit phrasing is not additional support for the disputed IBA process.
An independent reviewer checked the report against the cached primary sources.
No additional GO terms were adopted solely from this report; provider output is
preserved unmodified, with these corrections recorded here.
Final validation passes with one advisory: annotation decisions cite primary studies
rather than the available generated research file. Status is DRAFT to reflect this
warning; all 48 annotations are reviewed.